Insulin Resistance Type 2 Diabetes -cell Dysfunction Insulin Resistance Hyperglycaemia Insulin Concentration Insulin Action Euglycaemia -cell Failure
{"Image DocumentName": "Dual defect of type 2 diabetes: Treating a moving target", "Image ImageDescription": "Insulin. Resistance. Type 2. Diabetes. b-cell. Dysfunction. Hyperglycaemia. Insulin Action. b-cell Failure. Insulin. Concentration. Insulin. Resistance. Dual defect of type 2 diabetes: treating a moving target. The pathophysiology of type 2 diabetes is complex, and characterised by remorseless progression of the dual metabolic defects of insulin resistance and b-cell dysfunction. Initially, insulin resistance causes the glucose-lowering actions of insulin to be blunted, so that the pancreas secretes more insulin to overcome the deficit. At this stage the subject may develop impaired glucose tolerance, but is not yet diabetic. As insulin resistance progresses, however, the pancreas is no longer able to secrete enough insulin to control glycaemia, and increased hepatic glucose output and reduced glucose disposal by muscle and fat contribute to the chronic fasting and postprandial hyperglycaemia characteristic of type 2 diabetes. Eventually, insulin secretion from the b-cell begins to decline and the severity of the hyperglycaemia increases further. Adapted from DeFronzo RA, Bonadonna RC, Ferrannini E. Pathogenesis of NIDDM. A balanced overview. Diabetes Care 1992;15: Euglycaemia. Normal. IGT \u00b1 Obesity. Diagnosis of type 2 diabetes. Progression of type 2 diabetes. DeFronzo et al. Diabetes Care 1992;15:", "Image XResolution": "37", "Image YResolution": "37", "Image ResolutionUnit": "Pixels/Centimeter", "Image Software": "SlidePlayer", "Image YCbCrPositioning": "Centered"}