Adipose tissue dysfunction in obesity.
The incidence of obesity has increased dramatically during recent decades. Obesity will cause a decline in life expectancy for the first time in recent history due to numerous co-morbid disorders. Adipocyte and adipose tissue dysfunction belong to the primary defects in obesity and may link obesity to several health problems including increased risk of insulin resistance, type 2 diabetes, fatty liver disease, hypertension, dyslipidemia, atherosclerosis, dementia, airway disease and some cancers. However, not all obese individuals develop obesity related metabolic or cardiovascular disorders potentially due to a preserved normal adipose tissue architecture and function. The majority of patients with obesity have an impaired adipose tissue function caused by the interaction of genetic and environmental factors which lead to adipocyte hypertrophy, hypoxia, a variety of stresses and inflammatory processes within adipose tissue. Ectopic fat accumulation including visceral obesity may be considered as a consequence of adipose tissue dysfunction, which is further characterized by changes in the cellular composition, increased lipid storage and impaired insulin sensitivity in adipocytes, and secretion of a proinflammatory, atherogenic, and diabetogenic adipokine pattern. This review focuses on the discussion of mechanisms causing or maintaining impaired adipose tissue function in obesity and potentially linking obesity to its associated disorders. A model is proposed how different pathogenic factors and mechanisms may cause dysfunction of adipose tissue.
Blüher
M
M
Department of Medicine, University of Leipzig, Leipzig, Germany. bluma@medizin.uni-leipzig.de
D017667:Adipocytes / Q000378:metabolism* / Q000473:pathology; D054392:Adipokines / Q000235:genetics / Q000378:metabolism*; D000273:Adipose Tissue / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D050197:Atherosclerosis / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D015687:Cell Hypoxia / Q000235:genetics; D003704:Dementia / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D050171:Dyslipidemias / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D005234:Fatty Liver / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D015994:Incidence; D007333:Insulin Resistance / Q000235:genetics; D050356:Lipid Metabolism; D008171:Lung Diseases / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D008954:Models, Biological; D009369:Neoplasms / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D009765:Obesity / Q000150:complications / Q000453:epidemiology / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology
D054392:Adipokines