Beta-aminoisobutyric acid is released by contracting human skeletal muscle and lowers insulin release from INS-1 832/3 cells by mediating mitochondrial energy metabolism

Research output: Contribution to journalJournal articlepeer-review

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Beta-aminoisobutyric acid is released by contracting human skeletal muscle and lowers insulin release from INS-1 832/3 cells by mediating mitochondrial energy metabolism. / Barlow, Jonathan P; Karstoft, Kristian; Vigelsø, Andreas; Gram, Martin; Helge, Jørn W; Dela, Flemming; Pappan, Kirk; O'Neil, Donna; Dunn, Warwick; Solomon, Thomas P J.

In: Metabolism open, Vol. 7, 2020, p. 100053.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Barlow, JP, Karstoft, K, Vigelsø, A, Gram, M, Helge, JW, Dela, F, Pappan, K, O'Neil, D, Dunn, W & Solomon, TPJ 2020, 'Beta-aminoisobutyric acid is released by contracting human skeletal muscle and lowers insulin release from INS-1 832/3 cells by mediating mitochondrial energy metabolism', Metabolism open, vol. 7, pp. 100053. https://doi.org/10.1016/j.metop.2020.100053

APA

Barlow, J. P., Karstoft, K., Vigelsø, A., Gram, M., Helge, J. W., Dela, F., Pappan, K., O'Neil, D., Dunn, W., & Solomon, T. P. J. (2020). Beta-aminoisobutyric acid is released by contracting human skeletal muscle and lowers insulin release from INS-1 832/3 cells by mediating mitochondrial energy metabolism. Metabolism open, 7, 100053. https://doi.org/10.1016/j.metop.2020.100053

Vancouver

Barlow JP, Karstoft K, Vigelsø A, Gram M, Helge JW, Dela F et al. Beta-aminoisobutyric acid is released by contracting human skeletal muscle and lowers insulin release from INS-1 832/3 cells by mediating mitochondrial energy metabolism. Metabolism open. 2020;7:100053. https://doi.org/10.1016/j.metop.2020.100053

Author

Barlow, Jonathan P ; Karstoft, Kristian ; Vigelsø, Andreas ; Gram, Martin ; Helge, Jørn W ; Dela, Flemming ; Pappan, Kirk ; O'Neil, Donna ; Dunn, Warwick ; Solomon, Thomas P J. / Beta-aminoisobutyric acid is released by contracting human skeletal muscle and lowers insulin release from INS-1 832/3 cells by mediating mitochondrial energy metabolism. In: Metabolism open. 2020 ; Vol. 7. pp. 100053.

Bibtex

@article{528d8c4e0fe4450c97cce4a9ddd01519,
title = "Beta-aminoisobutyric acid is released by contracting human skeletal muscle and lowers insulin release from INS-1 832/3 cells by mediating mitochondrial energy metabolism",
abstract = "Aims/hypothesis: This study aimed to examine if beta-aminoisobutyric acid (BAIBA) is (i) secreted by skeletal muscle in humans during exercise, (ii) associated with insulin secretory function in vivo, and (iii) directly linked with acute glucose-mediated insulin release by pancreatic beta cells in vitro.Methods: Following 2-weeks of single-leg immobilization, plasma BAIBA concentrations were measured in the brachial artery and the femoral veins of each leg in healthy male subjects, at rest and during two-legged dynamic knee-extensor exercise. During a 2-h hyperglycamic clamp, insulin secretory function and levels of plasma BAIBA were assessed in non-diabetic individuals, non-diabetic individuals following 24-h hyperglycemia and patients with type 2 diabetes. Direct effects of BAIBA on acute glucose-mediated insulin release were probed in INS-1832/3 cells under normal and 'diabetes-like' conditions. Finally, the effect of BAIBA on mitochondrial function was assessed in INS-1832/3 cells using extracellular flux analysis.Results: (i) BAIBA is released from skeletal muscle at rest and during exercise under healthy conditions but is suppressed during exercise following leg immobilization, (ii) plasma BAIBA concentrations inversely associate with insulin secretory function in humans, (iii) BAIBA lowers mitochondrial energy metabolism in INS-1 832/3 cells in parallel with decreased insulin secretionConclusion/interpretation: BAIBA is a myokine released by skeletal muscle during exercise and indepedantly alters the triggering pathway of insulin secretion in cultured INS-1832/3 cells.",
author = "Barlow, {Jonathan P} and Kristian Karstoft and Andreas Vigels{\o} and Martin Gram and Helge, {J{\o}rn W} and Flemming Dela and Kirk Pappan and Donna O'Neil and Warwick Dunn and Solomon, {Thomas P J}",
note = "{\textcopyright} 2020 The Author(s).",
year = "2020",
doi = "10.1016/j.metop.2020.100053",
language = "English",
volume = "7",
pages = "100053",
journal = "Metabolism open",
issn = "2589-9368",

}

RIS

TY - JOUR

T1 - Beta-aminoisobutyric acid is released by contracting human skeletal muscle and lowers insulin release from INS-1 832/3 cells by mediating mitochondrial energy metabolism

AU - Barlow, Jonathan P

AU - Karstoft, Kristian

AU - Vigelsø, Andreas

AU - Gram, Martin

AU - Helge, Jørn W

AU - Dela, Flemming

AU - Pappan, Kirk

AU - O'Neil, Donna

AU - Dunn, Warwick

AU - Solomon, Thomas P J

N1 - © 2020 The Author(s).

PY - 2020

Y1 - 2020

N2 - Aims/hypothesis: This study aimed to examine if beta-aminoisobutyric acid (BAIBA) is (i) secreted by skeletal muscle in humans during exercise, (ii) associated with insulin secretory function in vivo, and (iii) directly linked with acute glucose-mediated insulin release by pancreatic beta cells in vitro.Methods: Following 2-weeks of single-leg immobilization, plasma BAIBA concentrations were measured in the brachial artery and the femoral veins of each leg in healthy male subjects, at rest and during two-legged dynamic knee-extensor exercise. During a 2-h hyperglycamic clamp, insulin secretory function and levels of plasma BAIBA were assessed in non-diabetic individuals, non-diabetic individuals following 24-h hyperglycemia and patients with type 2 diabetes. Direct effects of BAIBA on acute glucose-mediated insulin release were probed in INS-1832/3 cells under normal and 'diabetes-like' conditions. Finally, the effect of BAIBA on mitochondrial function was assessed in INS-1832/3 cells using extracellular flux analysis.Results: (i) BAIBA is released from skeletal muscle at rest and during exercise under healthy conditions but is suppressed during exercise following leg immobilization, (ii) plasma BAIBA concentrations inversely associate with insulin secretory function in humans, (iii) BAIBA lowers mitochondrial energy metabolism in INS-1 832/3 cells in parallel with decreased insulin secretionConclusion/interpretation: BAIBA is a myokine released by skeletal muscle during exercise and indepedantly alters the triggering pathway of insulin secretion in cultured INS-1832/3 cells.

AB - Aims/hypothesis: This study aimed to examine if beta-aminoisobutyric acid (BAIBA) is (i) secreted by skeletal muscle in humans during exercise, (ii) associated with insulin secretory function in vivo, and (iii) directly linked with acute glucose-mediated insulin release by pancreatic beta cells in vitro.Methods: Following 2-weeks of single-leg immobilization, plasma BAIBA concentrations were measured in the brachial artery and the femoral veins of each leg in healthy male subjects, at rest and during two-legged dynamic knee-extensor exercise. During a 2-h hyperglycamic clamp, insulin secretory function and levels of plasma BAIBA were assessed in non-diabetic individuals, non-diabetic individuals following 24-h hyperglycemia and patients with type 2 diabetes. Direct effects of BAIBA on acute glucose-mediated insulin release were probed in INS-1832/3 cells under normal and 'diabetes-like' conditions. Finally, the effect of BAIBA on mitochondrial function was assessed in INS-1832/3 cells using extracellular flux analysis.Results: (i) BAIBA is released from skeletal muscle at rest and during exercise under healthy conditions but is suppressed during exercise following leg immobilization, (ii) plasma BAIBA concentrations inversely associate with insulin secretory function in humans, (iii) BAIBA lowers mitochondrial energy metabolism in INS-1 832/3 cells in parallel with decreased insulin secretionConclusion/interpretation: BAIBA is a myokine released by skeletal muscle during exercise and indepedantly alters the triggering pathway of insulin secretion in cultured INS-1832/3 cells.

U2 - 10.1016/j.metop.2020.100053

DO - 10.1016/j.metop.2020.100053

M3 - Journal article

C2 - 32924003

VL - 7

SP - 100053

JO - Metabolism open

JF - Metabolism open

SN - 2589-9368

ER -

ID: 260692423