PPAR-gamma receptor agonists--a review of their role in diabetic management in Trinidad and Tobago.
The PPAR-gamma receptor agonists, as a relatively new and perhaps still not very widely used class of antidiabetic agent in the Caribbean and particularly the Trinidadian context, possess pharmacologic properties that certainly have been shown to have impact on many of the inflammatory, metabolic, biochemical and structural macrovascular aberrations that occur in the type 2 diabetic. Activation of PPAR(gamma) nuclear receptors regulates the transcription of insulin-responsive genes involved in the control of glucose production, transport, and utilization. PPAR(gamma)-responsive genes also participate in the regulation of fatty acid metabolism, an important contributory pathogenic factor in this subset of patients. The unique mode of action of this class of therapeutic agent addresses a range of anomalies occurring at the cellular and sub-cellular level that are injurious to the diabetic. My aim in addressing the issue of the potential impact of PPAR-gamma receptor agonists on cardiovascular disease (CVD) morbidity and mortality in the diabetic, is first, to seek to enhance both an awareness of, and greater familiarity among our own physicians, with this class of drug, and secondly, to effect a timely review of the recent literature as it relates to the tremendous possibilities for the potential clinical gains that might accrue from their use, in so far as this may serve to ameliorate the ravages of the CVD disease that all too tragically attends the type 2 diabetic, and more specifically those with the insulin resistance syndrome.
Smith
Steve Ian
SI
General Hospital, San Fernando, Trinidad. sismith@carib-link.net
D050260:Carbohydrate Metabolism; D002318:Cardiovascular Diseases / Q000209:etiology; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000453:epidemiology / Q000235:genetics / Q000378:metabolism; D003925:Diabetic Angiopathies / Q000209:etiology / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005260:Female; D005838:Genotype; D006801:Humans; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism; D009765:Obesity / Q000150:complications / Q000235:genetics / Q000378:metabolism; D047495:PPAR gamma / Q000819:agonists*; D011493:Protein Kinase C / Q000378:metabolism; D045162:Thiazolidinediones / Q000627:therapeutic use; D014300:Trinidad and Tobago / Q000453:epidemiology
D005230:Fatty Acids, Nonesterified; D008055:Lipids; D047495:PPAR gamma; D045162:Thiazolidinediones; D011493:Protein Kinase C; D048049:Extracellular Signal-Regulated MAP Kinases