Do diabetes and obesity affect the metabolic response to exercise?
Open accessAbstract
PURPOSE OF REVIEW: Exercise is recommended as therapeutic intervention for people at risk to develop type 2 diabetes to prevent or treat the disease. Recent studies on the influence of obesity and type 2 diabetes on the outcome of exercise programs are discussed. RECENT FINDINGS: Poor glycemic control before an intervention can be a risk factor of reduced therapeutic benefit from exercise. But the acute metabolic response to exercise and the transcriptional profile of the working muscle is similar in healthy controls and type 2 diabetic patients, including but not limited to intact activation of skeletal muscle AMP-activated kinase signaling, glucose uptake and expression of peroxisome proliferator-activated receptor gamma coactivator 1α. The increase in plasma acylcarnitines during exercise is not influenced by type 2 diabetes or obesity. The hepatic response to exercise is dependent on the glucagon/insulin ratio and the exercise-induced increase in hepatokines such as fibroblast growth factor 21 and follistatin is impaired in type 2 diabetes and obesity, but consequences for the benefit from exercise are unknown yet. SUMMARY: Severe metabolic dysregulation can reduce the benefit from exercise, but the intact response of key metabolic regulators in exercising skeletal muscle of diabetic patients demonstrates the effectiveness of exercise programs to treat the disease.
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Clinical studies in patients with insulin resistant conditions have described dampened upregulation of exercise-induced factors such as FGF21 and follistatin, most likely due to an altered glucagon-to-insulin ratio.
“Clinical studies in patients with insulin resistant conditions have described dampened upregulation of exercise-induced factors, such as FGF21 and follistatin, most likely due to an altered glucagon-to-insulin ratio [156,157,280]”
From The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review (2020) · cites this paper as [280]
The 'Effect on exercise-regulated hepatokines' section (p. 9) reports reduced exercise-induced follistatin secretion and blunted FGF21 secretion in type 2 diabetes, as well as an impaired FGF21 increase in obesity. It says both hepatokines are regulated by the glucagon-to-insulin ratio, but describes the cause of the impaired response as uncertain; 'most likely due to' states the mechanism more strongly than the source does. (LLM, conf=0.83)
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- Authors
- Plomgaard, P., & Weigert, C.
- Affiliations
- Copenhagen University Hospital (DK)
- Helmholtz Munich (DE)
- Corresponding author
- Weigert, Cora
- Venue
- Current Opinion in Clinical Nutrition & Metabolic Care
- Published
- 2017-07
- Volume
- 20
- Issue
- 4
- Pages
- 294-299
- ISSN
- 1363-1950 (ISSN-L)
- OpenAlex
- W2604763813
- Cited by
- 10
- References
- 38
- Citations by year
- 2025: 1 · 2023: 2 · 2022: 2 · 2020: 1 · 2019: 4
- FWCI
- 0.13
- Type
- journal article
- Language
- en
- Open access
- Licence
- other-oa
- Locations
- Current Opinion in Clinical Nutrition & Metabolic Care (publishedVersion)
- PubMed (publishedVersion)
- Site cant be reached (submittedVersion, other-oa)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology › Physical Activity and Health
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Keywords
- type 2 diabetes, obesity, exercise metabolism, glycemic control, AMPK, skeletal muscle glucose uptake, PPARγ coactivator-1α, acylcarnitines, glucagon/insulin ratio, FGF21, follistatin, hepatokines, exercise therapy
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Blood Glucose, Carnitine, Diabetes Mellitus, Type 2, Fatty Acids, Glucose, Glycogen, Humans, Liver, Obesity, Oxidation-Reduction, Signal Transduction, Exercise, Muscle, Skeletal, AMP-Activated Protein Kinases
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