Obesity and Excess Body Fat in Humans and Rats

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Table of Contents

Introduction
Discussion
References

Introduction

Obesity is a situation whereby an individual experiences a body mass index of 30 or more and this is very risky as it may have severe aftermath such as insulin resistance, heart problems, other forms of cancer and type 2 diabetes that can easily cause premature death. The brain stem has the ability to accept sugary or harsh foodstuff with the help of neural circuits which can be transformed by satisfaction or bodily starvation signs such as a drop in glucose metabolism or the availability of food in the digestive system. Obesity has been identified to be common in some families and in as much as this suggests that it may be genetic, it is so because the family members share a lot in common such as daily diet. The diet we take counts a lot on our weight and taking excess fats than our body needs will easily result to obesity. According to Dr. Marion Nestle, Professor and chair of the Department of Nutrition and Food Studies at New York University, it is clear that the rate of obesity in the United States has increased because there has been an increase in the intake of soft drinks and also the US agribusiness has increased produces in the past 30 years from 3,300 3,800 calories of food a day for every individual. This indicates that there is a higher energy intake. Taking too much trans-fats, refined white flour carbohydrates and low fiber intake often leads to metabolic and absorption difficulties and thus destabilize food and energy metabolism in the body which then results to excess fat storage. Our age greatly determines our metabolic rates and as we grow older our body requirements drop and we therefore have to reduce our intake.

Discussion

When studying insulin action in liver, adult male rats in groups of two were fed on isocaloric diet that was high in either carbohydrate or fat for a period of 24 days. The rodents fed on high fat diet ended up with a massive reduction in the whole body glucose consumption due to a drop in the glucose removal and failure to hold back liver glucose production. The group that had high carbohydrates experienced a high thermogenesis though there was no difference in the basal metabolic rate. Therefore the conclusion was that feeding on food with high fat leads to insulin resistance and obesity. The peptides orexin and melanin-concentrating hormone are secreted in the brain neurons whose functions involve in stimulus, motor and metabolism. Food deficiency enhances the intensity of these peptides and rats with a specified mutation not in favor of melanin-concentrating hormone eat less food. The release of ghrelin in the stomach (a circulating growth hormone-releasing peptide) is controlled by the brain. Ghrelin is responsible for motivation of food ingestion.

Motivation of the tangential hypothalamus with either current or excitatory amino acids fabricates ingestion whereas on the other hand application of glutamate rival lowers the eating rate. This action is monitored by a double group of neurons whose main work is to promote eating and lower metabolic rate. The discharge of neuropeptide Y in the hypothalamus stimulates eating an outcome that seems to be a result of the association of neuropeptide Y-secreting neurons with the orexin and melanin-concentrating hormone. The neuropeptide Y neurons at some level release a peptide called AGRP which enhances eating. When neuropeptide Y is permeated into the paraventricular nucleus, it reduces metabolic rate. Whenever one is hungry, his level of NPY rises and will only fall when he eats. Most of the people who are obese have soaring leptin levels and therefore experience a state of negative energy balance when their mass drops and leptin levels decline and thus almost all the people who lose their weight via dieting gain their original weight. This suggests that body weight is controlled physiologically and not psychologically therefore biological processes are the ones in question and digression in mass of a person whether lean or obese draws out an effective counter-response that opposes the change. Some individuals have obesity genes that predetermine molecular composition of the physiological aspect that controls body mass which is characterized by the hormone leptin which is produced by fat tissue. A rise in body fats is connected with a rise in the levels of leptin and mutation that end up in low leptin levels are characterized with massive obesity in both the rat family and humans

References

Anne Collins. Note on Causes of Obesity. Causes of Obesity & Excess Body Fat, Genetic Factors, Psychological & Environmental Reasons For Overweight.
Calle, E., Thun, M., Petrelli, J., Rodriquez, C. & Heath, C. Body-mass index and mortality in a prospective cohort of U.S. adults. N. Engl. J. Med. 341, 1097– 1105 (1999).
Elias, C. et al. Leptin differentially regulates NPY and POMC neurons projecting to the lateral Hypothalamic area. Neuron 23, 775–786 (1999).
F. Bourgoin, H. Bachelard, M. Badeau, S. Melancon, M. Pitre, R. Lariviere, and A. Nadeau. Endothelial and vascular dysfunctions and insulin resistance in rats fed a high-fat, high-Sucrose diet. Am J Physiol Heart Circ Physiol, 2008; 295(3): H1044 – H1055.
Wren AM, Small CJ, Abbott CR, Dhillo WS, Seal LJ, Cohen MA, Batterham RL, Taheri S, Stanley SA, Ghatei MA, Bloom SR.

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Obesity and Excess Body Fat in Humans and Rats

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