Insulin action and resistance in obesity and type 2 diabetes
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TLDR
This Perspective reviews alternate viewpoints and recent results on the temporal and mechanistic connections between hyperinsulinemia, obesity and insulin resistance and connects insulin resistance to extensive metabolic cross-talk between the liver, adipose tissue, pancreas and skeletal muscle.Abstract:
Nutritional excess is a major forerunner of type 2 diabetes. It enhances the secretion of insulin, but attenuates insulin's metabolic actions in the liver, skeletal muscle and adipose tissue. However, conflicting evidence indicates a lack of knowledge of the timing of these events during the development of obesity and diabetes, pointing to a key gap in our understanding of metabolic disease. This Perspective reviews alternate viewpoints and recent results on the temporal and mechanistic connections between hyperinsulinemia, obesity and insulin resistance. Although much attention has addressed early steps in the insulin signaling cascade, insulin resistance in obesity seems to be largely elicited downstream of these steps. New findings also connect insulin resistance to extensive metabolic cross-talk between the liver, adipose tissue, pancreas and skeletal muscle. These and other advances over the past 5 years offer exciting opportunities and daunting challenges for the development of new therapeutic strategies for the treatment of type 2 diabetes.read more
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LMO3 reprograms visceral adipocyte metabolism during obesity
Gabriel Wagner,Anna Fenzl,Josefine Lindroos-Christensen,Josefine Lindroos-Christensen,Elisa Einwallner,Julia Husa,Nadine Witzeneder,Sabine Rauscher,Marion Gröger,Sophia Derdak,Thomas Mohr,Hedwig Sutterlüty,Florian Klinglmüller,Silviya Wolkerstorfer,Silviya Wolkerstorfer,Martina Fondi,Gregor Hoermann,Lei Cao,Oswald Wagner,Florian W. Kiefer,Harald Esterbauer,Martin Bilban +21 more
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TL;DR: In this paper, the authors developed a genetically modified rat model bearing an orthologous AS160R693X mutation, which mimics human patients exhibiting post-prandial hyperglycemia and hyperinsulinemia.
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α-Lipoic Acid Reduces Ceramide Synthesis and Neuroinflammation in the Hypothalamus of Insulin-Resistant Rats, While in the Cerebral Cortex Diminishes the β-Amyloid Accumulation
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References
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