SGLT2 inhibitor protects cardiomyocytes against palmitate-induced lipotoxicity by increasing activation of AMPK and lipid oxidations
Lee, Han Byeol | Choi, Sung-E | Kang, Yup | Kim, Tae Ho | Seo, Mi Hye | Lee, Min Jeong | Lee, Nami | Moon, Hyun Uk | Han, Seung Jin | Kim, Dae Jung | Lee, Kwan-Woo
Low doses of palmitates evoked lipotoxicity in cardiomyocytes. Although SGLT2 expression was less in myocardial cells, treatment of SGLT2 inhibitor dramatically reduced palmitate-induced expression levels of inflammatory cytokines, such as IL-1beta and TNF-alpha. Immunoblotting analysis showed treatment of cardiomyocytes, with SGLT2 inhibitor, recovered impaired insulin signaling, such as phospho-AKT, but total AKT did not change. SGLT2 inhibitor also restored insulin-stimulated glucose uptake, which was destroyed by lipotoxicity. Treatment with SGLT2 inhibitor decreased the level of ER stress markers as well as inflammatory signaling markers. In particular, SGLT2 inhibitor stimulated phosphorylation of AMPK and fatty acid beta-oxidation. Cardiomyocyte exposure to high doses of palmitates evoked apoptotic features such as caspase 3 activation and DNA fragmentations. But pretreatment of SGLT2 inhibitor significantly protected palmitate-induced apoptotic features.
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