Endurance training improves GLP-1 sensitivity and glucose tolerance in overweight women

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Context and objective: Obesity and inactivity are risk factors for developing impaired glucose tolerance characterized by insulin resistance and reduced beta-cell function. The stimulatory effect of glucagon-like peptide 1 (GLP-1) on insulin secretion is also impaired in obese, inactive individuals. The aim of this study was to investigate whether endurance training influences beta-cell sensitivity to GLP-1. 

Participants and intervention: Twenty-four female participants, age 46 ± 2 years, body mass index 32.4 ± 0.9 kg/m2, and maximal oxygen consumption 24.7 ± 0.8 mL/kg/min participated in a 10-week exercise training study. 

Methods: Beta-cell sensitivity to GLP-1 was assessed in a subset of participants (n = 6) during a 120-minute hyperglycemic glucose clamp (8.5 mM) including a 1-hour GLP-1 (7-36 amide) infusion (0.4 pmol/kg/min). Changes in glucose tolerance, body composition, and cardiorespiratory fitness were assessed by oral glucose tolerance tests (OGTTs), dual-energy X-ray absorptiometry scans, magnetic resonance scans, and maximal oxygen consumption (VO2max) tests, respectively. 

Results: The c-peptide response to infusion of GLP-1 increased 28 ± 3% (P < 0.05) toward the end of the hyperglycemic clamp. The insulin response remained unchanged. Training improved glucose tolerance and reduced GLP-1, insulin, and glucagon levels during the OGTTs. Training increased VO2max (from 24.7 ± 0.8 to 27.0 ± 0.7 mL/kg/min; P < 0.05) and reduced visceral fat volume (from 4176 ± 265 to 3888 ± 266 cm3; P < 0.01). 

Conclusion: Along with improved glycemic control, endurance training improved beta-cell sensitivity to GLP-1 in overweight women. The study was deemed not to constitute a clinical trial and was not registered as such.

TidsskriftJournal of the Endocrine Society
Udgave nummer9
Sider (fra-til)1-8
Antal sider8
StatusUdgivet - 2022

Bibliografisk note

CURIS 2022 NEXS 218

Funding Information:
The Centre for Physical Activity Research (CFAS) is supported by TrygFonden (grants ID 101390, ID 20045, and ID 125132). During the study period, the Centre of Inflammation and Metabolism was supported by a grant from the Danish National Research Foundation (#02-512-55) and by the Commission of the European Communities (contract no. LSHM-CT-2004-005272 EXGENESIS). This study was further supported by the Danish Medical Research Council and by the Carla Thiel Kragh Foundation.

Publisher Copyright:
© 2022 The Author(s).

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