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• W2562251160 abstract "β-Cell dysfunction represents a pathophysiological hallmark of diabetes. It precedes the development of hyperglycemia and the progressive decline of the ability of β cells to compensate for coexisting insulin resistance sets the rate of conversion from normal to impaired glucose tolerance and, eventually, to overt diabetes. Insulin secretion is tightly controlled through a sophisticated integrated process encompassing finely tuned feedbacks between the β cell, plasma glucose, and other nutrient levels, insulin sensitivity, incretin hormones, neuropeptides, and neuronal control. The disruption of this network and the reduction of β-cell mass account for abnormal insulin secretion in type 2 diabetes. β-Cell abnormalities develop over a long period and this process can be schematized in three main steps: (i) genetic predisposition, (ii) early and progressive β-cell dysfunction and loss of β-cell mass, and (iii) development of metabolic alterations (hyperglycemia, obesity, hyperlipidemia) that can accelerate the rate of loss of β-cell function. In recent decades, a large number of genetic variants associated with increased risk of developing type 2 diabetes have been identified. The majority of these variants are believed to directly affect β-cell function and survival, accounting for the reduction in β-cell mass and, to a greater extent, impaired insulin secretion in people predisposed to diabetes and in those with prediabetes. A minimal increase in fasting plasma glucose levels is usually accompanied by loss of first-phase insulin secretion and loss of glucose sensitivity, that is, the ability of the β cell to sense and respond properly to changes in glucose concentrations. Obesity, development of hyperglycemia, dyslipidemia, increased plasma free fatty acid concentrations, and chronic overstimulation of insulin secretion can activate pathogenic mechanisms (glucolipotoxicity, oxidative stress, inflammation, endoplasmic reticulum stress, epigenetic modifications, amyloid deposition, etc.) that worsen β-cell abnormalities. The same mechanisms trigger apoptosis and, to some extent, autophagy, which, in the face of a lack of compensatory increase in β-cell regeneration/differentiation, result in a decrease in the β-cell mass. Based on this view, preservation of β-cell function is key to preventing deterioration of glucose tolerance and development of diabetes. Moreover, tight control of the accelerating factors may slow the progression of the disease and result in more durable glycemic control over the years." @default.
• W2562251160 created "2017-01-06" @default.
• W2562251160 creator A5005158952 @default.
• W2562251160 creator A5019711625 @default.
• W2562251160 creator A5076218609 @default.
• W2562251160 date "2016-12-09" @default.
• W2562251160 modified "2023-10-14" @default.
• W2562251160 title "Abnormalities of Insulin Secretion and β-Cell Defects in Type 2 Diabetes" @default.
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