Time of day determines postexercise metabolism in mouse adipose tissue

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The circadian clock is a cell-autonomous transcription–translation feedback mechanism that anticipates and adapts physiology and behavior to different phases of the day. A variety of factors including hormones, temperature, food-intake, and exercise can act on tissue-specific peripheral clocks to alter the expression of genes that influence metabolism, all in a time-of-day dependent manner. The aim of this study was to elucidate the effects of exercise timing on adipose tissue metabolism. We performed RNA sequencing on inguinal adipose tissue of mice immediately following maximal exercise or sham treatment at the early rest or early active phase. Only during the early active phase did exercise elicit an immediate increase in serum nonesterified fatty acids. Furthermore, early active phase exercise increased expression of markers of thermogenesis and mitochondrial proliferation in inguinal adipose tissue. In vitro, synchronized 3T3-L1 adipocytes showed a timing-dependent difference in Adrb2 expression, as well as a greater lipolytic activity. Thus, the response of adipose tissue to exercise is time-of-day sensitive and may be partly driven by the circadian clock. To determine the influence of feeding state on the time-of-day response to exercise, we replicated the experiment in 10-h-fasted early rest phase mice to mimic the early active phase metabolic status. A 10-h fast led to a similar lipolytic response as observed after active phase exercise but did not replicate the transcriptomic response, suggesting that the observed changes in gene expression are not driven by feeding status. In conclusion, acute exercise elicits timing-specific effects on adipose tissue to maintain metabolic homeostasis.

TidsskriftProceedings of the National Academy of Sciences of the United States of America
Udgave nummer8
StatusUdgivet - 2023

Bibliografisk note

Funding Information:
ACKNOWLEDGMENTS. This study was supported by the Novo Nordisk Foundation (NNF14OC0011493), Swedish Diabetes Foundation (DIA2021-645), Swedish Research Council for Sport Science (P2022-0013) and the Swedish Research Council (2015-00165). L.A.P. was supported by KID funding from Karolinska Institutet (2019). L.D. was supported by a Novo Nordisk postdoctoral fellowship run in partnership with Karolinska Institutet and by a Novo Nordisk Foundation postdoctoral fellowship for research abroad (NNF20OC0060969), as well as by EFSD/Novo Nordisk and EFSD/Lilly. The Novo Nordisk Foundation Center for Basic Metabolic Research is an independent research center at the University of Copenhagen, partially funded by an unrestricted donation from the Novo Nordisk Foundation.

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Copyright © 2023 the Author(s).

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