Effects of acute exercise and exercise training on plasma GDF15 concentrations and associations with appetite and cardiometabolic health in individuals with overweight or obesity – A secondary analysis of a randomized controlled trial
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Growth Differentiation Factor 15 (GDF15) is seemingly involved in appetite control. Acute exercise increases GDF15 concentrations in lean humans, but acute and long-term effects of exercise on GDF15 in individuals with overweight/obesity are unknown. We investigated the effects of acute exercise and exercise training on GDF15 concentrations in individuals with overweight/obesity and associations with appetite and cardiometabolic markers. 90 physically inactive adults (20–45 years) with overweight/obesity were randomized to 6-months habitual lifestyle (CON, n=16), or isocaloric exercise of moderate (MOD, n=37) or vigorous intensity (VIG, n=37), 5 days/week. Testing was performed at baseline, 3, and 6 months. Plasma GDF15 concentrations, other metabolic markers, and subjective appetite were assessed fasted and in response to acute exercise before an ad libitum meal. Cardiorespiratory fitness, body composition, insulin sensitivity, and intraabdominal adipose tissue were measured. At baseline, GDF15 increased 18% (95%CI: 4; 34) immediately after acute exercise and 32% (16; 50) 60 min post-exercise. Fasting GDF15 increased 21% (0; 46) in VIG after 3 months (p=0.045), but this attenuated at 6 months (13% (−11; 43), p=0.316) and was unchanged in MOD (11% (−6; 32), p=0.224, across 3 and 6 months). Post-exercise GDF15 did not change in MOD or VIG. GDF15 was not associated with appetite or energy intake. Higher GDF15 was associated with lower cardiorespiratory fitness, central obesity, dyslipidemia, and poorer glycemic control. In conclusion, GDF15 increased in response to acute exercise but was unaffected by exercise training. Higher GDF15 concentrations were associated with a less favorable cardiometabolic profile but not with markers of appetite. This suggests that GDF15 increases in response to acute exercise independent of training state. Whether this has an impact on free-living energy intake and body weight management needs investigation.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | 106423 |
| Tidsskrift | Appetite |
| Vol/bind | 182 |
| Antal sider | 11 |
| ISSN | 0195-6663 |
| DOI | |
| Status | Udgivet - 2023 |
Bibliografisk note
Funding Information:
The GO-ACTIWE study was funded by the University of Copenhagen Excellence Programme for Interdisciplinary Research (www.go.ku.dk), TrygFonden, and Gerda and Aage Haensch's Fund. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. During the trial, Jonas Salling Quist was supported by a PhD scholarship from the Faculty of Health and Medical Sciences, University of Copenhagen, Denmark, and was supported by grants from the Danish Diabetes Association, Novo Nordisk A/S, and the Danish Diabetes Academy which is supported by the Novo Nordisk Foundation during the present work. Analysis of GDF15 was supported by institutional funding from Steno Diabetes Center Copenhagen, University of Copenhagen, and the Novo Nordisk Foundation Center for Basic Metabolic Research which is an independent Research Center, based at the University of Copenhagen, Denmark, and partially funded by an unconditional donation from the Novo Nordisk Foundation (www.cbmr.ku.dk) (Grant number NNF18CC0034900).
Funding Information:
The GO-ACTIWE study was funded by the University of Copenhagen Excellence Programme for Interdisciplinary Research ( www.go.ku.dk ), TrygFonden , and Gerda and Aage Haensch’s Fund . The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. During the trial, Jonas Salling Quist was supported by a PhD scholarship from the Faculty of Health and Medical Sciences, University of Copenhagen, Denmark , and was supported by grants from the Danish Diabetes Association , Novo Nordisk A/S , and the Danish Diabetes Academy which is supported by the Novo Nordisk Foundation during the present work. Analysis of GDF15 was supported by institutional funding from Steno Diabetes Center Copenhagen , University of Copenhagen , and the Novo Nordisk Foundation Center for Basic Metabolic Research which is an independent Research Center, based at the University of Copenhagen, Denmark, and partially funded by an unconditional donation from the Novo Nordisk Foundation ( www.cbmr.ku.dk ) (Grant number NNF18CC0034900 ).
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