Obesity, inflammation, and vascular disease: the role of the adipose tissue as an endocrine organ.
Insulin resistance, both in nondiabetic and diabetic subjects, is frequently associated with obesity, particularly with an excess of central fat. With the growing prevalence of obesity, scientific interest in the biology of adipose tissue has been extended to the secretory products of adipocytes, since they are increasingly shown to influence several aspects in the pathogenesis of obesity-related diseases Until relatively recently, the role of fat itself in the development of obesity and its consequences was considered to be a passive one; adipocytes were considered to be little more than storage cells for fat. It is now clear that, in addition to storing calories as triglycerides, they also secrete a large variety of proteins, including cytokines, chemokines and hormone-like factors, such as leptin, adiponectin and resistin. This production of pro-atherogenic chemokines by adipose tissue is of particular interest since their local secretion, e.g. by perivascular adipose depots, may provide a novel mechanistic link between obesity and the associated vascular complications. Recent research has revealed many functions of adipocytokines extending far beyond metabolism, such as immunity, cancer and bone formation. This remarkable understanding is allowing us to more clearly define the role that adipocytes play in health and in obesity and how inflammatory mediators act as signaling molecules in this process. Moreover, on a molecular level, we are beginning to comprehend how such variables as hormonal control, exercise, food intake, and genetic variation interact and result in a given phenotype, and how pharmacological intervention may modulate adipose tissue biology.
Calabro
Paolo
P
Division of Cardiology, Department of Cardiothoracic Sciences, Second University of Naples, Italy, paolo.calabro@unina2.it
Yeh
Edward T
ET
D017667:Adipocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D000273:Adipose Tissue / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D003920:Diabetes Mellitus / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D004702:Endocrine Glands / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D007333:Insulin Resistance / Q000235:genetics / Q000276:immunology; D009369:Neoplasms / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009765:Obesity / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D010012:Osteogenesis / Q000235:genetics / Q000276:immunology; D036361:Peptide Hormones / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology; D014652:Vascular Diseases / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000473:pathology
D036361:Peptide Hormones