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9 août 2021
- doi: 10.3390/ijms22168555
- issn: 1422-0067
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info:eu-repo/semantics/altIdentifier/doi/10.3390/ijms22168555
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info:eu-repo/semantics/altIdentifier/pmid/34445261
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info:eu-repo/semantics/altIdentifier/eissn/1422-0067
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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_745478D849DF9
info:eu-repo/semantics/openAccess , CC BY 4.0 , https://creativecommons.org/licenses/by/4.0/
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Type II diabetes Ketosis resistant diabetes Adult onset diabetes Noninsulin-dependent diabetes NIDDM (Diabetes) Stable diabetes Maturity onset diabetes Type 2 diabetesCiter ce document
D. Aguilar-Recarte et al., « The PPARβ/δ-AMPK Connection in the Treatment of Insulin Resistance. », Serveur académique Lausannois, ID : 10.3390/ijms22168555
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The current treatment options for type 2 diabetes mellitus do not adequately control the disease in many patients. Consequently, there is a need for new drugs to prevent and treat type 2 diabetes mellitus. Among the new potential pharmacological strategies, activators of peroxisome proliferator-activated receptor (PPAR)β/δ show promise. Remarkably, most of the antidiabetic effects of PPARβ/δ agonists involve AMP-activated protein kinase (AMPK) activation. This review summarizes the recent mechanistic insights into the antidiabetic effects of the PPARβ/δ-AMPK pathway, including the upregulation of glucose uptake, muscle remodeling, enhanced fatty acid oxidation, and autophagy, as well as the inhibition of endoplasmic reticulum stress and inflammation. A better understanding of the mechanisms underlying the effects resulting from the PPARβ/δ-AMPK pathway may provide the basis for the development of new therapies in the prevention and treatment of insulin resistance and type 2 diabetes mellitus.