Involvement of the extracellular matrix and integrin signalling proteins in skeletal muscle glucose uptake

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Standard

Involvement of the extracellular matrix and integrin signalling proteins in skeletal muscle glucose uptake. / Draicchio, Fulvia; Behrends, Volker; Tillin, Neale A; Hurren, Nicholas M; Sylow, Lykke; Mackenzie, Richard.

I: Journal of Physiology, Bind 600, Nr. 20, 2022, s. 4393-4408.

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Harvard

Draicchio, F, Behrends, V, Tillin, NA, Hurren, NM, Sylow, L & Mackenzie, R 2022, 'Involvement of the extracellular matrix and integrin signalling proteins in skeletal muscle glucose uptake', Journal of Physiology, bind 600, nr. 20, s. 4393-4408. https://doi.org/10.1113/JP283039

APA

Draicchio, F., Behrends, V., Tillin, N. A., Hurren, N. M., Sylow, L., & Mackenzie, R. (2022). Involvement of the extracellular matrix and integrin signalling proteins in skeletal muscle glucose uptake. Journal of Physiology, 600(20), 4393-4408. https://doi.org/10.1113/JP283039

Vancouver

Draicchio F, Behrends V, Tillin NA, Hurren NM, Sylow L, Mackenzie R. Involvement of the extracellular matrix and integrin signalling proteins in skeletal muscle glucose uptake. Journal of Physiology. 2022;600(20):4393-4408. https://doi.org/10.1113/JP283039

Author

Draicchio, Fulvia ; Behrends, Volker ; Tillin, Neale A ; Hurren, Nicholas M ; Sylow, Lykke ; Mackenzie, Richard. / Involvement of the extracellular matrix and integrin signalling proteins in skeletal muscle glucose uptake. I: Journal of Physiology. 2022 ; Bind 600, Nr. 20. s. 4393-4408.

Bibtex

@article{26146c448c8d43e7b7fb1ebdb16be786,
title = "Involvement of the extracellular matrix and integrin signalling proteins in skeletal muscle glucose uptake",
abstract = "Whole-body euglycaemia is partly maintained by two cellular processes that encourage glucose uptake in skeletal muscle; 1) the insulin- and 2) contraction-stimulated pathways, with research suggesting convergence between these two previously separate processes. The normal structural integrity of the skeletal muscle requires an intact actin cytoskeleton as well as integrin-associated proteins, thus those structures are likely fundamental for effective glucose uptake in skeletal muscle. In contrast, excessive extracellular matrix (ECM) remodelling and integrin expression in skeletal muscle may contribute to insulin resistance owing to an increased physical barrier causing reduced nutrient and hormonal flux. This review paper explores the role of the ECM and the actin cytoskeleton in insulin- and contraction-mediated glucose uptake in skeletal muscle. This is a clinically important area of research given that defects in the structural integrity of the ECM and integrin-associated proteins may contribute to loss of muscle function and decreased glucose uptake in type 2 diabetes.",
keywords = "Faculty of Science, Integrin, ILK, Rac1, ECM, Actin cytoskeleton, Muscle contraction, Insulin, Insulin resistance",
author = "Fulvia Draicchio and Volker Behrends and Tillin, {Neale A} and Hurren, {Nicholas M} and Lykke Sylow and Richard Mackenzie",
note = "This article is protected by copyright. All rights reserved.",
year = "2022",
doi = "10.1113/JP283039",
language = "English",
volume = "600",
pages = "4393--4408",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "20",

}

RIS

TY - JOUR

T1 - Involvement of the extracellular matrix and integrin signalling proteins in skeletal muscle glucose uptake

AU - Draicchio, Fulvia

AU - Behrends, Volker

AU - Tillin, Neale A

AU - Hurren, Nicholas M

AU - Sylow, Lykke

AU - Mackenzie, Richard

N1 - This article is protected by copyright. All rights reserved.

PY - 2022

Y1 - 2022

N2 - Whole-body euglycaemia is partly maintained by two cellular processes that encourage glucose uptake in skeletal muscle; 1) the insulin- and 2) contraction-stimulated pathways, with research suggesting convergence between these two previously separate processes. The normal structural integrity of the skeletal muscle requires an intact actin cytoskeleton as well as integrin-associated proteins, thus those structures are likely fundamental for effective glucose uptake in skeletal muscle. In contrast, excessive extracellular matrix (ECM) remodelling and integrin expression in skeletal muscle may contribute to insulin resistance owing to an increased physical barrier causing reduced nutrient and hormonal flux. This review paper explores the role of the ECM and the actin cytoskeleton in insulin- and contraction-mediated glucose uptake in skeletal muscle. This is a clinically important area of research given that defects in the structural integrity of the ECM and integrin-associated proteins may contribute to loss of muscle function and decreased glucose uptake in type 2 diabetes.

AB - Whole-body euglycaemia is partly maintained by two cellular processes that encourage glucose uptake in skeletal muscle; 1) the insulin- and 2) contraction-stimulated pathways, with research suggesting convergence between these two previously separate processes. The normal structural integrity of the skeletal muscle requires an intact actin cytoskeleton as well as integrin-associated proteins, thus those structures are likely fundamental for effective glucose uptake in skeletal muscle. In contrast, excessive extracellular matrix (ECM) remodelling and integrin expression in skeletal muscle may contribute to insulin resistance owing to an increased physical barrier causing reduced nutrient and hormonal flux. This review paper explores the role of the ECM and the actin cytoskeleton in insulin- and contraction-mediated glucose uptake in skeletal muscle. This is a clinically important area of research given that defects in the structural integrity of the ECM and integrin-associated proteins may contribute to loss of muscle function and decreased glucose uptake in type 2 diabetes.

KW - Faculty of Science

KW - Integrin

KW - ILK

KW - Rac1

KW - ECM

KW - Actin cytoskeleton

KW - Muscle contraction

KW - Insulin

KW - Insulin resistance

U2 - 10.1113/JP283039

DO - 10.1113/JP283039

M3 - Review

C2 - 36054466

VL - 600

SP - 4393

EP - 4408

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - 20

ER -

ID: 318441179