1988 Fiscal Year Final Research Report Summary
Studies on Pathogenesis and Pathophysiology of Visceral Fat Obesity, a New Criteria of Obesity based on fat Topography
| Project/Area Number |
62480255
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
内分泌・代謝学
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| Research Institution | Osaka University |
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Principal Investigator |
MATSUZAWA Yuji Osaka University Medical School, Lecturer, 医学部, 講師 (70116101)
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| Co-Investigator(Kenkyū-buntansha) |
川本 俊治 大阪大学, 医学部附属病院, 医員
FUJIOKA Shigenori Osaka University Hospital, Medical Staff, 医学部附属病院, 医員 (40218988)
KAWAMOTO Toshiharu Osaka University Hospital, Medical Staff
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| Project Period (FY) |
1987 – 1988
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| Keywords | Visceral Fat Obesity / Subcutaneous Fat Obesity / VMH-lesioned Rat / Mesenteric Preadipocyte / Portal Free Fatty Acid / 脂肪分布 |
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| Research Abstract |
The frequency of metabolic complications associated with obesity has been shown to be related to the profile of body fat distribution. We have proposed a new anthropometric classification of obesity using CT scanning technique developed by us one is "visceral fat obesity" which is characterized by a marked fat accumulation in abdominal cavity and the other is "subcutaneous fat obesity" in which fat accumulations located mainly in subcutaneous area. The disturbance of glucose and lipid metabolism are more remarkable in visceral fat obesity than in subcutaneous fat obesity of obesity. In this study, we investigated pathogenesis and pathophysiology of visceral fat obesity.
Changes of fat distribution after weight reduction were investigated in visceral fat obesity. After weight reduction, visceral fat decreased more than any other part of body fat, and the extent of improvement of metabolic aberrations correlted with the extent of decrease in viscreal fat after weight reduction. Predominant fat accumulation in the abdominal cavity were also observed in normal weight patients with type 2 diabetes or hyperlipidemia.
Animal experiments using VMH-lesioned rats revealed that the extent of mesenteric fat accumulation is closely correlated to the extent of hyperglycemia and hypertriglyceridemia. Portal free fatty acid (FFA) were also higher in accordance with the volume of mesenteric fat. Excessive FFA flux into the liver may cause overproduction of lipoproteins and also might lead to reduction in insulin sensitivity and deranged glucose metabolism. As the factors which cause visceral fat accumulation, high sucrose diet promoted mesenteric fat accumulation in VMH-lesioned obese rats. Experiments using primary-cultured preadipocytes revealed that mesenteric preadipcytes were resistant to stimulation of replication and differentiation, consequently intending to increase cell volume of matured adipocytes at the development of adipose tissue.
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