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Where's the Fat?
Appendix

Insulin Resistance
The list of diseases above has been associated together under a different title, Syndrome X or the Metabolic Syndrome. This syndrome consists of insulin resistance at the center of a group of diseases the resistance may cause: impaired glucose tolerance, diabetes mellitus, hypertriglyceridemia and hypertension. return

Intra-Abdominal Adipose Depots
Abdominal girth is a result of the accumulation of adipose tissue occurring in any of three different compartments: abdominal skin, visceral (internal organs) and retroperitoneal (back and side, "love handles"). From a metabolic point of view, they are not equivalent. Retroperitoneal fat is the least active metabolically and thus appears to change least when all three areas are followed during weight loss. Of these three sites, only the fat tissue of the internal organs, whose veins drain into the liver, share a common circulation. This shared connection may help explain why abdominal obesity is more associated with disease processes than other fat tissue. return

Genetic Influence
Although the gene(s) for abdominal obesity remain to be identified, it appears that a recessive gene accounts for at least part of this metabolic disorder. The Quebec Family Study evaluated 382 men and women from 100 families using CT scans to measure visceral adiposity. Evidence pointed to a recessive gene, not linked to the X or Y sex chromosomes, that influenced abdominal fat levels in these families. However, all of the genetic variance could not be attributed to this gene and scientists continue to search for additional genetic or environmental influences. return

Insulin Resistance
FFA inhibits glucose utilization. Competition between FFA and glucose as cellular energy sources has been known for some time. Because muscles, the major site of insulin's actions, prefer to use FFA over glucose, it is theorized that FFA, in this way, reduces sensitivity to insulin.

FFA stimulate liver glucose production. FFA stimulate the liver's glucose production. Excess glucose production has been shown to occur in diabetes mellitus and also in patients with impaired glucose tolerance.

FFA stimulate insulin secretion and thus may contribute to the finding of hyperinsulinemia in these subjects. Hyperinsulinemia also appears to be due to decreased clearance of insulin by the liver in abdominal obesity.

FFA are needed by the liver for the production of triglycerides and VLDL. Unfortunately, studies on the above effects are not in agreement and medical scientists are left with a chicken and egg situation, that is, which came first -- the insulin resistance or the abdominal fat? More research is needed before we can be certain. return




  

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