TGF-β2 is an exercise-induced adipokine that regulates glucose and fatty acid metabolism
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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 subcutaneous white adipose tissue (scWAT) and 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.
Originalsprog | Engelsk |
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Tidsskrift | Nature Metabolism |
Vol/bind | 1 |
Udgave nummer | 2 |
Sider (fra-til) | 291-303 |
ISSN | 2522-5812 |
DOI | |
Status | Udgivet - 2019 |
Links
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6481955/pdf/nihms-1517151.pdf
Accepteret manuskript
ID: 240635834