Adipocyte-specific mTORC2 deficiency impairs BAT and iWAT thermogenic capacity without affecting glucose uptake and energy expenditure in cold-acclimated mice

Author:

Castro Érique1,Vieira Thayna S.1,Oliveira Tiago E.1,Ortiz-Silva Milene1,Andrade Maynara L.1,Tomazelli Caroline A.1,Peixoto Albert S.1,Sobrinho Cleyton R.1ORCID,Moreno Mayara F.1,Gilio Gustavo R.1,Moreira Rafael J.1,Guimarães Raphael C.1,Perandini Luiz A.1,Chimin Patricia2,Reckziegel Patricia3,Moretti Eduardo H.4,Steiner Alexandre A.4,Laplante Mathieu56ORCID,Festuccia William T.1ORCID

Affiliation:

1. Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil

2. Department of Physical Education, Physical Education and Sports Center, Londrina State University, Parana, Brazil

3. Department of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo (UNIFESP), Sao Paulo, Brazil

4. Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, Sao Paulo, Brazil

5. Institut Universitaire de Cardiologie et de Pneumologie de Quebec, Université Laval, Quebec, Quebec, Canada

6. Centre de recherche sur le cancer de l’Université Laval, Université Laval, Québec, Quebec, Canada

Abstract

BAT and iWAT mTORC2 is inhibited by cold acclimation, but its residual activity is required for cold-induced increases in total UCP-1 content and thermogenic capacity, but not glucose uptake and mTORC1 activity. The impaired BAT and iWAT total UCP-1 content and thermogenic capacity induced by adipocyte mTORC2 deficiency are compensated by activation of muscle shivering in cold-acclimated mice.

Funder

Fundação de Amparo à Pesquisa do Estado de São Paulo

MCTI | Conselho Nacional de Desenvolvimento Científico e Tecnológico

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology,Endocrinology, Diabetes and Metabolism

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