DM的最新研究及治疗信息.pptVIP

* * Presentation notes To be effective, treatment for type 2 diabetes must be intensified in line with the progressive failure of endogenous insulin production and increase in insulin resistance. Therapy generally progresses from non-pharmacological interventions such as improved diet and exercise, through the introduction of oral antidiabetic agents, to the introduction of insulin, the most effective blood glucose lowering treatment option available. * The primary metabolic defects of T2DM are pancreatic islet dysfunction (?-cell and ?-cell dysfunction) and impaired insulin action (insulin resistance); another contributing factor is uncompensated glucose influx. Many of these specific problems are addressed by one or another existing class of oral antihyperglycemic drugs, each of which has distinctive mechanisms.1 ?-Glucosidase inhibitors moderate glucose influx by delaying intestinal carbohydrate absorption, thereby mitigating postprandial glucose excursions.1 The utility of these agents depends in part on proper dietary compliance and is more effective in populations whose diet does not consist of highly processed foods. The widespread use of these agents in Japan and Spain is an excellent example of their utility in populations where a rice and fish diet is prevalent. Thiazolidinediones (TZDs) work primarily by enhancing both basal and insulin-mediated suppression of hepatic glucose production and to some extent by augmenting insulin-stimulated muscle glucose utilization.2 Metformin (of the biguanide drug class) lowers glucose levels, chiefly by reducing heptic glucose production.1 Sulfonylureas lower the glucose threshold for triggering ?-cell insulin release.1 Glinides resemble sulfonylureas in enhancing acute ?-cell function. Their short metabolic half-lives enable them to produce brief, episodic stimulation of insulin secretion.1 Of the glinides, nateglinide is rapidly reversible, whereas repaglinide is not. No currently available therapy addresses ?-cell f