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Abstract
Accumulation of toxic lipids is the most common etiology of insulin resistance in type 2 diabetes and associated metabolic disorders such as obesity and non-alcoholic fatty liver disease. Understanding of the underlying mechanisms has revealed various opportunities to target key regulators in lipid metabolic pathways for the treatment of metabolic diseases. Here, we review the discovery and development of potential anti-diabetic drugs with primary effects on cellular targets leading to reductions of intracellular lipids in key organs. We will particularly focus on AMPK, SIRT1, PGC-1α, SREBP-1c, ChREBP, ACC, PPARs and HSPs which either stimulate in fatty acid oxidation (energy expenditure) or inhibit de novo lipogenesis.
Keywords: Anti-diabetic drug targets, drug discovery, insulin resistance, lipid metabolism.
Current Drug Targets
Title:Discovery of Novel Anti-Diabetic Drugs by Targeting Lipid Metabolism
Volume: 16 Issue: 12
Author(s): Xiu Zhou, Jun Xu, Yuguang Shi and Ji-Ming Ye
Affiliation:
Keywords: Anti-diabetic drug targets, drug discovery, insulin resistance, lipid metabolism.
Abstract: Accumulation of toxic lipids is the most common etiology of insulin resistance in type 2 diabetes and associated metabolic disorders such as obesity and non-alcoholic fatty liver disease. Understanding of the underlying mechanisms has revealed various opportunities to target key regulators in lipid metabolic pathways for the treatment of metabolic diseases. Here, we review the discovery and development of potential anti-diabetic drugs with primary effects on cellular targets leading to reductions of intracellular lipids in key organs. We will particularly focus on AMPK, SIRT1, PGC-1α, SREBP-1c, ChREBP, ACC, PPARs and HSPs which either stimulate in fatty acid oxidation (energy expenditure) or inhibit de novo lipogenesis.
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Cite this article as:
Zhou Xiu, Xu Jun, Shi Yuguang and Ye Ji-Ming, Discovery of Novel Anti-Diabetic Drugs by Targeting Lipid Metabolism, Current Drug Targets 2015; 16 (12) . https://dx.doi.org/10.2174/1389450116666150223120829
DOI https://dx.doi.org/10.2174/1389450116666150223120829 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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