Category: Metabolic Disorders

This essay examines a research paper, Allometric scaling of maximal metabolic rate in mammals, written by Weibela and Hoppelera. The paper analyzes the existing facts on maximum metabolic rate (MMR) in several mammals (Weibel, Bacigalupe, Schmitt & Hoppeler, 2004). As illustrated in the paper, MMR depicts the rate at which oxygen is consumed by a homoeothermic animals body, when at maximum aerobic output, during maximum exercises. On the other hand, basal metabolic rate (BMR) refers to the lowest energy needed to fulfill an animals daily living needs, calculated when an animal is at rest, fasting and under its normal temperature (Weibel et al, 2004). All through their investigations and findings, the researchers attempt to uncover the papers hypothesis that stated, To determine the factors that influence MMR in mammals.

By examining the existing literature, the researchers noted how aerobic scope varied from one mammal to another. From their research findings, Weibela and Hoppelera confirmed that aerobic scope in large-sized mammals is much higher than in small-sized mammals (Weibel et al, 2004). Similarly, the report illustrated that athletic mammals posses a higher aerobic scope as compared to non- athletic mammals. Weibela and Hoppeleras work indicated that a lot of BMR related researches have been done as compared to MMR related researches. For instance, the report indicates that more than 600 mammal species have been used in the analysis of BMR, while less than 50 mammals species have contributed to the recent knowledge in MMR (Weibel et al, 2004). Through this, Weibela and Hoppelera were able to develop a comprehensive report on the topic.

These research findings did not only rely on other researchers works, but also on their own investigations (Weibel et al, 2004). During the research, many animals were used. To select the best data, the researchers employed the standardized approach used in the estimation of the VO2max. Under this approach, several animals were placed on a treadmill running on varying velocity. Thereafter, VO2max estimation, morph-metric examinations, and psychoanalysis were carried out on the animals (Weibel et al, 2004). Afterwards, the animals were killed, and their lungs replaced with intratracheal installation of glutaraldehyde. It was not long before some of their organs and muscles tissues were removed for further analysis. Using the collected information, the researchers correlated their data with the existing MMR and BMR information (Weibel et al, 2004).

After data correlation, morph-metric analysis was initiated. The animals half bodies were subdivided into several strata. With each stratum, the length, depth and circumference were measured and recorded to represent a three dimensional specimen (Weibel et al, 2004). From then on, the remaining animals half bodies were dissected and weighed. The weights were labeled Mm to represent approximations of the weighed carcasses. Subsequently, approximations of mitochondrial volume densities were evaluated and recorded as biased approximations. Thereafter, the samples were analyzed to obtain their capillary length densities. Finally, the volume densities were evaluated by multiplying capillary circumferences with length densities (Weibel et al, 2004).

From the collected data, the researchers compared their findings with the existing literatures. Out of all the samples, 57 approximations of Vo2max matched with the literature findings (Weibel et al, 2004). The estimates represented the 35 mammalian species selected. The findings were then represented using tables and graphs. With the help of these tables and graphs, scaling of VO2max, muscle capacity and capillary blood supply were deduced. From the findings, researchers confirmed that in mammals MMR scales largely varied with body mass than BMR scales. From the earlier findings, BMR exponents were recorded as 0.75; however, the researchers findings were recorded as 0.872 (Weibel et al, 2004). Similarly, it was observed that the factorial the ratio of MMR and BMR was higher in small mammals than in huge mammals. Reduced factorial ratio in large animals was attributed to their agility.

During the experiment, comprehensive data on Vo2max, functional and structural characteristics of loco-motor muscles were collected (Weibel et al, 2004). The mammals sampled ranged from 20g to 450 kg. The data collected represented the whole muscle mass of the carcasses, which in quadrupeds are active when animals work in MMR. In this range, the scale exponent was found to be 0.96 rather than the usual 0.87 for the entire samples (Weibel et al, 2004). Similarly, the researchers noted that the volume of the mitochondria obtained from the loco-motor musculature, scaled with the same exponent of 0.96. This implies that the total volume of the mitochondria is strictly proportional to the Vo2max for all animals. After evaluation, the researchers evaluated the ratio of VO2max and muscle capillary erythrocyte volume as 4.9 (Weibel et al, 2004). However, it should be noted that the value obtained varied from the standard metabolic capacity of mitochondria. As such, higher values have been obtained in similar experiments by increasing the degree of oxygen supply in the mitochondria. This limitation is attributed to the oxidative phosphorylation process in the mitochondria.

In animals, mitochondria, and capillary blood determine aerobic capacity of muscles. It should be noted that their proportions vary directly with the maximal metabolic rate an animal can achieve (Weibel et al, 2004). Weibela and Hoppelera generalized their findings on a subset of species with MMR scale of 0.87. Generalization was implemented for several reasons. First, in their findings the scaling components were not statistically different from the entire population. Similarly, the selected subset was evenly distributed over the entire range (Weibel et al, 2004). Equally, in the subset both athletic and non-athletic species were represented. With these, the authors confirmed that scaling of aerobic capacity of loco-motor muscle is directly proportional to Vo2max. Similarly, Weibela and Hoppelera illustrated the relationship between mechanistic explanations and scaling components(Weibel et al, 2004). In the article, the authors findings confirm that in mammals, MMR scales differently with BMR. In the article, the researchers emphasized that there is no prior reason why MMR should scale with BMR (Weibel et al, 2004). However, differences in their performance were attributed to the BMR oxygen and BMR blood flow. In general, the authors explanations clearly relate with the papers hypothesis.

In the papers conclusion, Weibela and Hoppelera acknowledged that their findings failed to indicate how the process relates with vasculature (Weibel et al, 2004). Using Darveaus model, the authors asserted that the approximations of partial scaling on the sequential functions depend on scaling exponents of metabolic rate. In their attempt to expound on this process, the authors examined several body organs analyzed during the examination of MMR and BMR (Weibel et al, 2004). Through this analysis, mechanistic explanations of the scaling of MMR are clearly outlined.

Reference

Weibela, E. R., & Hoppelera, H. (2004). Allometric scaling of maximal metabolic rate in mammals: muscle aerobic capacity as determinant factor. Respiratory Physiology & Neurobiology, 1(1), 18.

Introduction

The biochemical reactions that occur with living cells are all referred to as metabolic reactions. In all organisms, metabolic reactions can either take the form of anabolism or catabolism. Catabolism describes all metabolic reactions in which large molecules are broken down to smaller and in the process, a release of energy occurs (Bhagavan 34). Anabolism on the other hand describes metabolic reactions in which small molecules are joined together to form larger molecules. Anabolic reactions generally require energy to take place. An example of an anabolic reaction is the creation of proteins from amino acids.

In all organisms, metabolic reactions occur in series referred to as metabolic pathways. A metabolic pathway is a series of progressive biochemical reactions utilized by a cell to transform an input substance into an end product (Gropper and Smith 64). The pathways can be cyclic, in which the biochemical reactions reproduce the initial product, or linear, in which reactions produce a different product.

All life forms share the same metabolic pathways. In human beings, the main metabolic pathways include carbohydrate (glycolysis, gluconeogenesis, and glycogen) metabolism, lipid (fatty acid) metabolism, and protein (amino acid) metabolism (Garrett and Grisham 551). If consumed in adequate quantities, any of the three energy-creating nutrients i.e. carbohydrates, proteins, and fat, can avail energy to the body on a short-term basis. The biochemical pathways always occur in one direction and interact in a complex manner to enable ample regulation.

Interaction of Biochemical Pathways

A central array of metabolic pathways exists within all living things. These pathways are responsible for the breakdown of essential nutrients into Adenosine Triphosphate (ATP) and other molecules necessary for the release of energy into the body. As shown in figure 3, all metabolic pathways interact in one form or another during the energy production process. The interrelationships of metabolic pathways take various forms and always result in three junction points: glucose-6-phosphate, Pyruvate, and Acetyl CoA (Stoker 503). The fact that human beings can gain fat on a predominantly carbohydrate diet is evidence that the metabolic pathways interact and that nutrients can be converted from one form to another.

Connections of other sugars to glucose metabolism

In all animals, energy is stored in the glycogen molecule. In situations where the body has ample ATP present, excess glucose is converted into glycogen for storage (Rosenthal and Glew 57). Glycogen is prepared and stored in both the human muscles and the liver. When the blood sugar drops, glycogen monomers are broken down to form glucose. The carbohydrate (glycolytic) pathway occurs when the synthesis of glycogen monomers forms glucose-6-phosphate (G-6-P) which can later provide energy for the human body.

Sucrose, a disaccharide that consists of a fructose molecule plus a glucose molecule is broken down to form both fructose and glucose. Fructose plus galactose and glucose form the three main monosaccharide diets. Galactose is a milk product that is generally absorbed into the bloodstream directly after digestion. Glucose metabolism produces energy by converting glucose into pyruvate. Glycolysis consists of 10 biochemical reactions in which various intermediates act as the entry points for further reactions. The hexokinases enzymes carry out the phosphorylation of glucose to form glucose-6-phosphate. While the reaction utilizes ATP, it also maintains a low glucose concentration thus ensuring that glucose flows into the cell while at the same time blocking glucose from flowing out of the cell (Lee and Bishop 36). While glucose can be absorbed directly after digestion, living tissues can convert other sugars into glucose in the fast phase to provide energy or convert them in the fed state into fat to be stored for future use.

Connections of lipid and glucose metabolism

In metabolic connections, lipids link with glucose pathways through triglycerides and cholesterol. For animals, fat is very important for the storage and subsequent release of energy. All tissues utilize fatty acids as energy storage mechanisms as well as the means of creating cell membranes. The normal human body ingests lipids as triglycerides that are impossible to absorb by the intestines (Gropper and Smith 63). The pancreatic lipase enzyme breaks down these lipid molecules into glycerol and free fatty acids. Triglycerides can be both broken down or created through phases of the glucose metabolism pathways. Glycolysis occurs by the way of the phosphorylation of glycerol into glycerol-3-phosphate. Glycogen from muscles and the liver can feed into the catabolic pathways for carbohydrates (Stoker 545).

The catabolism of lipids occurs through beta-oxidation that occurs in the matrix of mitochondria and changes fatty acids into acetyl groups. Tissues then incorporate these groups into CoA to create Acetyl CoA that continues further into the Krebs cycle.

In certain situations, the body oxidizes carbohydrates to create both the fatty acid and glycerol portions of triacylglycerol (TAG). The transformation of fatty acids into carbohydrates is however impossible as the dehydrogenase reaction of pyruvate goes in one direction and is irreversible.

Connections of Proteins to Glucose Metabolism

The hydrolysis of proteins in human cells occurs through a variety of enzymes. Generally, tissues synthesize amino acids into new proteins when needed. However, if the body is starving, or in a situation where there are excess amino acids, part of these amino acids will be pushed into the glucose catabolic pathways (Gropper and Smith 251). Before an amino acid enters the glucose metabolic pathway, its amino group is detached and transformed into ammonia. Amino acids are metabolized into both the ketogenic amino groups and the glucogenic amino groups (Grisham and Garrett 101). Through oxidation, both the ketogenic and non-essential amino acids can indirectly from fatty acids. Carbohydrates can also result from the oxidation of the non-essential glucogenic amino acids.

Fed-Fast Cycle

The fed-fast cycle provides a very concise description of the interrelationship of the different metabolic pathways. During the fed state, glucose is readily available in various tissues and is usually absorbed directly to provide the required energy. In this state, enzymes in the liver convert excess glucose into fatty acids and glycogen (Gropper and Smith 252). The transformation of glucose into fatty acids only takes place when energy use is far lower than the intake.

During the post-absorptive phase, the tissues are unable to obtain energy from consumed glucose and the other nutrients but must rely on other energy sources. During this phase, glycogenolysis occurs in the liver where the synthesis of triacylglycerol and glycogen occurs to maintain the glucose levels in the blood (Grisham and Garrett 761). In the muscles, lactate is stored and released as required and becomes an essential energy source. The amino group alanine from the liver enters the glucose-alanine cycle and glycogenolysis occurs to transform this amino group into pyruvate.

In the fasting state, the hydrolysis of proteins in the muscles to create glucogenic amino acids increases. In this state, amino acids from protein breakdown form the bulk of the substrates needed for gluconeogenesis (Stoker 613). Through lipolysis, glycerol is also a chief provider of energy in this phase. Apart from this, anaerobic metabolism occurs in the muscles to create lactate that also offers a means for energy provision. In this phase, all the macronutrients offer a means of energy through various reactions in the body.

In the starvation phase, the body struggles to conserve essential proteins required for antibodies, hemoglobin, and enzymes. In this phase, fat stores in the body act as the major source of energy. Metabolic reactions shift from gluconeogenesis to lipolysis (Gropper and Smith 258). However, the brain cannot utilize fatty acids as a source of energy as they cannot move across the blood-brain barrier. The brain thus utilizes ketone as its main source of energy during the starvation phase. At this phase, an organism can only continue to exist depending on the amount of fat stored earlier.

Conclusion

Metabolism is a porous reaction in the body in which all metabolic pathways interact to provide the necessary energy required. Carbohydrates, lipids, and amino acids all interact at the three junction points to provide the required molecules needed for energy production. The intersection points are Acetyl CoA, glucose-6-phosphate, and Pyruvate. Carbohydrates, lipids, and amino acids can all provide energy through different processes in the body. The glucose pathway relates to all the other pathways and is a major provider of energy in the body during the fed-fast phase. All living things require energy and share the same metabolic reaction. The three main metabolic reactions interrelate to provide essential energy-providing molecules for any living thing.

References

Bhagavan, Natali. Medical Biochemistry. Malaysia: Academic Press, 2012. Print.

Grisham, Charles and Reginald Garrett. Biochemistry. 5^th ed. Belmont, CA: Brooks/Cole Cengage Learning, 2013. Print.

Gropper, Sareen and Jack Smith. Advanced Nutrition and Human Metabolism. 6^th ed. Belmont, CA: Wadsworth-Cengage Learning, 2012. Print.

Lee, Gary and Penny Bishop. Microbiology and Infection Control for Health Proffessionals. French Forest: Pearson Australia, 2012. Print.

Rosenthal, Miriam and Robert Glew. Medical Biochemistry: Human Metabolism in Health and Diseases. New Jersey, NJ: John Wiley and Sons, 2009. Print.

Stoker, Stephen. Organic and Biological Chemistry. 7^th ed. Boston, MA: Cengage Learning, 2015. Print.

Recent discoveries bring up new insights on the processes by which muscles connect with other organs and modulate the positive effects of physical exertion due to the application of molecular approaches to the biology of physical exercise. Previous studies looked at metabolic responses to exercise and the molecular processes that underpin skeletal muscle adaptation to training. It became apparent that the biology that underpins maximal exercise performance has applications outside of sports. High-intensity exercise causes a large drop in SaO2, which compromises the supply of O2 to contract skeletal muscles and leads to a decline in physical performance in certain well-trained endurance athletes. These modifications help to explain why, following training, activities with any given submaximal intensity of effort result in decreased heart rate and blood pressure. They also lead to a long-term drop in blood pressure following physical activity.

At least in animal models, many adaptive responses of skeletal muscles to training may be replicated via genetic modification and/or pharmacological therapy. Given the multiple health advantages of exercise, the finding of genetic and orally-active medicines that imitate or improve the effects of endurance exercise is a long-standing, if elusive, medical objective,” according to one source. Recognizing the known advantages of exercise for health outcomes and the population’s increasing inactivity, researchers are looking for orally-active molecules that imitate or improve the effects of exercise. Multiple and obviously repeated molecular pathways implicated in several essential acute and chronic responses to physical activity have been found in skeletal muscles and other tissues using molecular approaches in the biology of physical exercise. Clearly, a major challenge for physical fitness experts in the next 40 years will be to correlate diverse signaling cascades to metabolic responses and changes in skeletal muscles that occur after exercise.

This essay examines a research paper, Allometric scaling of maximal metabolic rate in mammals, written by Weibela and Hoppelera. The paper analyzes the existing facts on maximum metabolic rate (MMR) in several mammals (Weibel, Bacigalupe, Schmitt & Hoppeler, 2004). As illustrated in the paper, MMR depicts the rate at which oxygen is consumed by a homoeothermic animal’s body, when at maximum aerobic output, during maximum exercises. On the other hand, basal metabolic rate (BMR) refers to the lowest energy needed to fulfill an animal’s daily living needs, calculated when an animal is at rest, fasting and under its normal temperature (Weibel et al, 2004). All through their investigations and findings, the researchers attempt to uncover the paper’s hypothesis that stated, “To determine the factors that influence MMR in mammals.”

By examining the existing literature, the researchers noted how aerobic scope varied from one mammal to another. From their research findings, Weibela and Hoppelera confirmed that aerobic scope in large-sized mammals is much higher than in small-sized mammals (Weibel et al, 2004). Similarly, the report illustrated that athletic mammals posses a higher aerobic scope as compared to non- athletic mammals. Weibela and Hoppelera’s work indicated that a lot of BMR related researches have been done as compared to MMR related researches. For instance, the report indicates that more than 600 mammal species have been used in the analysis of BMR, while less than 50 mammals’ species have contributed to the recent knowledge in MMR (Weibel et al, 2004). Through this, Weibela and Hoppelera were able to develop a comprehensive report on the topic.

These research findings did not only rely on other researchers’ works, but also on their own investigations (Weibel et al, 2004). During the research, many animals were used. To select the best data, the researchers employed the standardized approach used in the estimation of the VO2max. Under this approach, several animals were placed on a treadmill running on varying velocity. Thereafter, VO2max estimation, morph-metric examinations, and psychoanalysis were carried out on the animals (Weibel et al, 2004). Afterwards, the animals were killed, and their lungs replaced with intratracheal installation of glutaraldehyde. It was not long before some of their organs and muscles tissues were removed for further analysis. Using the collected information, the researchers correlated their data with the existing MMR and BMR information (Weibel et al, 2004).

After data correlation, morph-metric analysis was initiated. The animals’ half bodies were subdivided into several strata. With each stratum, the length, depth and circumference were measured and recorded to represent a three dimensional specimen (Weibel et al, 2004). From then on, the remaining animals’ half bodies were dissected and weighed. The weights were labeled Mm to represent approximations of the weighed carcasses. Subsequently, approximations of mitochondrial volume densities were evaluated and recorded as biased approximations. Thereafter, the samples were analyzed to obtain their capillary length densities. Finally, the volume densities were evaluated by multiplying capillary circumferences with length densities (Weibel et al, 2004).

From the collected data, the researchers compared their findings with the existing literatures. Out of all the samples, 57 approximations of Vo2max matched with the literature findings (Weibel et al, 2004). The estimates represented the 35 mammalian species selected. The findings were then represented using tables and graphs. With the help of these tables and graphs, scaling of VO2max, muscle capacity and capillary blood supply were deduced. From the findings, researchers confirmed that in mammals MMR scales largely varied with body mass than BMR scales. From the earlier findings, BMR exponents were recorded as 0.75; however, the researchers’ findings were recorded as 0.872 (Weibel et al, 2004). Similarly, it was observed that the factorial the ratio of MMR and BMR was higher in small mammals than in huge mammals. Reduced factorial ratio in large animals was attributed to their agility.

During the experiment, comprehensive data on Vo2max, functional and structural characteristics of loco-motor muscles were collected (Weibel et al, 2004). The mammals sampled ranged from 20g to 450 kg. The data collected represented the whole muscle mass of the carcasses, which in quadrupeds are active when animals work in MMR. In this range, the scale exponent was found to be 0.96 rather than the usual 0.87 for the entire samples (Weibel et al, 2004). Similarly, the researchers noted that the volume of the mitochondria obtained from the loco-motor musculature, scaled with the same exponent of 0.96. This implies that the total volume of the mitochondria is strictly proportional to the Vo2max for all animals. After evaluation, the researchers evaluated the ratio of VO2max and muscle capillary erythrocyte volume as 4.9 (Weibel et al, 2004). However, it should be noted that the value obtained varied from the standard metabolic capacity of mitochondria. As such, higher values have been obtained in similar experiments by increasing the degree of oxygen supply in the mitochondria. This limitation is attributed to the oxidative phosphorylation process in the mitochondria.

In animals, mitochondria, and capillary blood determine aerobic capacity of muscles. It should be noted that their proportions vary directly with the maximal metabolic rate an animal can achieve (Weibel et al, 2004). Weibela and Hoppelera generalized their findings on a subset of species with MMR scale of 0.87. Generalization was implemented for several reasons. First, in their findings the scaling components were not statistically different from the entire population. Similarly, the selected subset was evenly distributed over the entire range (Weibel et al, 2004). Equally, in the subset both athletic and non-athletic species were represented. With these, the authors confirmed that scaling of aerobic capacity of loco-motor muscle is directly proportional to Vo2max. Similarly, Weibela and Hoppelera illustrated the relationship between mechanistic explanations and scaling components(Weibel et al, 2004). In the article, the authors’ findings confirm that in mammals, MMR scales differently with BMR. In the article, the researchers emphasized that there is no prior reason why MMR should scale with BMR (Weibel et al, 2004). However, differences in their performance were attributed to the BMR oxygen and BMR blood flow. In general, the authors’ explanations clearly relate with the paper’s hypothesis.

In the paper’s conclusion, Weibela and Hoppelera acknowledged that their findings failed to indicate how the process relates with vasculature (Weibel et al, 2004). Using Darveau’s model, the authors asserted that the approximations of partial scaling on the sequential functions depend on scaling exponents of metabolic rate. In their attempt to expound on this process, the authors examined several body organs analyzed during the examination of MMR and BMR (Weibel et al, 2004). Through this analysis, mechanistic explanations of the scaling of MMR are clearly outlined.

Reference

Weibela, E. R., & Hoppelera, H. (2004). Allometric scaling of maximal metabolic rate in mammals: muscle aerobic capacity as determinant factor. Respiratory Physiology & Neurobiology, 1(1), 18.

Introduction

The biochemical reactions that occur with living cells are all referred to as metabolic reactions. In all organisms, metabolic reactions can either take the form of anabolism or catabolism. Catabolism describes all metabolic reactions in which large molecules are broken down to smaller and in the process, a release of energy occurs (Bhagavan 34). Anabolism on the other hand describes metabolic reactions in which small molecules are joined together to form larger molecules. Anabolic reactions generally require energy to take place. An example of an anabolic reaction is the creation of proteins from amino acids.

In all organisms, metabolic reactions occur in series referred to as metabolic pathways. A metabolic pathway is a series of progressive biochemical reactions utilized by a cell to transform an input substance into an end product (Gropper and Smith 64). The pathways can be cyclic, in which the biochemical reactions reproduce the initial product, or linear, in which reactions produce a different product.

All life forms share the same metabolic pathways. In human beings, the main metabolic pathways include carbohydrate (glycolysis, gluconeogenesis, and glycogen) metabolism, lipid (fatty acid) metabolism, and protein (amino acid) metabolism (Garrett and Grisham 551). If consumed in adequate quantities, any of the three energy-creating nutrients i.e. carbohydrates, proteins, and fat, can avail energy to the body on a short-term basis. The biochemical pathways always occur in one direction and interact in a complex manner to enable ample regulation.

Interaction of Biochemical Pathways

A central array of metabolic pathways exists within all living things. These pathways are responsible for the breakdown of essential nutrients into Adenosine Triphosphate (ATP) and other molecules necessary for the release of energy into the body. As shown in figure 3, all metabolic pathways interact in one form or another during the energy production process. The interrelationships of metabolic pathways take various forms and always result in three junction points: glucose-6-phosphate, Pyruvate, and Acetyl CoA (Stoker 503). The fact that human beings can gain fat on a predominantly carbohydrate diet is evidence that the metabolic pathways interact and that nutrients can be converted from one form to another.

Connections of other sugars to glucose metabolism

In all animals, energy is stored in the glycogen molecule. In situations where the body has ample ATP present, excess glucose is converted into glycogen for storage (Rosenthal and Glew 57). Glycogen is prepared and stored in both the human muscles and the liver. When the blood sugar drops, glycogen monomers are broken down to form glucose. The carbohydrate (glycolytic) pathway occurs when the synthesis of glycogen monomers forms glucose-6-phosphate (G-6-P) which can later provide energy for the human body.

Sucrose, a disaccharide that consists of a fructose molecule plus a glucose molecule is broken down to form both fructose and glucose. Fructose plus galactose and glucose form the three main monosaccharide diets. Galactose is a milk product that is generally absorbed into the bloodstream directly after digestion. Glucose metabolism produces energy by converting glucose into pyruvate. Glycolysis consists of 10 biochemical reactions in which various intermediates act as the entry points for further reactions. The hexokinases enzymes carry out the phosphorylation of glucose to form glucose-6-phosphate. While the reaction utilizes ATP, it also maintains a low glucose concentration thus ensuring that glucose flows into the cell while at the same time blocking glucose from flowing out of the cell (Lee and Bishop 36). While glucose can be absorbed directly after digestion, living tissues can convert other sugars into glucose in the fast phase to provide energy or convert them in the fed state into fat to be stored for future use.

Connections of lipid and glucose metabolism

In metabolic connections, lipids link with glucose pathways through triglycerides and cholesterol. For animals, fat is very important for the storage and subsequent release of energy. All tissues utilize fatty acids as energy storage mechanisms as well as the means of creating cell membranes. The normal human body ingests lipids as triglycerides that are impossible to absorb by the intestines (Gropper and Smith 63). The pancreatic lipase enzyme breaks down these lipid molecules into glycerol and free fatty acids. Triglycerides can be both broken down or created through phases of the glucose metabolism pathways. Glycolysis occurs by the way of the phosphorylation of glycerol into glycerol-3-phosphate. Glycogen from muscles and the liver can feed into the catabolic pathways for carbohydrates (Stoker 545).

The catabolism of lipids occurs through beta-oxidation that occurs in the matrix of mitochondria and changes fatty acids into acetyl groups. Tissues then incorporate these groups into CoA to create Acetyl CoA that continues further into the Krebs cycle.

In certain situations, the body oxidizes carbohydrates to create both the fatty acid and glycerol portions of triacylglycerol (TAG). The transformation of fatty acids into carbohydrates is however impossible as the dehydrogenase reaction of pyruvate goes in one direction and is irreversible.

Connections of Proteins to Glucose Metabolism

The hydrolysis of proteins in human cells occurs through a variety of enzymes. Generally, tissues synthesize amino acids into new proteins when needed. However, if the body is starving, or in a situation where there are excess amino acids, part of these amino acids will be pushed into the glucose catabolic pathways (Gropper and Smith 251). Before an amino acid enters the glucose metabolic pathway, its amino group is detached and transformed into ammonia. Amino acids are metabolized into both the ketogenic amino groups and the glucogenic amino groups (Grisham and Garrett 101). Through oxidation, both the ketogenic and non-essential amino acids can indirectly from fatty acids. Carbohydrates can also result from the oxidation of the non-essential glucogenic amino acids.

Fed-Fast Cycle

The fed-fast cycle provides a very concise description of the interrelationship of the different metabolic pathways. During the fed state, glucose is readily available in various tissues and is usually absorbed directly to provide the required energy. In this state, enzymes in the liver convert excess glucose into fatty acids and glycogen (Gropper and Smith 252). The transformation of glucose into fatty acids only takes place when energy use is far lower than the intake.

During the post-absorptive phase, the tissues are unable to obtain energy from consumed glucose and the other nutrients but must rely on other energy sources. During this phase, glycogenolysis occurs in the liver where the synthesis of triacylglycerol and glycogen occurs to maintain the glucose levels in the blood (Grisham and Garrett 761). In the muscles, lactate is stored and released as required and becomes an essential energy source. The amino group alanine from the liver enters the glucose-alanine cycle and glycogenolysis occurs to transform this amino group into pyruvate.

In the fasting state, the hydrolysis of proteins in the muscles to create glucogenic amino acids increases. In this state, amino acids from protein breakdown form the bulk of the substrates needed for gluconeogenesis (Stoker 613). Through lipolysis, glycerol is also a chief provider of energy in this phase. Apart from this, anaerobic metabolism occurs in the muscles to create lactate that also offers a means for energy provision. In this phase, all the macronutrients offer a means of energy through various reactions in the body.

In the starvation phase, the body struggles to conserve essential proteins required for antibodies, hemoglobin, and enzymes. In this phase, fat stores in the body act as the major source of energy. Metabolic reactions shift from gluconeogenesis to lipolysis (Gropper and Smith 258). However, the brain cannot utilize fatty acids as a source of energy as they cannot move across the blood-brain barrier. The brain thus utilizes ketone as its main source of energy during the starvation phase. At this phase, an organism can only continue to exist depending on the amount of fat stored earlier.

Conclusion

Metabolism is a porous reaction in the body in which all metabolic pathways interact to provide the necessary energy required. Carbohydrates, lipids, and amino acids all interact at the three junction points to provide the required molecules needed for energy production. The intersection points are Acetyl CoA, glucose-6-phosphate, and Pyruvate. Carbohydrates, lipids, and amino acids can all provide energy through different processes in the body. The glucose pathway relates to all the other pathways and is a major provider of energy in the body during the fed-fast phase. All living things require energy and share the same metabolic reaction. The three main metabolic reactions interrelate to provide essential energy-providing molecules for any living thing.

References

Bhagavan, Natali. Medical Biochemistry. Malaysia: Academic Press, 2012. Print.

Grisham, Charles and Reginald Garrett. Biochemistry. 5^th ed. Belmont, CA: Brooks/Cole Cengage Learning, 2013. Print.

Gropper, Sareen and Jack Smith. Advanced Nutrition and Human Metabolism. 6^th ed. Belmont, CA: Wadsworth-Cengage Learning, 2012. Print.

Lee, Gary and Penny Bishop. Microbiology and Infection Control for Health Proffessionals. French Forest: Pearson Australia, 2012. Print.

Rosenthal, Miriam and Robert Glew. Medical Biochemistry: Human Metabolism in Health and Diseases. New Jersey, NJ: John Wiley and Sons, 2009. Print.

Stoker, Stephen. Organic and Biological Chemistry. 7^th ed. Boston, MA: Cengage Learning, 2015. Print.

A cataleptic African-American male was taken into the emergency unit. The patient was brought directly from a building and construction site. The physician noted that his skin was warm and flushed. He also exhibited a fruity odor breath and tachycardia. As such, his family and friends did not accompany him. Similarly, his records indicated that he had a history of uncontrolled type 1 diabetes mellitus.

Condition

Based on the above symptoms and laboratory tests, the patient is suffering from metabolic acidosis (Gordis, 2007). There are numerous forms of metabolic acidosis. They include diabetic acidosis, lactic acidosis, and hyperchloremic acidosis. Because the patient had been diagnosed with diabetes mellitus type 1, he had a higher risk of developing metabolic acidosis. The complication is experienced when the body generates excess acid. Metabolic acidosis can also be exhibited when kidneys fail to get rid of excess acid from the body. The symptoms for the above symptoms include grapey odor, reddened skin, and rapid breathing (Symposium, 2007). Notably, the patient in the case study exhibited the above symptoms.

Laboratory analysis

The patient’s laboratory examination indicated a glucose level of 750mg/dL, a pH level of 7.12, a CO2 rate of 44, and a HCO3 rate at 12. A person with the diabetic acidosis will exhibit a blood glucose level above 250.0mg/dl, a pH level between 7.00 and 7.30, and a HCO3 level of less than 15 (Sirotina, 2005). Notably, the patient in the case study has tested positive for all the above complications (Van & Pijpe, 2005). Thus, the laboratory analysis provided the basis of my identification.

Cause of rapid breathing

In our bodies, sugar is a principal source of energy required by the muscular and tissue muscles (Miller, 2006). Usually, insulin aids the absorption of sugar into the body cells. In the absence of adequate insulin, the patient’s body will not be able to utilize adequate sugar. Under such situations, the body triggers the production of hormones that disintegrate fats to produce energy. The process leads to the generation of ketones. When surplus ketones accumulate in the blood, they are released through the urine. The above complication stabilizes the body pH.

Usually, human bodies are adapted to a constant internal environment and stable pH levels of around 7.4 or above. Lesser pH levels exhibited by the patient in the case study make the body more acidic. Because of this, the human body will attempt to retain stable pH by involving the buffer systems. The buffer systems comprise of chemical constituents, which consume or release H+ that are liable for acidity. CO₃^– is a significant compound of these buffer systems. It can disintegrate hydrogen ions into very frail H₂CO_3, which breaks down into H2O and CO₂. Carbon dioxide generated through this process accrues in the body. With increased CO_2, the patient will experience a hasty breathing. Rapid respirations try to eliminate excess carbon dioxide in the body.

Treatment modalities

After establishing the level of dehydration from the laboratory analysis, treatment should be initiated. As such, intravenous fluid should be administered to the patient. The patient should be offered with saline of 0.90% at 15.0 to 20.0 mL per kg every hour (Repina, 2007). During the process, the fluids standing, electrolyte rates, and cardiac condition should be monitored. Equally, urine production and blood pressure ought to be evaluated. As the client becomes stable, the fluids should be reduced to between 4 mL to 14 mL per kg every hour or 250.0 to 500.0 mL hourly (Gordis, 2007). When sodium concentration stabilizes, a saline solution of 0.450% should be offered. Dextrose is supplemented once glucose rate drops to 200.0 mg for every dL.

Insulin should be introduced after one or two hours to stabilize the patient’s situation. A preliminary bolus of 0.10 units per kg is given with a mixture of 0.10 units per kg hourly. A mixture of 0.140 units per kg per hour should be used if a bolus is not available. During this process, glucose level is expected to lessen to around 50.0 to 70.0 mg per dL every hour. Therefore, insulin mixture should be attuned to attain this objective.

When the glucose level diminishes to 200.0 mg per dL, insulin mixture ought to be reduced to 0.05 to 0.100 units for every kg every hour. Similarly, dextrose fluids ought to be supplemented with the intravenous solutions at this level to maintain a sugar level ranging from 150.0 mg and 00.0 mg for every dL. The disorder is fixed when the sugar level is below 200.0 mg for every dL, the pH level is higher than 7.3, and when the HCO3 level is 18 mEq per L or more. When the above situations are met, the patient should be initiated on an insulin routine. Because the patient is diabetic, changes should be made on his outpatient prescription to enhance management of the disease. Similarly, the patient should be encouraged to adhere to his medication and diet as instructed by a physician.

References

Gordis, L. (2007). Using epidemiology to identify the causes of disease Epidemiology. 6(1),215-229.

Miller, W. (2006). Infectious Disease in Epidemiology. Epidemiology, 21(5), 593-594.

Repina, E. (2007). Mechanisms of adaptive immunity exemplified by type 1 diabetes mellitus. DM Journal, 13(2), 51-56.

Sirotina, O. (2005). Thymus in children with type 1 diabetes mellitus. DM Journal, 14(2), 75-76.

Symposium, C. (2007). Metabolic Acidosis. Hoboken: John Wiley & Sons.

Van, G., & Pijpe, A. (2005). E-epidemiology: a comprehensive update. A Epidemiology, 1(1), 172-179.

Introduction

Phenylketonuria (PKU) is a hereditary disease with an autosomal recessive type of inheritance. Phenylketonuria is caused by insufficient activity of the enzyme called phenylalanine hydroxylase. As a result, it leads to the gradual accumulation of amino acid phenylalanine and its derivatives, which have a toxic effect on the central nervous system of a patient. Phenotypic manifestations of the disorder are microcephaly, convulsions, allergic dermatitis, hypopigmentation of hair, skin, and iris. Without timely treatment, patients with the problem have severe mental degeneration, and the seriousness of the PKU depends on the type of mutation.

In order to fully understand the hereditary nature of the disorder, it important to identify and describe the genes involved. The genes are autosomal recessive (AR), their location is 12q23.2, and the MIM number is 612349 in the locus PAH (“Phenylketonuria; PKU,” 2020). It is stated that transient phenylalanine titration treatment can have a detrimental effect on the control of the patients’ metabolism (Barbosa et al., 2018). Phenylketonuria is a genetic violation of the metabolism of amino acids and the reason is the lack of liver enzymes involved in the phenylalanine to tyrosine metabolism.

Main body

The early signs of phenylketonuria are vomiting, lethargy or hyperactivity, the smell of mold from urine and skin, and a delay in psychomotor development. Typical late symptoms include oligophrenia, physical developmental retardation, cramps, and eczematous skin changes. Screening of newborns for phenylketonuria is still in the maternity hospital. Subsequent diagnostics include molecular genetic testing, determination of blood phenylalanine concentration, urine biochemical analysis, and brain MRI. The treatment of phenylketonuria is to follow a special diet. Disruption of amino acid metabolism is accompanied by a violation of myelination of nerve fibers, a decrease in the formation of neurotransmitters, triggering pathogenetic mechanisms of mental retardation, and progressive dementia.

Newborns with phenylketonuria do not have clinical signs of the disease. Typically, the manifestation of phenylketonuria in children occurs at an early age. With the inception of feeding, the breast milk proteins or their substitutes begin to enter the baby’s body, which leads to the development of the early, non-specific symptoms such as lethargy, anxiety, and hyperexcitability, regurgitation, muscle dystonia, convulsive syndrome. One of the early pathognomonic signs of phenylketonuria is vomiting, which can be mistakenly treated as a manifestation of pyloric stenosis. By the following period, the child’s lag in the development of psychomotor functions becomes noticeable. The child can become inactive, irresponsive, stops to recognize parents, and does not attempt to stand on his feet or sit down. A fundamental factor in the treatment of phenylketonuria is a diet that restricts the intake of protein in the body.

Conclusion

Conducting a mass screening for phenylketonuria in the neonatal period allows organizing early diet therapy and prevent severe cerebral damage, impaired liver function. With the early appointment of an elimination diet in classical phenylketonuria, the prognosis for the development of children is good. With late treatment, the prognosis for mental development is poor. Prevention of complications of phenylketonuria consists of mass screening of newborns, early prescribing, and long-term dietary compliance. In order to assess the risk of giving birth to a child with phenylketonuria, preliminary genetic counseling should be given to couples who already have a sick child, are in a consanguineous relationship, and have relatives with this disease. Women with phenylketonuria who are planning a pregnancy should follow a strict diet.

References

Barbosa, C. S., Almeida, M. F., Sousa, C., Rocha, S., Guimas, A., Ribeiro, R., … Rocha, J. C. (2018). Metabolic control in patients with phenylketonuria pre- and post-sapropterin loading test. Journal of Inborn Errors of Metabolism and Screening, 6, 1-6.

Phenylketonuria; PKU. (2020). Web.

Abstract

This paper aims at analyzing some of the problems associated with poor nutrition intake or intake of unbalanced diet. Beside that, the paper aims at describing the risk factors associated with bad feeding habit or other metabolic syndrome.

This is a collection of various hazardous factors caused by high body weight, obesity and other fatty associated diseases in the body. Accumulation of too much fat in the lining of cardiovascular arteries and other organs of the body may result to health problems such as hypertensions, stroke and heart diseases.

Introduction

Metabolic syndrome is a feature detected to the obese patients, diabetics, and patients with heart problems. This is a malfunction caused by poor and prolonged feeding habits, poor nutrition and lack of exercises. Therefore, metabolic syndrome can highly be avoided through proper nutrition and doing exercises. The risk of getting heart problems increases with the patients who suffer from metabolic syndrome. C-reactive protein hypersensitivity to the patients is a good indicator of one having high risks of getting heart problems or any other problem associated with high fatty tissues.

Heart diseases are the main factors that drive doctors to diagnose metabolic syndrome in the suspicious patient. Some of the medical conditions associated with this syndrome include patients with fatty and extended waste line. Obese abdomen is cause of accumulated fat in the abdomen adipose tissue. This increases the risks of getting heart problems as opposed to accumulation of fat in other body parts. Another factor that increases risks of heart diseases is too much triglyceride in the blood.

Patients with metabolic syndrome have high risks of getting heart diseases, stroke, diabetes and hypertension than those who do not have metabolic syndrome. Beside metabolic syndrome, too much low-density lipoprotein cholesterol, abuse of drugs, alcoholism etc increases the risks of getting heart problems.

The only cure to avoid heart problems and metabolic syndrome is by having proper balanced diet and doing exercises.

Aim of the study

1. To examine C – reactive protein titer in patients with metabolic syndrome and its effect in cardiovascular diseases.
2. To measure the risk factors for developing heart diseases
3. To investigate whether obese have high chances of getting cardiovascular problems

Sub problems

• Does the feeding habit of an individual goes hand in hand with the cardiovascular problems?
• Does doing exercises mitigate the problems?

Methodology

I have decided to use questionnaire, direct interview, cross examination and recorded date of the inpatients

The procedure was as follows

1. First, a population of one hundred health individuals was selected.
2. The population was divided into two groups. One consisted of 43 men and 47 women.
3. Then examination of each group was done whereby smokers, those who suffer from deadly infections, cardiovascular diseases, diabetics, and other chronic and acute infections were eliminated.
4. After that physical examination of health persons was done to give a positive result.
5. The main procedure included check up of clinical and laboratory results beside normal features such as waist circumference, body mass index, height and weight, and finally waist to hip ratio. The life histories of the persons were taken whereby full medical history was recorded.
6. Physical analysis of the control population was done. This included urinalysis, counting of blood cells, analytical chemistry of the blood was carried out whereby blood glucose was measured using Behring apparatus, individuals with hepatitis b and a were examined through serological tests and fried ward formula, chest radiography was done, this was followed by electrocardiogram, respiratory and digestive systems were also examined.
7. Going on, systolic and diastolic pressure was measured using a sphygmomanometer whereby each individual was given ten minutes for resting.
8. Korotkolfs sound were used to define the pressures whereby reading were recorded to the nearest even number with a mean of 2.5
9. Plasma analysis was done whereby cholesterol concentration was measured and triglycerides. Finally, the difference between the two data was recorded and analyzed.

Findings

From the data of both control and the population under investigation, the following results emerged. First, from the two groups, it emerged that there is no difference in age and sex, meaning that even young and obese children have got high chances of getting cardiovascular problems.

From the laboratory results, in the two groups men who suffered from metabolic syndrome were 24 and 26 women. The control group had a lower level of systolic and diastolic blood pressure. the metabolic syndrome group had a higher blood pressure whereby the systolic was at 142 and diastolic at 85 as compared to 124 and 76 respectively for the control group. Another finding is that hanging belly and obesity was more frequent to women than men.

Of course the metabolic syndrome group had higher Lower Density Lipoprotein cholesterol concentration and triglycerides while High Density Lipoprotein cholesterol was lower in metabolic syndrome. The CRP concentrations were higher in metabolic syndrome compared to the control group.

Lastly, computing of logistic regression shows that waist circumference and plasma glucose both at (p<0.012) gives independent correlation with plasma C – reactive protein. Again, smokers, obese, and the aged have got high chances of getting levels of C – reactive protein increasing. Therefore, they have high chances of contracting cardiovascular problems that is associated with the metabolic syndrome patients.

Discussion

Since C – reactive protein is associated with the metabolic syndrome individuals, it means that metabolic individuals have got high chances of getting cardiovascular problems. Therefore, hypersensitivity C-reactive protein is an indicator of cardiovascular diseases. This is because, metabolic syndrome playa a major role in development of coronary problems.

Metabolic syndrome is a feature detected to the obese patients, diabetics, and patients with heart problems. This is a malfunction caused by poor and prolonged feeding habits, poor nutrition and lack of exercises. Therefore, metabolic syndrome can highly be avoided through proper nutrition and doing exercises. The risk of getting heart problems increases with the patients who suffer from metabolic syndrome. C-reactive protein hypersensitivity to the patients is a good indicator of one having high risks of getting heart problems or any other problem associated with high fatty tissues.

Conclusion

From the findings, it is apparent that individuals, who are obese, have insulin problems, coronary artery problems and with too much fatty tissue are associated with metabolic syndrome. This syndrome is further associated with patients who suffer often from cardiovascular diseases. Therefore, metabolic syndrome individuals have got high chances of getting cardiovascular problems. This is especially when they eat too much fatty food and they do not do a lot of exercises.

Since obesity and insulin is associated with high level of C – reactive protein, taking food free of cholesterol and weight loss would help to reduce chances of CRP. This again would lessen body inflammation. By doing this the reduction of acute coronary infection may be enhanced.

Comments and recommendation

Metabolic syndrome is a feature detected to the obese patients, diabetics, and patients with heart problems. This is a malfunction caused by poor and prolonged feeding habits, poor nutrition and lack of exercises. Therefore, metabolic syndrome can highly be avoided through proper nutrition and doing exercises. The risk of getting heart problems increases with the patients who suffer from metabolic syndrome. C-reactive protein hypersensitivity to the patients is a good indicator of one having high risks of getting heart problems or any other problem associated with high fatty tissues.

References

Aytekin G and Ali C (2006) metabolic syndrome and hypersensitivity, Sage publisher, New York.

High sensitivity and metabolic syndrome, 2007.

Patel N, Sathanur.R (2005) Metabolic syndrome and correlation of plasma C- reactive protein

The heart rate is one of the cardiovascular measurements employed during exercise to measure the strength of the heart relative to the exercise and the rate of recovery from the exercise. This is important in terms of specifying exercise intensities for different individuals. The maximal heart rate entails the maximum increase in cardiac output, which cannot be surpassed relative to an increase in the intensity of the exercise. According to Robergs and Landwehr (2), the maximal heart rate can be predicted using the equation, HRmax = 220-age.

This equation was developed in 1938 by Robinson and it is the most accepted formula in the prediction of the maximum heart rate. When starting any physical activity, there is a direct proportional increase in the heart rate with the level of intensity of the physical activity in question. This condition proceeds until the maximum intensity is reached. At this point, the heart rate begins to flatten gradually despite that the exercise continues and the intensity increases. This indicates that the highest point of the heart rate is approaching and this value remains constant until an individual gets exhausted. Moreover, an individual’s maximal heart rate remains constant each day (Robergs and Landwehr 3).

However, Robinson noted that the maximal heart rate can decrease annually relative to an increase in age as from 10-15 years. Therefore, the maximal heart rate depends on an individual’s age. Consequently, when the age of a person is subtracted from 220, we are then able to approximate the heart rate of such an individual.

However, a large error of prediction (Sxy=7-11 beats per minute) is involved in using the equation, HRmax=220-age. Besides, Robergs and Landwehr (4), reveal that the equation, HRmax=220-age was not developed using primary data and that the data used in developing the prediction equation was obtained from more than 11 published and unpublished studies (Robergs and Landwehr 6).

Due to the inherent errors in the equation, HRmax=220-age, other equations that predict the maximal heart rate relative to age were developed. A review of these equations also notes that there is a large inherent error of prediction when using these equations to predict the maximal heart rate. These errors are attributable to lack of a mode-specific method of HRmax prediction relative to age because most regression equations are mode-specific (Robergs and Landwehr 7). Besides, mode-specificity as one of the variables in the prediction of HRmax has not been accurately incorporated into most of the equations used to determine the maximal heart rate.

Therefore, because of the presence of other factors such as different exercise procedures and the motivating factors affecting different people during the exercise, there is the need to allow for prediction errors in the equations used to predict the heart rate. Here, the prediction error for accurate measurements of HRmax is equal to ±3 beats per minute (Robergs and Landwehr 7). And since HRmax is the basis of other cardiovascular measurements such as estimation of the exercise intensities and the volume of oxygen consumption during exercise (VO₂max), there is a paramount need to consider the error of prediction involved in estimating the maximal heart rate.

On the other hand, the best equation for estimation of the heart beat is HRmax=208-(0.7 × age). According to this equation, when an individual is exercising at a constant rate and sub-maximal intensity, the heart rate increases steadily until it reaches a maximum, which is also the optimum heart rate. Subsequently, any further increments in the intensity will give rise to a new optimum heart rate that meets the demands of the circulatory system. This equation can be used on different populations of people under different circumstances.

Works cited

Robergs, Robert and Landwehr, Roberto. “The surprising history of the “HRmax=220 age” equation.” Journal of Exercise Physiology Online 5.2 (2002): 1-10.

Introduction

The healthcare industry has had to cope with the emergence of ‘new’ diseases in the recent past. Although the health care sector has the means to fully treat these diseases, the increasing trend is devastating and causes psychological torture to the infected and affected. Times and life patterns have significantly changed and explains the rise in certain disorders (Barlow & Dietz, 1998). Global climate change and change in eating habits have played a crucial role in causing such disorders. Some of the diseases that are being focused on today include skin cancer and metabolic syndrome.

It is worrying to note that such diseases target children and the youth who end up not attaining the age of maturity. A participatory approach is therefore the way to go if levels of such disorders are to be set within acceptable limits. The essay provides an elaborate description of metabolic syndrome.

Signs and Symptoms

For a long period of time, the definition of metabolic syndrome is not clear even to the medical professionals. Several definitions have been proposed to try and explain the disorder. More than 40 definitions have been suggested. However, a definition brought forth by a National Cholesterol Education Program indicates that metabolic syndrome is associated with the following; obesity, high fasting glucose, hypertension and hypertriglyceridimia. Low HDL cholesterol is another risk factor associated with the disorder. These factors increase the probability of getting a heart-related disease. A research conducted by Ribeiro, Guerra, Mota, et al. (2004) indicated that if at least three of these risk factors manifest themselves then one is said to have metabolic syndrome. The syndrome is also called insulin resistance syndrome.

The major signs and symptoms of metabolic syndrome vary with age and sex. Most of the mentioned risk factors show no symptoms or warning manifestations. However, a large waistline is noted for those affected. Standards for BMI (Body Mass Index), blood pressure, height and weight differ between sexes and depend on age (Barlow & Dietz, 1998). Children with metabolic syndrome recorded abnormal values of high density lipoprotein cholesterol and blood glucose of about 100mg/dl. Children are associated with growth and developmental changes thereby making it difficult to decide on the bench mark for risk factors.

These variations in age also make the symptoms of metabolic syndrome different among those affected. Symptoms of high blood sugar characterized by unending thirst, increased frequency of urination, impaired vision, and fatigue are observed for those who are diabetic. Later stages of high blood pressure show no signs. People who are in early stages experience headaches, dizzy moments, and unusual nosebleeds. Metabolic syndrome is also characterized by abnormal clotting of blood as well as continued inflammation of the body.

Causes and Prevalence of Metabolic Syndrome

Several factors acting together cause metabolic syndrome. Whereas some of these factors are beyond human explanation, some are controllable. Being overweight and obese, living an inactive lifestyle and having insulin resistance causes the syndrome. Some uncontrollable factors such as ageing also play a role. Genetics is also uncontrollable and may increase the risk of insulin resistance. Other unexplored research findings indicate that metabolic syndrome may also be caused by a fatty liver, polycystic ovarian syndrome, gallstones and breathing problems during sleep. A recent study by Ribeiro et al. (2004) carried out on children and adolescents aged between 12 and19 showed a prevalence of 4.2%.

Other researchers found that a prevalence of about 3.6% in young people aged 8-17 years. The research findings revealed much higher prevalence rates among the overweight children. More to this study indicated that 89% of those whose BMI z-score was 2.0-2.5 had 38.7% prevalence (Barlow & Dietz, 1998). The patients who were severely obese and whose BMI z-score was more than 2.5 had the syndrome (about 49.7%). A prevalence of 6.8% was observed for those whose BMI z-score ranged between 1.5 and 2.0.

The study also indicated that the prevalence of Metabolic Syndrome showed some variability on the basis of sex and ethnicity among the youth (Ribeiro et al., 2004). Males showed a significant 6.1% prevalence compared to that of females that stood at 2.1%. Another revelation by Kolbe, Kann, and Brener (2001) showed that whites were more prone to the syndrome as compared to African Americans.

Prevalence rates of 5.6% and 2.0% for whites and African Americans respectively were noted on the basis of lipids bench mark. Children who were overweight aged between 5 and 15 years and had a waist-to-height ratio of more than 0.5 were at a great risk of having metabolic syndrome (Barlow & Dietz, 1998). The study revealed that normal-weight children were 8 times safe from the syndrome compared to their overweight counter parts. Obese children characterized by large waist circumference were also at a higher risk. Several growth stages influence the metabolism of the body systems.

A good example is the puberty stage that has been found to affect the insulin-glucose homeostasis. It is a fact that insulin resistance is increased during puberty. Compensation for this resistance is countered by an increase in insulin secretion (McMurray, Harrell & Levine, 2002). This super normal secretion of insulin found in adolescents may explain the recent increase in metabolic syndrome. The sensitivity in insulin during puberty was associated with sex and body composition.

Metabolic Risk Factors

Several factors among them abdominal obesity, an inactive lifestyle and insulin resistance pose a great likelihood of metabolic syndrome. Some people who are usually under medication may be at risk because of the medicines’ effect on weight gain, blood cholesterol and levels of blood sugar. In USA about 47% adults are prone to metabolic syndrome. A recent finding indicated that some other groups were also at risk for metabolic syndrome (Ribeiro et al., 2004). Genetically, people whose siblings or parents are diabetic or have a history of diabetes are prone to the syndrome. Women who showed a tendency of developing cysts in the ovaries are also not very safe.

A large waistline, a major symptom of metabolic syndrome, is a clear indication that excess weight is carried around the waist. A waist circumference that is greater than the standard measurement for men and women is a risk factor for metabolic syndrome and hence an increase in heart disease risks. The situation of overweight cases in children is recognized as a risk factor for cardiovascular disease (CVD) and diabetes. Cases of overweight children showed an increase from 1974 to 2000 (Kolbe et al., 2001). A recent study conducted by Kolbe in 2001indicated that indeed the percentage of overweight children had increased to 16%. The blacks recorded the highest overweight prevalence of 20.5% while the whites had 13.6% prevalence.

Blood contains several forms of fats. One example is triglycerides. Usually a level of less than 150 milligrams per deciliter (mg/dl) is acceptable. Any value beyond this limit is a metabolic risk factor. Cholesterol is usually found in most foods. Too much cholesterol in the foods we eat is detrimental to our health. The body produces its own HDL cholesterol which helps to remove the cholesterol trapped within the arteries. Any values below the normal HDL cholesterol level in both men and women are metabolic risk factors.

The blood pressure is usually measured in millimeters of mercury. The recommended pressure is 130/85 mmHg. Any value that exceeds either of the two values is a metabolic risk factor. Blood sugar level is a key component in metabolic syndrome. The set benchmark for metabolic risk factor is values greater than 100mg/dl (McMurray et al., 2004). People are considered pre-diabetic if the levels are 100-125 mg/dl and diabetic if the sugar level exceeds the 126 mg/dl mark.

Prevention and Treatment

Preventive measures are usually considered better than curative measures. The most appropriate way in the prevention of metabolic syndrome is making informed lifestyle choices. Maintaining a healthy weight can be a challenge but is important as a preventive measure. Waist measurement and body mass index if known frequently, risks of metabolic syndrome may be curtailed. A body mass index of 25 should be maintained to prevent the syndrome. Those who have the syndrome should cut down the BMI by 7-10% during the first year in which treatment is administered (Barlow & Dietz, 1998).

Over eating should be discouraged and following a healthy diet emphasized. A variety of fruits and vegetables, fish, beans, lean meats and low-fat milk should be taken. Foods that are high in cholesterol and added sugar should be avoided. Whole-grain products should also be given a priority in diets. Foods with too much salt cause blood pressure and should be avoided (McMurray et al., 2002).

Regular exercises are crucial to the maintenance of healthy weight. It is important to see a doctor who would advice on the best exercise to be undertaken. Some of these exercises are aerobic, bone strengthening, muscle strengthening and stretching. Smoking is not only hazardous to the liver but poses a great risk in causing metabolic syndrome and heart attacks. Those who find quitting smoking a challenge should join hands together with support groups. In most cases lifestyle changes may never work at all. Doctors prescribe drugs in a bid to control risk factors. Statins, nicotinic acid and fibrates are used to treat low cholesterol levels. The risk of blood clots can be reduced by taking low-dose aspirin.

Conclusion

It is important to acknowledge that metabolic syndrome exposes one to heart diseases. The health care sector is faced with enormous challenges that would reduce metabolic syndrome if addressed. The present and future of the youth is at risk. The health care key players should be involved in educative forums to ensure that children and the youth are aware of their state. This awareness will ensure that chances of occurrence of metabolic syndrome are minimal. A participatory approach between health care key players and the community will not only bear fruits in the short-term but also in the long-term. Heart diseases have become a menace and failure to address these issues may cause more pain in future.

References

Barlow, S. E. & Dietz, W. H. (1998). Evaluation and Treatment of Obesity: Recommendations. Journal of Health Resources and Services, 3 (2); Pp. 134-146.

Kolbe, L. J, Kann, L, & Brener, N. D. (2001). Overview and summary of findings: School Health Policies and Programs Study. McGraw Hill Plc.

McMurray, R. G, Harrell, J. S., & Levine, A. (2002). Metabolic Syndrome: A School-Based Intervention can Reduce Body Fat and Blood Pressure in Young Adolescents. Journal of Adolescent Health, 3 (1): Pp.125 -132.

Ribeiro, J. C, Guerra, S., Mota, J., et al. (2004). Understanding Physical activity and biological risk factors clustering in pediatric population. Cengage Learning.