title: Insulin resistance and body fat distribution.
abstract: Body fat distribution can be assessed by computed tomography (CT). The ratio of umbilicus was used to classify obese subjects as having visceral fat obesity (VFO) or subcutaneous fat obesity (SFO). Serum triglyceride and total cholesterol levels and plasma glucose area in an oral glucose tolerance test were higher in patients with VFO than in those with SFO. Significant positive correlations were demonstrated between V/S ratio and plasma glucose area, serum triglyceride level, and total cholesterol level as well as systolic or diastolic blood pressure. VFO was more frequently associated with coronary artery disease. Moreover, VFO was more often accompanied by multiple risk factors than was SFO. Steady-state plasma glucose (SSPG) level was significantly higher in patients with VFO than with SFO, suggesting that insulin resistance may be more remarkable in VFO than in SFO. Furthermore, visceral fat accumulation was also associated with these complications even in nonobese subjects. Visceral fat area (VFA) was significantly correlated with fasting plasma glucose, serum triglyceride, and total cholesterol levels. Animal models such as Goto-Kakizaki (GK) rats with ventromedial hypothalamus (VMH) lesions and Otsuka-Long-Evans-Tokushima-Fatty (OLETF) rats were accompanied by visceral fat accumulation and an early stage of aortic atherosclerosis. Aging, sex hormone, genetic, and dietary factors and physical inactivity may induce visceral fat accumulation. Visceral fat is characterized by its high lipogenic activity as well as its accelerated lipolytic activity. High levels of portal free fatty acids (FFAs) may eventually result in an enhancement of hepatic triglyceride synthesis, causing hyperlipidemia. High portal FFA levels would also induce insulin resistance, thereby causing glucose intolerance, hypertension, and finally atherosclerosis. We propose a term, "visceral fat syndrome," as a highly atherogenic state, which includes visceral fat accumulation, glucose intolerance (insulin resistance), hyperlipidemia, and hypertension.
authors: Second Department of Internal Medicine, Osaka University Medical School, Japan.
authors: S
authors: S
authors: Yamashita
authors: T
authors: T
authors: Nakamura
authors: I
authors: I
authors: Shimomura
authors: M
authors: M
authors: Nishida
authors: S
authors: S
authors: Yoshida
authors: K
authors: K
authors: Kotani
authors: K
authors: K
authors: Kameda-Takemuara
authors: K
authors: K
authors: Tokunaga
authors: Y
authors: Y
authors: Matsuzawa
mesh_terms: D000273:Adipose Tissue / Q000033:anatomy & histology* / Q000502:physiology; D000328:Adult; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition; D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000503:physiopathology*; D003920:Diabetes Mellitus / Q000097:blood / Q000503:physiopathology*; D018149:Glucose Intolerance / Q000097:blood / Q000503:physiopathology; D006801:Humans; D007333:Insulin Resistance; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000503:physiopathology*; D012867:Skin; D014057:Tomography, X-Ray Computed; D014280:Triglycerides / Q000097:blood; D014781:Viscera
chemical_list: D001786:Blood Glucose; D014280:Triglycerides; D002784:Cholesterol