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An overview of pathophysiology and treatment of insulin resistance Umrani DN; Goyal RKIndian J Physiol Pharmacol 2001[Jan]; 45 (1): 22-36Insulin resistance has emerged out as a concept linking diabetes mellitus and hypertension. Clinically it is characterized by hyperinsulinemia, hypertension, central obesity, abnormal lipid profile and cardiovascular complications. Insulin resistance is often associated with presence of anti-insulin antibodies and absent or dysfunctional insulin receptors. At molecular level insulin resistance appears to occur at the level of G-protein, kinase activation, glucose carriers (GLUT) and gene expression. Although with advent or research, the molecular mechanisms of insulin resistance are becoming more clear and there is development of new therapeutic agents like insulin sensitizers (thizolidinediones), in clinical practice, as of today, a patient with insulin resistance is looked upon as hypertensive or having diabetes mellitus. Accordingly he is taking either antihypertensives or antidiabetic drugs or both. It is thus essential to look into effects of these agents on insulin sensitivity. In recent years some scattered studies have been conducted to evaluate the effect of various antihypertensives and antidiabetics on insulin sensitivity. An antihypertensive or antidiabetic drug should directly benefit the cardiovascular risk profile of these patients. Although various newer approaches are explored to have a therapeutic benefit in insulin resistance, it is still a long way in the research, when a suitable pharmacological agent with least untoward effects will be available for the treatment of insulin residence.|*Insulin Resistance/physiology[MESH]|Animals[MESH]|Enzyme Inhibitors/*therapeutic use[MESH]|GTP-Binding Proteins/metabolism[MESH]|Heart Failure/etiology[MESH]|Humans[MESH]|Hyperglycemia/complications/*drug therapy/physiopathology[MESH]|Hypertension/etiology[MESH]|Hypoglycemic Agents/*therapeutic use[MESH]|Monosaccharide Transport Proteins/metabolism[MESH]|Phosphatidylinositol 3-Kinases/metabolism[MESH]|Phosphotransferases/metabolism[MESH]|Signal Transduction/physiology[MESH] |
