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• W2100040836 abstract "AB~T~S affects ~,5% of people in the United States of America and the incidence is much higher in sporadic populations such as Pima Indians in North America and Australian Aborigines. There are two major forms of diabetes, referred to as insulin-dependent diabetes (IDD) ~ and non-insulin-dependent diabetes (NIDD). The etiology of these diseases is quite different despite similarities in their pathophysiologies. IDD often arises in early life and is due to autoimmune destruction of pancreatic/3 cells resulting in partial or complete loss of/3 cell function. NIDD is more common in later life (>40 yr) and ,x,85 % of all diabetics have this form. The increased prevalence of NIDD in developed countries together with its association with heart disease and stroke makes this one of the most devastating diseases in the western world. NIDD appears to be due to a defect in glucose disposal (DeFronzo et al., 1992). Both glucose per se and insulin, play important roles in facilitating glucose uptake into target organs (for review see DeFronzo et ai., 1992). Following ingestion of a carbohydrate meal, glucose uptake into many organs is increased simply due to the elevated blood glucose. A more pronounced increase which is evoked by insulin, is observed specifically in muscle and adipose tissue. The net result is that in the postprandial state, glucose is rapidly and efficiently cleared from the blood and stored primarily in muscle and adipose. Each of these processes is defective in NIDD making it extremely difficult to identify the primary lesion. Studies in first degree relatives of NIDDs indicate that one of the earliest detectable defects is impaired insulin action in muscle and adipose tissue or insulin resistance (Martin et al., 1992). Thus, identifying the physiological and molecular biological processes that control insulin-stimulated glucose utilization in these organs is of major significance." @default.
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• W2100040836 date "1994-09-01" @default.
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• W2100040836 title "Insulin resistance, diabetes, and the insulin-regulated trafficking of GLUT-4." @default.
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• W2100040836 doi "https://doi.org/10.1083/jcb.126.5.1123" @default.
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