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Apolipoprotein A-I enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle

Therapeutic interventions that increase plasma high density lipoprotein (HDL) and apolipoprotein (apo) A-I levels have been reported to reduce plasma glucose levels and attenuate insulin resistance. The present study asks if this is a direct effect of increased glucose uptake by skeletal muscle. Inc...

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Autores principales: Tang, Shudi, Tabet, Fatiha, Cochran, Blake J., Cuesta Torres, Luisa F., Wu, Ben J., Barter, Philip J., Rye, Kerry-Anne
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6362284/
https://www.ncbi.nlm.nih.gov/pubmed/30718702
http://dx.doi.org/10.1038/s41598-018-38014-3
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author Tang, Shudi
Tabet, Fatiha
Cochran, Blake J.
Cuesta Torres, Luisa F.
Wu, Ben J.
Barter, Philip J.
Rye, Kerry-Anne
author_facet Tang, Shudi
Tabet, Fatiha
Cochran, Blake J.
Cuesta Torres, Luisa F.
Wu, Ben J.
Barter, Philip J.
Rye, Kerry-Anne
author_sort Tang, Shudi
collection PubMed
description Therapeutic interventions that increase plasma high density lipoprotein (HDL) and apolipoprotein (apo) A-I levels have been reported to reduce plasma glucose levels and attenuate insulin resistance. The present study asks if this is a direct effect of increased glucose uptake by skeletal muscle. Incubation of primary human skeletal muscle cells (HSKMCs) with apoA-I increased insulin-dependent and insulin–independent glucose uptake in a time- and concentration-dependent manner. The increased glucose uptake was accompanied by enhanced phosphorylation of the insulin receptor (IR), insulin receptor substrate-1 (IRS-1), the serine/threonine kinase Akt and Akt substrate of 160 kDa (AS160). Cell surface levels of the glucose transporter type 4, GLUT4, were also increased. The apoA-I-mediated increase in glucose uptake by HSKMCs was dependent on phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt, the ATP binding cassette transporter A1 (ABCA1) and scavenger receptor class B type I (SR-B1). Taken together, these results establish that apoA-I increases glucose disposal in skeletal muscle by activating the IR/IRS-1/PI3K/Akt/AS160 signal transduction pathway. The findings suggest that therapeutic agents that increase apoA-I levels may improve glycemic control in people with type 2 diabetes.
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spelling pubmed-63622842019-02-07 Apolipoprotein A-I enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle Tang, Shudi Tabet, Fatiha Cochran, Blake J. Cuesta Torres, Luisa F. Wu, Ben J. Barter, Philip J. Rye, Kerry-Anne Sci Rep Article Therapeutic interventions that increase plasma high density lipoprotein (HDL) and apolipoprotein (apo) A-I levels have been reported to reduce plasma glucose levels and attenuate insulin resistance. The present study asks if this is a direct effect of increased glucose uptake by skeletal muscle. Incubation of primary human skeletal muscle cells (HSKMCs) with apoA-I increased insulin-dependent and insulin–independent glucose uptake in a time- and concentration-dependent manner. The increased glucose uptake was accompanied by enhanced phosphorylation of the insulin receptor (IR), insulin receptor substrate-1 (IRS-1), the serine/threonine kinase Akt and Akt substrate of 160 kDa (AS160). Cell surface levels of the glucose transporter type 4, GLUT4, were also increased. The apoA-I-mediated increase in glucose uptake by HSKMCs was dependent on phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt, the ATP binding cassette transporter A1 (ABCA1) and scavenger receptor class B type I (SR-B1). Taken together, these results establish that apoA-I increases glucose disposal in skeletal muscle by activating the IR/IRS-1/PI3K/Akt/AS160 signal transduction pathway. The findings suggest that therapeutic agents that increase apoA-I levels may improve glycemic control in people with type 2 diabetes. Nature Publishing Group UK 2019-02-04 /pmc/articles/PMC6362284/ /pubmed/30718702 http://dx.doi.org/10.1038/s41598-018-38014-3 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Tang, Shudi
Tabet, Fatiha
Cochran, Blake J.
Cuesta Torres, Luisa F.
Wu, Ben J.
Barter, Philip J.
Rye, Kerry-Anne
Apolipoprotein A-I enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle
title Apolipoprotein A-I enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle
title_full Apolipoprotein A-I enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle
title_fullStr Apolipoprotein A-I enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle
title_full_unstemmed Apolipoprotein A-I enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle
title_short Apolipoprotein A-I enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle
title_sort apolipoprotein a-i enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6362284/
https://www.ncbi.nlm.nih.gov/pubmed/30718702
http://dx.doi.org/10.1038/s41598-018-38014-3
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