A role for β-catenin in diet-induced skeletal muscle insulin resistance

Journal article


Mason, Stewart W. C., Dissanayake, Waruni C., Broome, Sophie C., Hedges, Christopher P., Peters, Wouter M., Gram, Martin, Rowlands, David S., Shepherd, Peter R. and Merry, Troy L.. (2023). A role for β-catenin in diet-induced skeletal muscle insulin resistance. Physiological Reports. 11(4), p. Article e15536. https://doi.org/10.14814/phy2.15536
AuthorsMason, Stewart W. C., Dissanayake, Waruni C., Broome, Sophie C., Hedges, Christopher P., Peters, Wouter M., Gram, Martin, Rowlands, David S., Shepherd, Peter R. and Merry, Troy L.
Abstract

A central characteristic of insulin resistance is the impaired ability for insulin to stimulate glucose uptake into skeletal muscle. While insulin resistance can occur distal to the canonical insulin receptor-PI3k-Akt signaling pathway, the signaling intermediates involved in the dysfunction are yet to be fully elucidated. β-catenin is an emerging distal regulator of skeletal muscle and adipocyte insulin-stimulated GLUT4 trafficking. Here, we investigate its role in skeletal muscle insulin resistance. Short-term (5-week) high-fat diet (HFD) decreased skeletal muscle β-catenin protein expression 27% (p = 0.03), and perturbed insulin-stimulated β-cateninS552 phosphorylation 21% (p = 0.009) without affecting insulin-stimulated Akt phosphorylation relative to chow-fed controls. Under chow conditions, mice with muscle-specific β-catenin deletion had impaired insulin responsiveness, whereas under HFD, both mice exhibited similar levels of insulin resistance (interaction effect of genotype × diet p < 0.05). Treatment of L6-GLUT4-myc myocytes with palmitate lower β-catenin protein expression by 75% (p = 0.02), and attenuated insulin-stimulated β-catenin phosphorylationS552 and actin remodeling (interaction effect of insulin × palmitate p < 0.05). Finally, β-cateninS552 phosphorylation was 45% lower in muscle biopsies from men with type 2 diabetes while total β-catenin expression was unchanged. These findings suggest that β-catenin dysfunction is associated with the development of insulin resistance.

Keywordsglucose transport; insulin resistance; obesity; Wnt-signaling
Year2023
JournalPhysiological Reports
Journal citation11 (4), p. Article e15536
PublisherWiley Periodicals LLC
ISSN2051-817X
Digital Object Identifier (DOI)https://doi.org/10.14814/phy2.15536
PubMed ID36807886
Scopus EID2-s2.0-85148588218
PubMed Central IDPMC9937784
Open accessPublished as ‘gold’ (paid) open access
Page range1-13
FunderMinistry of Business, Innovation and Employment (MBIE), Aotearoa New Zealand
Royal Society Te Apārangi
University of Auckland
Publisher's version
License
File Access Level
Open
Output statusPublished
Publication dates
Online17 Feb 2023
Publication process dates
Accepted20 Nov 2022
Deposited17 Nov 2023
Grant IDUOOX1404
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