J Korean Med Assoc.  2007 Aug;50(8):725-728. 10.5124/jkma.2007.50.8.725.

Visceral Obesity

• Yoo HJ

• KMID: 2184900
• DOI: http://doi.org/10.5124/jkma.2007.50.8.725

Abstract

Multiple lines of evidence support the thesis that visceral adiposity is causally related to insulin resistance and the metabolic syndrome. Visceral adipose tissue is biochemically quite distinct from subcutaneous adipose tissue. It has become increasingly evident that the effects of visceral adiposity must be mediated by multiple factors. The release of free fatty acid from visceral adipose tissue in obese individuals has been reported to account for 20% of that delivered to the liver, and it is unlikely that the contribution of visceral fat to the free fatty acid flux in the circulation is the major mechanism of insulin resistance. Adiponectin and other newly discovered adipokines are likely to contribute to attenuate the effects of visceral obesity onto insulin resistance and metabolic syndrome. Insulin resistance and the metabolic impacts are the consequence of the metabolic effects of the products being released from the adipose tissue rather than an effect of the absolute mass of the fat. Adipose tissue releases free fatty acids and cytokines and modulates the secretion of a large number of metabolically active adipokines. Abdominal circumference is one of indicators for visceral obesity. The abdominal circumference values among Koreans are discussed by active groups.

Keyword

Visceral obesity; Insulin resistance; Adipokines; Free fatty acids; Oxidative stress; Waist circumference

MeSH Terms

Adipokines
Adiponectin
Adipose Tissue
Adiposity
Cytokines
Fatty Acids, Nonesterified
Insulin Resistance
Intra-Abdominal Fat
Liver
Obesity, Abdominal*
Oxidative Stress
Subcutaneous Fat
Waist Circumference
Adipokines
Adiponectin
Cytokines
Fatty Acids, Nonesterified

Figure

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  Figure 1 Lipotoxicity hypothesis in metabolic syndrome.

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  Figure 2 Oxidative stress of fat tissues and metabolic syndrome.

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