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10.4239/wjd.v6.i12.1207

http://scihub22266oqcxt.onion/10.4239/wjd.v6.i12.1207
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C4598604!4598604!26464759
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suck abstract from ncbi

pmid26464759      World+J+Diabetes 2015 ; 6 (12): 1207-22
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  • Treatment of prediabetes #MMPMID26464759
  • Kanat M; DeFronzo RA; Abdul-Ghani MA
  • World J Diabetes 2015[Sep]; 6 (12): 1207-22 PMID26464759show ga
  • Progression of normal glucose tolerance (NGT) to overt diabetes is mediated by a transition state called impaired glucose tolerance (IGT). Beta cell dysfunction and insulin resistance are the main defects in type 2 diabetes mellitus (type 2 DM) and even normoglycemic IGT patients manifest these defects. Beta cell dysfunction and insulin resistance also contribute to the progression of IGT to type 2 DM. Improving insulin sensitivity and/or preserving functions of beta-cells can be a rational way to normalize the GT and to control transition of IGT to type 2 DM. Loosing weight, for example, improves whole body insulin sensitivity and preserves beta-cell function and its inhibitory effect on progression of IGT to type 2 DM had been proven. But interventions aiming weight loss usually not applicable in real life. Pharmacotherapy is another option to gain better insulin sensitivity and to maintain beta-cell function. In this review, two potential treatment options (lifestyle modification and pharmacologic agents) that limits the IGT-type 2 DM conversion in prediabetic subjects are discussed.
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