Literature DB >> 11590996

Visceral obesity and the metabolic syndrome: effects of weight loss.

L Busetto1.   

Abstract

A large body of experimental and epidemiological evidence has established an association between visceral obesity and the metabolic syndrome, which retains its power throughout the spectrum of adiposity and is still clinically meaningful in severe obesity. The association may be due to an overload of liver free fatty acids (FFA) produced by the high lipolytic activity of omental fat. A substantial improvement in all aspects of the metabolic syndrome with only a moderate degree of weight loss has been observed in a large number of randomised controlled studies and can also be obtained in severe obesity, despite the fact that the patients remain obese. The reasons for this apparent dissociation between weight loss and metabolic improvement are not yet clearly understood, but may involve the relationship between visceral fat and metabolic alterations. The results of some studies suggest that the favourable metabolic changes observed in obese patients with weight loss may be directly attributable to a reduction in visceral fat, and other studies have recently shown that a rapid and preferential reduction in visceral fat mass occurs during the first phase of weight loss in morbidly obese patients possibly as a result of sympathetic nervous system activation. It is therefore possible that the apparent dissociation between weight loss and metabolic improvement is partially due to a difference in the responsiveness of visceral and subcutaneous adipose tissue to energy restriction: i.e. the fact that the metabolic profile of patients with visceral obesity may substantially improve after the loss of only a few kilograms of body weight could be related to a greater relative reduction in the amount of visceral rather than other fat. In this respect, the characteristically high rate of visceral fat mobilisation can also be seen as a good target for interventions aimed at reducing cardiovascular risk factors.

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Mesh:

Year:  2001        PMID: 11590996

Source DB:  PubMed          Journal:  Nutr Metab Cardiovasc Dis        ISSN: 0939-4753            Impact factor:   4.222


  23 in total

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