title: Type 2 diabetes and cardiovascular disease: getting to the fat of the matter.
abstract: The increasing national prevalence of obesity is a major public health concern and a substantial burden on the health care resources of Canada. In addition to the direct health impact of obesity, this condition is a well-established risk factor for the development of various prevalent comorbidities including type 2 diabetes, hypertension, and cardiovascular disease. Historically, adipose tissue has been regarded primarily as an organ for energy storage. However, the discovery of leptin in the mid 1990's revolutionized our understanding of this tissue and has focused attention on the endocrine function of adipose tissue as a source of secreted bioactive peptides. These compounds, collectively termed adipokines, regulate a number of biological functions including appetite and energy balance, insulin sensitivity, lipid metabolism, blood pressure, and inflammation. The physiological importance of adipokines has led to the hypothesis that changes in the synthesis and secretion of these compounds in the obese are a causative factor contributing to the development of obesity and obesity-related diseases in these individuals. Following from this it has been proposed that pharmacologic manipulation of adipokine levels may provide novel effective therapeutic strategies to treat and prevent obesity, type 2 diabetes, and cardiovascular disease.
authors.affiliation: College of Pharmacy, Department of Pharmacology, Dalhousie University, Halifax, NS B3H 1X5, Canada.
authors.forename: Kerry B
authors.initials: KB
authors.lastname: Goralski
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Sinal
mesh_terms: D052242:Adiponectin / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000378:metabolism; D003167:Complement Activation; D015926:Complement C3a / Q000378:metabolism; D011416:Complement Factor D / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000209:etiology / Q000378:metabolism; D005342:Fibrinolysis; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000378:metabolism; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000378:metabolism; D020738:Leptin / Q000378:metabolism; D054409:Nicotinamide Phosphoribosyltransferase; D009765:Obesity / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D012084:Renin-Angiotensin System; D052243:Resistin / Q000378:metabolism; D012177:Retinol-Binding Proteins / Q000378:metabolism; D054839:Retinol-Binding Proteins, Plasma; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D052242:Adiponectin; D016207:Cytokines; D015850:Interleukin-6; D020738:Leptin; D017395:Plasminogen Activator Inhibitor 1; C101326:RBP4 protein, human; D052243:Resistin; D012177:Retinol-Binding Proteins; D054839:Retinol-Binding Proteins, Plasma; D014409:Tumor Necrosis Factor-alpha; C044541:complement C3a, des-Arg-(77)-; D000804:Angiotensin II; D015926:Complement C3a; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human; D011416:Complement Factor D