Pathophysiology and pathogenesis of visceral fat obesity - PubMed (original) (raw)

Review

Pathophysiology and pathogenesis of visceral fat obesity

Y Matsuzawa et al. Obes Res. 1995 Sep.

Free article

Abstract

Based on the analysis of fat distribution by computed tomography (CT) scans, the classification scheme for obesity should include visceral fat obesity in which fat accumulation is predominant in the intra-abdominal cavity. Obese subjects with visceral fat accumulation more frequently demonstrate impairment of glucose and lipid metabolism than those with subcutaneous fat accumulation. We have shown that visceral fat obesity is present in almost 90% of obese patients with ischemic heart disease. Even in non-obese subjects, visceral fat accumulation is correlated with glucose intolerance, hyperlipidemia and hypertension. Forty percent of non-obese subjects with coronary artery disease (CAD) had increased visceral fat. In non-obese subjects, visceral fat area assessed by abdominal CT at the level of the umbilicus correlates with metabolic risk factors, whereas in obese subjects the visceral fat area to subcutaneous fat area ratio provides a more significant correlation. From clinical and basic investigations, aging, sex hormones, excess intake of sucrose and lack of physical exercise have been suggested to be determinants for visceral fat accumulation. Since intra-abdominal fat (mesenteric and omentum fat) has been shown to have high activities of both lipogenesis and lipolysis, its accumulation can induce high levels of free fatty acids, a product of lipolysis, in portal circulation which go into the liver. Excess free fatty acids may cause the enhancement of lipid synthesis and gluconeogenesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance and hypertension and finally atherosclerosis. Thus we propose a disease entity, visceral fat syndrome, which may increase susceptibility to atherosclerosis due to multiple risk factors induced by visceral fat accumulation.

PubMed Disclaimer

Cited by

Advancement in genetic variants conferring obesity susceptibility from genome-wide association studies.
Wang T, Jia W, Hu C. Wang T, et al. Front Med. 2015 Jun;9(2):146-61. doi: 10.1007/s11684-014-0373-8. Epub 2014 Dec 29. Front Med. 2015. PMID: 25556696 Review.
Fat tissue, aging, and cellular senescence.
Tchkonia T, Morbeck DE, Von Zglinicki T, Van Deursen J, Lustgarten J, Scrable H, Khosla S, Jensen MD, Kirkland JL. Tchkonia T, et al. Aging Cell. 2010 Oct;9(5):667-84. doi: 10.1111/j.1474-9726.2010.00608.x. Epub 2010 Aug 15. Aging Cell. 2010. PMID: 20701600 Free PMC article. Review.
New risk prediction model of coronary heart disease in participants with and without diabetes: Assessments of the Framingham risk and Suita scores in 3-year longitudinal database in a Japanese population.
Hirai H, Asahi K, Yamaguchi S, Mori H, Satoh H, Iseki K, Moriyama T, Yamagata K, Tsuruya K, Fujimoto S, Narita I, Konta T, Kondo M, Shibagaki Y, Kasahara M, Watanabe T, Shimabukuro M. Hirai H, et al. Sci Rep. 2019 Feb 26;9(1):2813. doi: 10.1038/s41598-019-39049-w. Sci Rep. 2019. PMID: 30808962 Free PMC article.
Aging and atherosclerosis in human and nonhuman primates.
Cefalu WT, Wagner JD. Cefalu WT, et al. Age (Omaha). 1997 Jan;20(1):15-28. doi: 10.1007/s11357-997-0002-4. Age (Omaha). 1997. PMID: 23604288 Free PMC article.
Perivascular Adipocytes Store Norepinephrine by Vesicular Transport.
Ahmad MF, Ferland D, Ayala-Lopez N, Contreras GA, Darios E, Thompson J, Ismail A, Thelen K, Moeser AJ, Burnett R, Anantharam A, Watts SW. Ahmad MF, et al. Arterioscler Thromb Vasc Biol. 2019 Feb;39(2):188-199. doi: 10.1161/ATVBAHA.118.311720. Arterioscler Thromb Vasc Biol. 2019. PMID: 30567483 Free PMC article.

Pathophysiology and pathogenesis of visceral fat obesity - PubMed (original) (raw)