TGF-β2 is an exercise-induced adipokine that regulates glucose and fatty acid metabolism
Open accessAbstract
Exercise improves health and well-being across diverse organ systems, and elucidating mechanisms underlying the beneficial effects of exercise can lead to new therapies. Here, we show that transforming growth factor-β2 (TGF-β2) is secreted from adipose tissue in response to exercise and improves glucose tolerance in mice. We identify TGF-β2 as an exercise-induced adipokine in a gene expression analysis of human subcutaneous adipose tissue biopsies after exercise training. In mice, exercise training increases TGF-β2 in scWAT, serum, and its secretion from fat explants. Transplanting scWAT from exercise-trained wild type mice, but not from adipose tissue-specific Tgfb2-/- mice, into sedentary mice improves glucose tolerance. TGF-β2 treatment reverses the detrimental metabolic effects of high fat feeding in mice. Lactate, a metabolite released from muscle during exercise, stimulates TGF-β2 expression in human adipocytes. Administration of the lactate-lowering agent dichloroacetate during exercise training in mice decreases circulating TGF-β2 levels and reduces exercise-stimulated improvements in glucose tolerance. Thus, exercise training improves systemic metabolism through inter-organ communication with fat via a lactate-TGF-β2-signaling cycle.
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TGF-β2, an exercise-induced adipokine, is stimulated by exercise-induced lactate, enhancing glucose uptake in skeletal muscle and boosting mitochondrial function.
“Transforming growth factor-beta 2 (TGF-β2), an exercise-induced adipokine, is stimulated by exercise-induced lactate, enhancing glucose uptake in skeletal muscle and boosting mitochondrial function, shedding light on adipose–muscle tissue crosstalk [79] (Table 1).”
From Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis (2025) · cites this paper as [79]
Exercise-trained white adipose tissue fosters the generation of thermogenic brown-like adipocytes with specific adipokines including TGF-β, apelin, follistatin, and myostatin.
“Moreover, exercise-trained WAT fosters the generation of thermogenic brown-like adipocytes with specific adipokines, including TGF-β [79], apelin, follistatin, and myostatin (Figure 3) [80,81].”
From Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis (2025) · cites this paper as [79]
Exercise-related paracrine effects occur in the nervous system, adipose tissue, bone, cartilage, extracellular matrix and immune system.
“Exercise-related paracrine effects are also observed in the nervous system53, adipose tissue42,54–58, bone59–61, cartilage62, extracellular matrix63,64 and the immune system65,66.”
From Exerkines in health, resilience and disease (2022) · cites this paper as [42]
In a mouse model, lactate exposure in vitro and in vivo increased adipocyte TGFβ2 expression.
“In a mouse model, specific lactate exposure in vitro and in vivo increased adipocyte expression of TGFβ2 (REF.42).”
From Exerkines in health, resilience and disease (2022) · cites this paper as [42]
In a mouse model of chronic exercise, increased adipocyte TGFβ2 expression and secretion were associated with improved glucose metabolism, lipid oxidation and possible reduction of adipose inflammation.
“in a mouse model of chronic exercise, increased adipocyte levels of TGFβ2 expression and secretion were associated with improvements in glucose metabolism, lipid oxidation and a possible reduction of adipose tissue inflammation.”
From Exerkines in health, resilience and disease (2022) · cites this paper as [42]
Parallel findings to the mouse TGFβ2 results were observed in humans undertaking chronic exercise, though less pronounced.
“Parallel findings were also observed in humans undertaking chronic exercise, albeit to a less pronounced degree than the animal model observations42.”
From Exerkines in health, resilience and disease (2022) · cites this paper as [42]
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- Authors
- Takahashi, H., Alves, C. R. R., Stanford, K. I., Middelbeek, R. J. W., Nigro, P., Ryan, R. E., Xue, R., Sakaguchi, M., Lynes, M. D., So, K., Mul, J. D., Lee, M.-Y., Balan, E., Pan, H., Dreyfuss, J. M., Hirshman, M. F., Azhar, M., Hannukainen, J. C., Nuutila, P., Kalliokoski, K. K., Nielsen, S., Pedersen, B. K., Kahn, C. R., Tseng, Y.-H., & Goodyear, L. J.
- Affiliations
- Joslin Diabetes Center (US)
- University of South Carolina (US)
- University of Turku (FI)
- University of Copenhagen (DK)
- Corresponding author
- Goodyear, Laurie J.
- ORCID
- Takahashi, Hirokazu
- Alves, Christiano R. R.
- Stanford, Kristin I.
- Middelbeek, Roeland J. W.
- Nigro, Pasquale
- Sakaguchi, Masaji
- Lynes, Matthew D.
- Mul, Joram D.
- Pan, Hui
- Dreyfuss, Jonathan M.
- Hirshman, Michael F.
- Azhar, Mohamad
- Hannukainen, Jarna C.
- Nuutila, Pirjo
- Kalliokoski, Kari K.
- Nielsen, Søren
- Pedersen, Bente K.
- Kahn, C. Ronald
- Tseng, Yu-Hua
- Goodyear, Laurie J.
- Venue
- Nature Metabolism
- Published
- 2019-02-11
- Volume
- 1
- Issue
- 2
- Pages
- 291-303
- ISSN
- 2522-5812 (ISSN-L)
- PMC
- PMC6481955
- OpenAlex
- W2912468419
- Cited by
- 204
- References
- 66
- Citations by year
- 2026: 16 · 2025: 25 · 2024: 34 · 2023: 31 · 2022: 31 · 2021: 33 · 2020: 22 · 2019: 10
- FWCI
- 18.19
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Metabolism (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, other-oa)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Heart Association (R01HL126705, 17GRNT33650018, R01DK102898)
- Joslin Diabetes Center (P30DK36836, K23-DK114550)
- TrygFonden
- National Institutes of Health (17GRNT33650018, DK 36836, 5r01dk112283-03)
- Japan Society for the Promotion of Science (18K16208)
- National Heart, Lung, and Blood Institute (R01HL126705, R01HL138738, R01HL145064)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01-DK112283, R01DK077097, R01DK102898, K01DK111714, K23DK114550, R01DK033201, F32DK102320, T32DK007260, R01DK101043, P30DK036836, R01DK082659, R01DK099511)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Keywords
- TGF-beta2, glucose tolerance, fatty acid metabolism, subcutaneous white adipose tissue, lactate, dichloroacetate, inter-organ communication, myokines, high-fat feeding, exercise training, adipocytes
- MeSH terms
- Adipose Tissue, Animals, Fatty Acids, Glucose, Physical Conditioning, Animal, Mice, Transforming Growth Factor beta2, Adipokines
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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