Hypoadiponectinemia: A common basis for diseases associated with overnutrition

被引:15
作者
Funahashi T. [1 ]
Matsuzawa Y. [1 ]
机构
[1] Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka 565-0871
关键词
NASH; Adiponectin Level; Transverse Aortic Constriction; Plasma Adiponectin Level; Overnutrition;
D O I
10.1007/s11883-006-0042-8
中图分类号
学科分类号
摘要
Adiponectin is a plasma protein derived from adipose tissue, which we discovered from a human adipose cDNA project. Adiponectin exists in circulating plasma at concentrations ranging from 4 to 30 μg/mL, which is much higher than the concentrations of various other hormones and cytokines. Adiponectin has a sticky nature, binding to collagen I, III, and V, which are present in vascular intima. Adiponectin exhibits various antiatherogenic effects on vascular cells, suppressing the expression of adhesion molecules in vascular endothelial cells, proliferation of smooth muscle cells, and cholesteryl-ester accumulation in macrophages. However, its plasma levels are low in subjects with excess intra-abdominal fat. Adiponectin also has antidiabetic properties, and plasma adiponectin levels correlate positively with insulin sensitivity. Several clinical studies have demonstrated that hypoadiponectinemia is a risk factor for new-onset diabetes. Recent studies suggest that hypoadiponectinemia may partly contribute to the development of salt-sensitive hypertension and hypertensive heart failure, and can be also a risk factor for overnutrition-related cancers such as breast, colon, uterine, and prostate cancers. Hypoadiponectinemia might be at least in part the molecular basis of various diseases associated with overnutrition. Copyright © 2006 by Current Science Inc.
引用
收藏
页码:433 / 438
页数:5
相关论文
共 48 条
[1]  
The IDF consensus worldwide definition of the metabolic syndrome, (2006)
[2]  
Kissebah A.H., Vydelingum N., Murray R., Et al., Relation of body fat distribution to metabolic complications of obesity, J Clin Endocrinol Metab, 54, pp. 254-260, (1982)
[3]  
Larsson B., Svardsudd K., Welin L., Et al., Abdominal adipose tissue distribution, obesity, and risk of cardiovascular disease and death: 13 year follow up of participants in the study of men born in 1913, Br Med J Clin Res Ed, 288, pp. 1401-1404, (1984)
[4]  
Fujioka S., Matsuzawa Y., Tokunaga K., Tarui S., Contribution of intraabdominal fat accumulation to the impairment of glucose and lipid metabolism in human obesity, Metabolism, 36, pp. 54-59, (1987)
[5]  
Nakamura T., Tokunaga K., Shimomura I., Et al., Contribution of visceral fat accumulation to the development of coronary artery disease in non-obese men, Atherosclerosis, 107, pp. 239-246, (1994)
[6]  
Kaplan N.M., The deadly quartet. Upper-body obesity, glucose intolerance, hypertriglyceridemia, and hypertension, Arch Intern Med, 149, pp. 1514-1520, (1989)
[7]  
Funahashi T., Nakamura T., Shimomura I., Et al., Role of adipocytokines on the pathogenesis of atherosclerosis in visceral obesity, Intern Med, 38, pp. 202-206, (1999)
[8]  
Maeda K., Okubo K., Shimomura I., Et al., cDNA cloning and expression of a novel adipose specific collagen-like factor, apMa (Adipose Most Abundant gene transcript 1), Biochem Biophys Res Commun, 221, pp. 286-289, (1996)
[9]  
Arita Y., Kihara S., Ouchi N., Et al., Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity, Biochem Biophys Res Commun, 257, pp. 79-83, (1999)
[10]  
Reaven G.M., Banting lecture 1988. Role of insulin resistance in human disease?, Diabetes, 37, pp. 1595-1607, (1988)