Sequelae of Altered Metabolism in Visceral

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Intraabdominal adipose tissue has metabolic characteristics that are different from those of adipose tissue from other sites. These differences seem to be most pronounced in the regions that are drained by the portal circulation. These 'portal adipose tissues' have a sensitive system for the mobilization of free fatty acids due to a preponderance of ^-adrenergic receptors and little a-adrenergic inhibition.

The hypothesis has been advanced that the heightened responsiveness of intraabdominal fat to lipo-lytic agents results in increased lipolysis with venous drainage of the released free fatty acids directly to the liver. These fatty acids may contribute to increases in triacylglycerol synthesis and hyperinsulinemia secondary to decrements in insulin degradation. Hyper-insulinemia could produce insulin resistance and eventually type 2 diabetes in susceptible individuals. However, the hypothesis that increased release of free fatty acids from intraabdominal adipose tissue leads to insulin resistance through effects on the liver lacks supporting evidence in vivo.

The proposed mechanism of action of fat patterning on metabolic syndrome is linked to hyperinsulinemia. Hyperinsulinemia may lead to increased blood pressure through increased sympathetic stimulation of the vessels, heart, and kidneys. In addition, insulin resistance combined with a relative increase in androgenic activity may lead to an unfavorable lipid profile. In addition to the effects of free fatty acids on insulin and glucose, an increased visceral depot decreases the activity of LPL. This causes an increase in very low-density lipoprotein (VLDL) secretion and a decrease in its catabolism. The production of high-density lipoprotein (HDL) therefore decreases, the transfer of lipids (i.e., VLDL to LDL and HDL) increases, and an enrichment of triacylglycerols results.

In obesity and type 2 diabetes, there is an increased content of lipids within and around muscle fibers. Researchers have suggested that the accumulation of triaclyglycerols within the skeletal muscle may play an important role in insulin resistance. In obese individuals with elevated amounts of visceral adipose tissue, there is a strong correlation between visceral adipose tissue and insulin resistance independent of subcutaneous (abdominal and nonabdominal) adipose tissue and cardiovascular fitness. It has been suggested that the discrepancies in the literature regarding the independent effect of visceral or subcutaneous adipose tissue on insulin resistance are due to the large variations of abdominal obesity within the study populations.

Leptin is a hormone that is produced in the adipose cells and can act on the hunger center in the hypothalamus to reduce hunger and appetite and thereby lower food intake. Plasma leptin levels are correlated with body fat. Researchers have discovered a leptin receptor gene that is responsible for obesity due to the mutation or absence of the gene. This condition is extremely rare in humans. In general, in obese humans the leptin levels are elevated (hyperleptinemia).

There is a progressive increase in plasma levels during puberty in girls due to the increase in body fat during this period and in response to the effect of estrogens. Circulating leptin levels tend to decrease in response to testosterone in boys, thus resulting in higher plasma leptin levels in women compared to men. Leptin levels are also affected by insulin and glucocorticoids.

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