Altered amyloid precursor protein processing regulates glucose uptake and oxidation in cultured rodent myotubes
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- 作者：D. Lee Hamilton (1)
John A. Findlay (1)
Gemma Montagut (1)
Paul J. Meakin (1)
Dawn Bestow (1)
Susan M. Jalicy (1)
Michael L. J. Ashford (1) - 关键词：Amyloid ; BACE1 ; Glucose uptake ; Glut4 ; Insulin ; PI3K ; Skeletal muscle ; Type 2 diabetes
- 刊名：Diabetologia
- 出版年：2014
- 出版时间：August 2014
- 年：2014
- 卷：57
- 期：8
- 页码：1684-1692
- 全文大小：781 KB
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John A. Findlay (1)
Gemma Montagut (1)
Paul J. Meakin (1)
Dawn Bestow (1)
Susan M. Jalicy (1)
Michael L. J. Ashford (1)
1. Division of Cardiovascular and Diabetes Medicine, Medical Research Institute, Ninewells Hospital & Medical School, University of Dundee, Dundee, DD1 9SY, Scotland, UK - ISSN：1432-0428
文摘
Aims/hypothesis Impaired glucose uptake in skeletal muscle is an important contributor to glucose intolerance in type 2 diabetes. The aspartate protease, beta-site APP-cleaving enzyme 1 (BACE1), a critical regulator of amyloid precursor protein (APP) processing, modulates in vivo glucose disposal and insulin sensitivity in mice. Insulin-independent pathways to stimulate glucose uptake and GLUT4 translocation may offer alternative therapeutic avenues for the treatment of diabetes. We therefore addressed whether BACE1 activity, via APP processing, in skeletal muscle modifies glucose uptake and oxidation independently of insulin. Methods Skeletal muscle cell lines were used to investigate the effects of BACE1 and α-secretase inhibition and BACE1 and APP overexpression on glucose uptake, GLUT4 cell surface translocation, glucose oxidation and cellular respiration. Results In the absence of insulin, reduction of BACE1 activity increased glucose uptake and oxidation, GLUT4myc cell surface translocation, and basal rate of oxygen consumption. In contrast, overexpressing BACE1 in C2C12 myotubes decreased glucose uptake, glucose oxidation and oxygen consumption rate. APP overexpression increased and α-secretase inhibition decreased glucose uptake in C2C12 myotubes. The increase in glucose uptake elicited by BACE1 inhibition is dependent on phosphoinositide 3-kinase (PI3K) and mimicked by soluble APPα (sAPPα). Conclusions/interpretation Inhibition of muscle BACE1 activity increases insulin-independent, PI3K-dependent glucose uptake and cell surface translocation of GLUT4. As APP overexpression raises basal glucose uptake, and direct application of sAPPα increases PI3K–protein kinase B signalling and glucose uptake in myotubes, we suggest that α-secretase-dependent shedding of sAPPα regulates insulin-independent glucose uptake in skeletal muscle.