Glycogen metabolism links glucose homeostasis to thermogenesis in adipocytes

Omer Keinan, Joseph M. Valentine, Haopeng Xiao, Sushil K. Mahata, Shannon M. Reilly, Mohammad Abu-Odeh, Julia H. Deluca, Benyamin Dadpey, Leslie Cho, Austin Pan, Ruth T. Yu, Yang Dai, Christopher Liddle, Michael Downes, Ronald M. Evans, Aldons J. Lusis, Markku Laakso, Edward T. Chouchani, Mikael Rydén and Alan R. Saltiel ()
Additional contact information
Omer Keinan: University of California San Diego
Joseph M. Valentine: University of California San Diego
Haopeng Xiao: Dana–Farber Cancer Institute
Sushil K. Mahata: VA San Diego Healthcare System and University of California San Diego
Shannon M. Reilly: University of California San Diego
Mohammad Abu-Odeh: University of California San Diego
Julia H. Deluca: University of California San Diego
Benyamin Dadpey: University of California San Diego
Leslie Cho: University of California San Diego
Austin Pan: University of California San Diego
Ruth T. Yu: Salk Institute for Biological Sciences
Yang Dai: Salk Institute for Biological Sciences
Christopher Liddle: University of Sydney
Michael Downes: Salk Institute for Biological Sciences
Ronald M. Evans: Salk Institute for Biological Sciences
Aldons J. Lusis: University of California
Markku Laakso: University of Eastern Finland
Edward T. Chouchani: Dana–Farber Cancer Institute
Mikael Rydén: Karolinska University Hospital
Alan R. Saltiel: University of California San Diego

Nature, 2021, vol. 599, issue 7884, 296-301

Abstract: Abstract Adipocytes increase energy expenditure in response to prolonged sympathetic activation via persistent expression of uncoupling protein 1 (UCP1)1,2. Here we report that the regulation of glycogen metabolism by catecholamines is critical for UCP1 expression. Chronic β-adrenergic activation leads to increased glycogen accumulation in adipocytes expressing UCP1. Adipocyte-specific deletion of a scaffolding protein, protein targeting to glycogen (PTG), reduces glycogen levels in beige adipocytes, attenuating UCP1 expression and responsiveness to cold or β-adrenergic receptor-stimulated weight loss in obese mice. Unexpectedly, we observed that glycogen synthesis and degradation are increased in response to catecholamines, and that glycogen turnover is required to produce reactive oxygen species leading to the activation of p38 MAPK, which drives UCP1 expression. Thus, glycogen has a key regulatory role in adipocytes, linking glucose metabolism to thermogenesis.

Date: 2021
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DOI: 10.1038/s41586-021-04019-8

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