Abdominal Obesity - Pathophysiology of Visceral Obesity

Pathophysiology of Visceral Obesity

There is enough evidence in the scientific community where an impaired non-esterified fatty acid (NEFA) metabolism could give way to the insulin-resistant state of individuals with this type of obesity. Hypertrophy of intra-abdominal adipose cells causes it to be in a hyperlipolytic state in which it is resistant to the antilipolytic effect of insulin. The resulting NEFA flux to the liver causes impairment of liver metabolism which leads to over production of glucose in the liver. Individuals with obesity are more likely to develop weakened non-esterified fatty acid (NEFA), which can weaken the metabolism of the liver causing high glucose production. An individual is at a higher risk of developing ischemic heart disease if they have hyperinsulinemia-dyslipidemia while being abdominal obese.

Visceral fat, unlike subcutaneous fat, is implicated in many aging-associated diseases. Surgical removal of visceral fat, but not subcutaneous fat, has been shown to extend the mean and maximum lifespan of rodents. Abdominal adipose tissue is a major source of increased inflammatory Interleukin-6 (IL-6) associated with aging. Induction of cellular senescence by visceral fat contributes to the inflammation.