Insulin resistance: a phosphorylation-based uncoupling of insulin signaling. |
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| Authors: | Y Zick |
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| Affiliation: | 1. Department of Food Science and Technology, Central Taiwan University of Science and Technology, Taichung, Taiwan;2. Department of Bioindustry Technology, Da-Yeh University, Changhua, Taiwan;1. Clermont Université, Université d''Auvergne, Unité de Nutrition Humaine, BP 10448, F-63000 Clermont-Ferrand, France;2. INRA, UMR 1019, UNH, CRNH Auvergne, F-63000 Clermont-Ferrand, France;3. Plateforme d''Exploration du Métabolisme, INRA, Centre Clermont-Ferrand–Theix, UMR 1019 , Nutrition Humaine, Saint-Genès-Champanelle, France |
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| Abstract: | Insulin resistance refers to a decreased capacity of circulating insulin to regulate nutrient metabolism. It is associated with the development of type 2 diabetes--an ever-increasing epidemic of the 21st century. Recent studies reveal that agents that induce insulin resistance exploit phosphorylation-based negative-feedback control mechanisms, otherwise utilized by insulin itself, to uncouple the insulin receptor from its downstream effectors and thereby terminate insulin signal transduction. This article describes recent findings that present novel viewpoints of the molecular basis of insulin resistance, focusing on the cardinal role of Ser/Thr protein kinases as emerging key players in this arena. |
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