The data on the role of increased visceral fat as a cause of insulin resistance are conflicting. There are probably several reasons for the confusion. Methodologic imprecision in the measurement of body fat depots and real biological variation in lipolytic activity of fat depots may both play a role. It appears that visceral fat has very little if any role in the oversupply of FFAs to extrahepatic tissues in insulin-resistant states. Instead, subcutaneous fat, especially in the upper body, is the major contributor to this known mediator of insulin resistance. Increases in visceral fat mass, even among normal-weight individuals, are accompanied by increases in subcutaneous fat mass. Thus, the weight of evidence suggests that visceral fat may be responsible for hepatic insulin resistance in some circumstances but is no more than a marker for insulin resistance in extrahepatic tissues. Future studies should focus on the relationship between upper-body subcutaneous and visceral fat depots, regulation of FFA metabolism, and the relative contribution of insulin resistance in liver versus that in skeletal muscle to systemic insulin resistance.
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism
- Advanced and Specialized Nursing