Augmenting Vacuolar H-ATPase Function Prevents Cardiomyocytes from Lipid-Overload Induced Dysfunction.
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ID: 100644
2020
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Abstract
The diabetic heart is characterized by a shift in substrate utilization from glucose to lipids, which may ultimately lead to contractile dysfunction. This substrate shift is facilitated by increased translocation of lipid transporter CD36 (SR-B2) from endosomes to the sarcolemma resulting in increased lipid uptake. We previously showed that endosomal retention of CD36 is dependent on the proper functioning of vacuolar H-ATPase (v-ATPase). Excess lipids trigger CD36 translocation through inhibition of v-ATPase function. Conversely, in yeast, glucose availability is known to enhance v-ATPase function, allowing us to hypothesize that glucose availability, via v-ATPase, may internalize CD36 and restore contractile function in lipid-overloaded cardiomyocytes. Increased glucose availability was achieved through (a) high glucose (25 mM) addition to the culture medium or (b) adenoviral overexpression of protein kinase-D1 (a kinase mediating GLUT4 translocation). In HL-1 cardiomyocytes, adult rat and human cardiomyocytes cultured under high-lipid conditions, each treatment stimulated v-ATPase re-assembly, endosomal acidification, endosomal CD36 retention and prevented myocellular lipid accumulation. Additionally, these treatments preserved insulin-stimulated GLUT4 translocation and glucose uptake as well as contractile force. The present findings reveal v-ATPase functions as a key regulator of cardiomyocyte substrate preference and as a novel potential treatment approach for the diabetic heart.
| Reference Key |
wang2020augmentinginternational
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| Authors | Wang, Shujin;Wong, Li-Yen;Neumann, Dietbert;Liu, Yilin;Sun, Aomin;Antoons, Gudrun;Strzelecka, Agnieszka;Glatz, Jan F C;Nabben, Miranda;Luiken, Joost J F P; |
| Journal | International journal of molecular sciences |
| Year | 2020 |
| DOI |
E1520
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| URL | |
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