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Increase of Fat Oxidation and Weight Loss in Obese Mice Caused by Chronic Treatment with Human Growth Hormone or a Modified C-Terminal Fragment

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Exenatide activated eNOS and NO production in endothelial cells, induced dose-dependent vasorelaxation, and mitigated high-glucose or lipid-induced endothelial dysfunction in arterioles ex vivo, effects which were reduced by AMPK (AMP-activated protein kinase) inhibition [86]