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

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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.

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