Relationship Between Visceral Fat and Its Role in the Human Body Metabolism

It is important to note that the harmful effects of obesity are a well-known phenomenon. However, obesity is a complex health condition that is not solely based on the accumulation of adipose tissue. There is a range of differential manifestations of obesity, which vary between sexes as well as regions in the human body. The given analysis of visceral fat and its role in the human body metabolism reveals that the former increases the risk of cardiovascular complications, insulin resistance, chronic inflammation, and immunosuppression.

Firstly, the link between obesity and cardiovascular diseases is well-established, but visceral adipose tissue (VAT) is significantly more contributive compared to subcutaneous adipose tissue (SAT). A study found that “the development of abdominal-visceral obesity is combined with unfavorable metabolic activity and an increased risk of cardiovascular complications” (Gruzdeva et al., 2018, p. 2). The main reason is that VAT is much more active hormonally compared to SAT, which initiates a cascade of processes and signals of pro-inflammatory cytokines (e.g., TNF-α and IL-1) release (Gruzdeva et al., 2018). In other words, systematic changes in human metabolism begin with an increased accumulation of VAT, leading to plaque formation and atherosclerosis manifested in a range of cardiovascular complications, such as heart failure, stroke, and stenocardia.

Secondly, insulin resistance is a major indicator of type 2 diabetes. It is stated that “chronic, low-grade inflammation of VAT, and eventually systemically, is one of the major drivers of obesity-associated insulin resistance and metabolic abnormalities” (Li et al., 2020, p. 114). The metabolic pathways are controlled by regulatory T cells or Tregs, which “keeps inflammation in check and regulates organismal metabolism” (Li et al., 2020, p. 114). As a result, the insulin sensitivity of cells is downregulated, meaning more insulin needs to be released in order to prompt the necessary response in terms of glucose absorption into cells. Insulin resistance creates an environment of elevated blood glucose, which is toxic long-term and a defining symptom of type 2 diabetes. In addition, chronic inflammation is maintained by Tregs released and supported by VAT.

Thirdly, visceral fat causes immunosuppression directly through poor metabolism of immune systems as well as indirectly through inflammatory cytokines. The most recent evidence on immunosuppression is COVID-19, where it was found that “VAT is a marker of worse clinical outcomes in patients with COVID-19” (Watanabe et al., 2020, p. 154319). Findings suggest that “visceral fat (VAT) was significantly higher in patients requiring intensive care (p = 0.032), together with age (p = 0.009), inflammation markers CRP and LDH (p < 0.0001, p = 0.003, respectively), and interstitial pneumonia severity” (Watanabe et al., 2020, p. 154319). Thus, C-reactive protein (CPR) and lactate dehydrogenase (LDH) are metabolic markers of inflammation and weakened immunity, and antiviral immune response. It explains why COVID-19 manifests and develops in a much more complicated manner among young obese individuals compared to lighter young people.

In conclusion, the assessment of visceral fat and its role in the human body metabolism shows that the former increases the risk of cardiovascular complications, insulin resistance, chronic inflammation, and immunosuppression. There is a range of differential manifestations of obesity, where visceral adipose tissue (VAT) is significantly more contributive to diseases compared to subcutaneous adipose tissue (SAT). Therefore, obesity is a complex health condition, and it is not merely based on the accumulation of adipose tissue VAT is more hormonally active than SAT. VAT drives plaque formation and atherosclerosis manifested in a range of cardiovascular complications, such as heart failure, stroke, and stenocardia. In addition, chronic inflammation is maintained by Tregs released and supported by VAT leading to immunosuppression and diabetes.

References

Gruzdeva, O., Borodkina, D., Uchasova, E., Dyleva, Y., & Barbarash, O. (2018). . Lipids in Health and Disease, 17(218), 1-9. Web.

Li, C., Spallanzani, R. G., & Mathis, D. (2020). . Immunological Reviews, 295(1), 114-125. Web.

Watanabe, M., Caruso, D., Tuccinardi, D., Risi, R., Zerunian, M., Polici, M., Pucciarelli, F., Tarallo, M., Strigari, L., Manfrini, S., Mariani, S., Basciani, S., Lubrano, C., Laghi, A., & Gnessi, L. (2020). . Metabolism, 111, 154319. Web.

Calcium and Phosphorus Metabolism

Hypophosphatemia is a metabolic derangement characterized by an abnormally low phosphate level in the blood serum. Rickets in children occurs due to low phosphate serum levels, while Osteomalacia is due to phosphorus deficit in adults 1. Osteoporosis may be brought on by an imbalance in the body’s phosphorus and calcium levels in bone metabolism. If the body does not have enough calcium in the blood, metabolic derangement called hypocalcemia develops. Over time, cataracts, dental changes, and other abnormalities may develop due to hypocalcemia. Nails become brittle, hair grows slowly, and the skin becomes delicate and thin due to a lack of calcium. Muscle cramping, mental disorientation, and numb lips and hands are hypocalcemia’s severe symptoms. Calcium and phosphate ions release promote bone repair by controlling osteoblast and osteoclast activation. The calcium in the serum is affected by the phosphate level. There is an inverse relationship between calcium and phosphate in the body, meaning that phosphate levels decrease as calcium levels in the serum increase. PTH regulates calcium and phosphorus concentrations in the serum. Therefore, calcium and phosphorus interact to affect bone metabolism in the body.

Low blood calcium causes the release of PTH from the parathyroid gland (step 1).

PTH leads to the release of calcium from bones (step 2), leading to an increase in the serum calcium level (step 6a).

PTH affects the kidney by increasing the kidney’s conversion of 25-dihydroxy cholecalciferol to calcitriol (step 3). Calcitriol enhances calcium absorption in the brush borders of the intestine (step 6c), increasing serum calcium levels.

PTH acts on the kidney (step 4) to reduce calcium loss in urine by increasing its reabsorption, leading to increased serum calcium levels (step 6b).

Bibliography

Hall JE, Hall ME. Guyton and Hall Textbook of Medical Physiology. 14th ed. Elsevier – Health Science; 2020.

Shaker JL, Deftos L. PubMed. Published 2000. Web.