What are the effects of peroxisome proliferator-activated receptor agonists on adiponectin, tumor necrosis factor-alpha, and other cytokines in insulin resistance?

Abstract	Patients with type 2 diabetes are at high risk of cardiovascular disease. In addition to treating hyperglycemia, the thiazolidinedione (TZD) class of antidiabetic agents may also benefit the cardiovascular complications associated with the disease. The two available TZDs, pioglitazone and rosiglitazone, are peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists that influence gene expression of key proteins involved in regulating glucose and lipid metabolism. Tumor necrosis factor-alpha (TNF-alpha) and adiponectin are believed to be important in the development of insulin resistance and atherosclerosis. Understanding the role of these cytokines in the inflammatory processes that trigger plaque development might lead to identification of other potential mechanisms that could be exploited to enhance future treatments for patients with diabetes and atherosclerosis.
Authors	Patrick J Boyle
Journal	Clinical cardiology (Clin Cardiol) Vol. 27 Issue 7 Suppl 4 Pg. IV11-6 (Jul 2004) ISSN: 0160-9289 [Print] United States
PMID	15470906 (Publication Type: Journal Article, Review)
Chemical References	Adiponectin Apolipoproteins E Cytokines Intercellular Signaling Peptides and Proteins Proteins Receptors, Cytoplasmic and Nuclear Thiazolidinediones Transcription Factors Tumor Necrosis Factor-alpha Glucose
Topics	Adiponectin Animals Apolipoproteins E (deficiency, physiology) Arteriosclerosis (physiopathology) Cardiovascular Diseases (physiopathology) Cytokines (drug effects, immunology) Diabetes Mellitus, Type 2 (physiopathology) Glucose (metabolism) Humans Insulin Resistance (immunology, physiology) Intercellular Signaling Peptides and Proteins Lipid Metabolism Proteins (drug effects, immunology) Receptors, Cytoplasmic and Nuclear (agonists) Thiazolidinediones (agonists, pharmacology) Transcription Factors (agonists, pharmacology) Tumor Necrosis Factor-alpha (drug effects, immunology)

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