Personalized phosphoproteomics of skeletal muscle insulin resistance and exercise links MINDY1 to insulin action

Elise J. Needham; Janne R. Hingst; Johan D. Onslev; Alexis Diaz-Vegas; Magnus R. Leandersson; Hannah Huckstep; Jonas M. Kristensen; Kohei Kido; Erik A. Richter; Kurt Højlund; Benjamin L. Parker; Kristen Cooke; Guang Yang; Christian Pehmøller; Sean J. Humphrey; David E. James; Jørgen F.P. Wojtaszewski

doi:10.1016/j.cmet.2024.10.020

Personalized phosphoproteomics of skeletal muscle insulin resistance and exercise links MINDY1 to insulin action

Elise J. Needham
, Janne R. Hingst
, Johan D. Onslev
, Alexis Diaz-Vegas
, Magnus R. Leandersson
, Hannah Huckstep
, Jonas M. Kristensen
, Kohei Kido
, Erik A. Richter
, Kurt Højlund
, Benjamin L. Parker
, Kristen Cooke
, Guang Yang
, Christian Pehmøller
, Sean J. Humphrey^*
, David E. James
, Jørgen F.P. Wojtaszewski

^*Corresponding author af dette arbejde

August Krogh Sektionen for Human og Molekylær Fysiologi

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

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Abstract

Type 2 diabetes is preceded by a defective insulin response, yet our knowledge of the precise mechanisms is incomplete. Here, we investigate how insulin resistance alters skeletal muscle signaling and how exercise partially counteracts this effect. We measured parallel phenotypes and phosphoproteomes of insulin-resistant (IR) and insulin-sensitive (IS) men as they responded to exercise and insulin (n = 19, 114 biopsies), quantifying over 12,000 phosphopeptides in each biopsy. Insulin resistance involves selective and time-dependent alterations to signaling, including reduced insulin-stimulated mTORC1 and non-canonical signaling responses. Prior exercise promotes insulin sensitivity even in IR individuals by “priming” a portion of insulin signaling prior to insulin infusion. This includes MINDY1 S441, which we show is an AKT substrate. We found that MINDY1 knockdown enhances insulin-stimulated glucose uptake in rat myotubes. This work delineates the signaling alterations in IR skeletal muscle and identifies MINDY1 as a regulator of insulin action.

Originalsprog	Engelsk
Tidsskrift	Cell Metabolism
Vol/bind	36
Udgave nummer	12
Sider (fra-til)	2542-2559
ISSN	1550-4131
DOI	https://doi.org/10.1016/j.cmet.2024.10.020
Status	Udgivet - 2024

Bibliografisk note

Publisher Copyright:
© 2024 The Author(s)

Finansiering

We thank Betina Bolmgreen, Nikoline R. Andersen, Jesper B. Birk, and Irene B. Nielsen (Department of Nutrition, Exercise, and Sports) for their skilled technical help in the laboratory. We would like to thank Professor Bente Kiens for scientific discussion, Kasper E. Villumsen and Kim A. Sj\u00F8berg for assistance during the experimental trials, and Le Lene S. Stevner for support on data regulation and protection. This work was funded by a Pfizer, Inc. grant (to D.E.J., J.F.P.W., and C.P.) and a grant from the National Health and Medical Research Council (NHMRC; GNT2011083 to S.J.H., D.E.J., and J.F.P.W.). E.J.N. was supported by an Australian Government Research Training Program Scholarship, the University of Sydney Val Street Scholarship, EMBO (ALTF 1071-2021), and was supported by the Schmidt Science Fellows, in partnership with the Rhodes Trust. S.J.H. is supported by an NHMRC Investigator Grant (2026905). D.E.J. is an Australian Research Council (ARC) Laureate Fellow. J.F.P.W. was supported by The Novo Nordisk Foundation (no. NN0070370, NNF082659, and NNF0079480) and The University of Sydney University of Copenhagen Partnership Collaboration Awards (to J.F.P.W. and D.E.J.). J.D.O. and M.R.L. were supported by a research grant from the Danish Diabetes and Endocrinology Academy, which is funded by the Novo Nordisk Foundation, grant no. NNF17SA0031406; Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research 19K20007 (to K.K.); and the European Foundation for the Study of Diabetes JDS Fellowship Program (to K.K.). B.L.P. is supported by an NHMRC Investigator Grant (2009642). E.J.N. was supported by core funding from the British Heart Foundation (RG/18/13/33946); NIHR Cambridge Biomedical Research Centre (BRC-1215-20014 and NIHR203312); Cambridge BHF Centre of Research Excellence (RE/18/1/34212); BHF Chair Award (CH/12/2/29428); Health Data Research UK, which is funded by the UK Medical Research Council; the Engineering and Physical Sciences Research Council; the Economic and Social Research Council; the Department of Health and Social Care (England); the Chief Scientist Office of the Scottish Government Health and Social Care Directorates; the Health and Social Care Research and Development Division (Welsh Government); the Public Health Agency (Northern Ireland); the British Heart Foundation; and Wellcome. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NHMRC, ARC, the NIHR, or the Department of Health and Social Care. The authors acknowledge the facilities and support of the Sydney Mass Spectrometry Facility (SydneyMS), University of Sydney. We thank Betina Bolmgreen, Nikoline R. Andersen, Jesper B. Birk, and Irene B. Nielsen (Department of Nutrition, Exercise, and Sports) for their skilled technical help in the laboratory. We would like to thank Professor Bente Kiens for scientific discussion, Kasper E. Villumsen and Kim A. Sj\u00F8berg for assistance during the experimental trials, and Le Lene S. Stevner for support on data regulation and protection. This work was funded by a Pfizer, Inc. grant (to D.E.J., J.F.P.W., and C.P.) and a grant from the National Health and Medical Research Council (NHMRC; GNT2011083 to S.J.H., D.E.J., and J.F.P.W.). E.J.N. was supported by an Australian Government Research Training Program Scholarship , the University of Sydney Val Street Scholarship , and the Schmidt Science Fellows, in partnership with the Rhodes Trust . S.J.H. is supported by an NHMRC Investigator Grant ( 2026905 ). D.E.J. is an Australian Research Council (ARC) Laureate Fellow supported by The Novo Nordisk Foundation (no. NN0070370 , NNF082659 , and NNF0079480 to J.F.P.W.) and The University of Sydney University of Copenhagen Partnership Collaboration Awards (to J.F.P.W. and D.E.J.). J.D.O. and M.R.L. were supported by a research grant from the Danish Diabetes and Endocrinology Academy , which is funded by the Novo Nordisk Foundation , grant no. NNF17SA0031406 ; Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research 19K20007 (to K.K.); and the European Foundation for the Study of Diabetes JDS Fellowship Program (to K.K.). B.L.P. is supported by an NHMRC Investigator Grant ( 2009642 ). E.J.N. was supported by core funding from EMBO ( ALTF 1071-2021 ); the British Heart Foundation ( RG/18/13/33946 ); NIHR Cambridge Biomedical Research Centre ( BRC-1215-20014 and NIHR203312 ); Cambridge BHF Centre of Research Excellence ( RE/18/1/34212 ); BHF Chair Award ( CH/12/2/29428 ); Health Data Research UK , which is funded by the UK Medical Research Council ; the Engineering and Physical Sciences Research Council ; the Economic and Social Research Council ; the Department of Health and Social Care (England) ; the Chief Scientist Office of the Scottish Government Health and Social Care Directorates ; the Health and Social Care Research and Development Division (Welsh Government) ; the Public Health Agency (Northern Ireland) ; the British Heart Foundation ; and Wellcome. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NHMRC, ARC, the NIHR, or the Department of Health and Social Care. The authors acknowledge the facilities and support of the Sydney Mass Spectrometry Facility (SydneyMS), University of Sydney .

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Needham, E. J., Hingst, J. R., Onslev, J. D., Diaz-Vegas, A., Leandersson, M. R., Huckstep, H., Kristensen, J. M., Kido, K., Richter, E. A., Højlund, K., Parker, B. L., Cooke, K., Yang, G., Pehmøller, C., Humphrey, S. J., James, D. E., & Wojtaszewski, J. F. P. (2024). Personalized phosphoproteomics of skeletal muscle insulin resistance and exercise links MINDY1 to insulin action. Cell Metabolism, 36(12), 2542-2559. https://doi.org/10.1016/j.cmet.2024.10.020

Needham, EJ, Hingst, JR, Onslev, JD, Diaz-Vegas, A, Leandersson, MR, Huckstep, H, Kristensen, JM, Kido, K, Richter, EA, Højlund, K, Parker, BL, Cooke, K, Yang, G, Pehmøller, C, Humphrey, SJ, James, DE & Wojtaszewski, JFP 2024, 'Personalized phosphoproteomics of skeletal muscle insulin resistance and exercise links MINDY1 to insulin action', Cell Metabolism, bind 36, nr. 12, s. 2542-2559. https://doi.org/10.1016/j.cmet.2024.10.020

@article{f51723917baa4afbb7e3cb0cff7ee70c,

title = "Personalized phosphoproteomics of skeletal muscle insulin resistance and exercise links MINDY1 to insulin action",

abstract = "Type 2 diabetes is preceded by a defective insulin response, yet our knowledge of the precise mechanisms is incomplete. Here, we investigate how insulin resistance alters skeletal muscle signaling and how exercise partially counteracts this effect. We measured parallel phenotypes and phosphoproteomes of insulin-resistant (IR) and insulin-sensitive (IS) men as they responded to exercise and insulin (n = 19, 114 biopsies), quantifying over 12,000 phosphopeptides in each biopsy. Insulin resistance involves selective and time-dependent alterations to signaling, including reduced insulin-stimulated mTORC1 and non-canonical signaling responses. Prior exercise promotes insulin sensitivity even in IR individuals by {\textquotedblleft}priming{\textquotedblright} a portion of insulin signaling prior to insulin infusion. This includes MINDY1 S441, which we show is an AKT substrate. We found that MINDY1 knockdown enhances insulin-stimulated glucose uptake in rat myotubes. This work delineates the signaling alterations in IR skeletal muscle and identifies MINDY1 as a regulator of insulin action.",

keywords = "cell signaling, exercise, insulin, insulin resistance, MINDY1, phosphoproteomics, proteomics, skeletal muscle",

author = "Needham, \{Elise J.\} and Hingst, \{Janne R.\} and Onslev, \{Johan D.\} and Alexis Diaz-Vegas and Leandersson, \{Magnus R.\} and Hannah Huckstep and Kristensen, \{Jonas M.\} and Kohei Kido and Richter, \{Erik A.\} and Kurt H{\o}jlund and Parker, \{Benjamin L.\} and Kristen Cooke and Guang Yang and Christian Pehm{\o}ller and Humphrey, \{Sean J.\} and James, \{David E.\} and Wojtaszewski, \{J{\o}rgen F.P.\}",

note = "Funding Information: We thank Betina Bolmgreen, Nikoline R. Andersen, Jesper B. Birk, and Irene B. Nielsen (Department of Nutrition, Exercise, and Sports) for their skilled technical help in the laboratory. We would like to thank Professor Bente Kiens for scientific discussion, Kasper E. Villumsen and Kim A. Sj\textbackslash{}u00F8berg for assistance during the experimental trials, and Le Lene S. Stevner for support on data regulation and protection. This work was funded by a Pfizer, Inc. grant (to D.E.J., J.F.P.W., and C.P.) and a grant from the National Health and Medical Research Council (NHMRC; GNT2011083 to S.J.H., D.E.J., and J.F.P.W.). E.J.N. was supported by an Australian Government Research Training Program Scholarship, the University of Sydney Val Street Scholarship, EMBO (ALTF 1071-2021), and was supported by the Schmidt Science Fellows, in partnership with the Rhodes Trust. S.J.H. is supported by an NHMRC Investigator Grant (2026905). D.E.J. is an Australian Research Council (ARC) Laureate Fellow. J.F.P.W. was supported by The Novo Nordisk Foundation (no. NN0070370, NNF082659, and NNF0079480) and The University of Sydney University of Copenhagen Partnership Collaboration Awards (to J.F.P.W. and D.E.J.). J.D.O. and M.R.L. were supported by a research grant from the Danish Diabetes and Endocrinology Academy, which is funded by the Novo Nordisk Foundation, grant no. NNF17SA0031406; Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research 19K20007 (to K.K.); and the European Foundation for the Study of Diabetes JDS Fellowship Program (to K.K.). B.L.P. is supported by an NHMRC Investigator Grant (2009642). E.J.N. was supported by core funding from the British Heart Foundation (RG/18/13/33946); NIHR Cambridge Biomedical Research Centre (BRC-1215-20014 and NIHR203312); Cambridge BHF Centre of Research Excellence (RE/18/1/34212); BHF Chair Award (CH/12/2/29428); Health Data Research UK, which is funded by the UK Medical Research Council; the Engineering and Physical Sciences Research Council; the Economic and Social Research Council; the Department of Health and Social Care (England); the Chief Scientist Office of the Scottish Government Health and Social Care Directorates; the Health and Social Care Research and Development Division (Welsh Government); the Public Health Agency (Northern Ireland); the British Heart Foundation; and Wellcome. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NHMRC, ARC, the NIHR, or the Department of Health and Social Care. The authors acknowledge the facilities and support of the Sydney Mass Spectrometry Facility (SydneyMS), University of Sydney. Funding Information: We thank Betina Bolmgreen, Nikoline R. Andersen, Jesper B. Birk, and Irene B. Nielsen (Department of Nutrition, Exercise, and Sports) for their skilled technical help in the laboratory. We would like to thank Professor Bente Kiens for scientific discussion, Kasper E. Villumsen and Kim A. Sj\textbackslash{}u00F8berg for assistance during the experimental trials, and Le Lene S. Stevner for support on data regulation and protection. This work was funded by a Pfizer, Inc. grant (to D.E.J., J.F.P.W., and C.P.) and a grant from the National Health and Medical Research Council (NHMRC; GNT2011083 to S.J.H., D.E.J., and J.F.P.W.). E.J.N. was supported by an Australian Government Research Training Program Scholarship , the University of Sydney Val Street Scholarship , and the Schmidt Science Fellows, in partnership with the Rhodes Trust . S.J.H. is supported by an NHMRC Investigator Grant ( 2026905 ). D.E.J. is an Australian Research Council (ARC) Laureate Fellow supported by The Novo Nordisk Foundation (no. NN0070370 , NNF082659 , and NNF0079480 to J.F.P.W.) and The University of Sydney University of Copenhagen Partnership Collaboration Awards (to J.F.P.W. and D.E.J.). J.D.O. and M.R.L. were supported by a research grant from the Danish Diabetes and Endocrinology Academy , which is funded by the Novo Nordisk Foundation , grant no. NNF17SA0031406 ; Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research 19K20007 (to K.K.); and the European Foundation for the Study of Diabetes JDS Fellowship Program (to K.K.). B.L.P. is supported by an NHMRC Investigator Grant ( 2009642 ). E.J.N. was supported by core funding from EMBO ( ALTF 1071-2021 ); the British Heart Foundation ( RG/18/13/33946 ); NIHR Cambridge Biomedical Research Centre ( BRC-1215-20014 and NIHR203312 ); Cambridge BHF Centre of Research Excellence ( RE/18/1/34212 ); BHF Chair Award ( CH/12/2/29428 ); Health Data Research UK , which is funded by the UK Medical Research Council ; the Engineering and Physical Sciences Research Council ; the Economic and Social Research Council ; the Department of Health and Social Care (England) ; the Chief Scientist Office of the Scottish Government Health and Social Care Directorates ; the Health and Social Care Research and Development Division (Welsh Government) ; the Public Health Agency (Northern Ireland) ; the British Heart Foundation ; and Wellcome. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NHMRC, ARC, the NIHR, or the Department of Health and Social Care. The authors acknowledge the facilities and support of the Sydney Mass Spectrometry Facility (SydneyMS), University of Sydney . Publisher Copyright: {\textcopyright} 2024 The Author(s)",

year = "2024",

doi = "10.1016/j.cmet.2024.10.020",

language = "English",

volume = "36",

pages = "2542--2559",

journal = "Cell Metabolism",

issn = "1550-4131",

publisher = "Cell Press",

number = "12",

}

TY - JOUR

T1 - Personalized phosphoproteomics of skeletal muscle insulin resistance and exercise links MINDY1 to insulin action

AU - Needham, Elise J.

AU - Hingst, Janne R.

AU - Onslev, Johan D.

AU - Diaz-Vegas, Alexis

AU - Leandersson, Magnus R.

AU - Huckstep, Hannah

AU - Kristensen, Jonas M.

AU - Kido, Kohei

AU - Richter, Erik A.

AU - Højlund, Kurt

AU - Parker, Benjamin L.

AU - Cooke, Kristen

AU - Yang, Guang

AU - Pehmøller, Christian

AU - Humphrey, Sean J.

AU - James, David E.

AU - Wojtaszewski, Jørgen F.P.

N1 - Funding Information: We thank Betina Bolmgreen, Nikoline R. Andersen, Jesper B. Birk, and Irene B. Nielsen (Department of Nutrition, Exercise, and Sports) for their skilled technical help in the laboratory. We would like to thank Professor Bente Kiens for scientific discussion, Kasper E. Villumsen and Kim A. Sj\u00F8berg for assistance during the experimental trials, and Le Lene S. Stevner for support on data regulation and protection. This work was funded by a Pfizer, Inc. grant (to D.E.J., J.F.P.W., and C.P.) and a grant from the National Health and Medical Research Council (NHMRC; GNT2011083 to S.J.H., D.E.J., and J.F.P.W.). E.J.N. was supported by an Australian Government Research Training Program Scholarship, the University of Sydney Val Street Scholarship, EMBO (ALTF 1071-2021), and was supported by the Schmidt Science Fellows, in partnership with the Rhodes Trust. S.J.H. is supported by an NHMRC Investigator Grant (2026905). D.E.J. is an Australian Research Council (ARC) Laureate Fellow. J.F.P.W. was supported by The Novo Nordisk Foundation (no. NN0070370, NNF082659, and NNF0079480) and The University of Sydney University of Copenhagen Partnership Collaboration Awards (to J.F.P.W. and D.E.J.). J.D.O. and M.R.L. were supported by a research grant from the Danish Diabetes and Endocrinology Academy, which is funded by the Novo Nordisk Foundation, grant no. NNF17SA0031406; Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research 19K20007 (to K.K.); and the European Foundation for the Study of Diabetes JDS Fellowship Program (to K.K.). B.L.P. is supported by an NHMRC Investigator Grant (2009642). E.J.N. was supported by core funding from the British Heart Foundation (RG/18/13/33946); NIHR Cambridge Biomedical Research Centre (BRC-1215-20014 and NIHR203312); Cambridge BHF Centre of Research Excellence (RE/18/1/34212); BHF Chair Award (CH/12/2/29428); Health Data Research UK, which is funded by the UK Medical Research Council; the Engineering and Physical Sciences Research Council; the Economic and Social Research Council; the Department of Health and Social Care (England); the Chief Scientist Office of the Scottish Government Health and Social Care Directorates; the Health and Social Care Research and Development Division (Welsh Government); the Public Health Agency (Northern Ireland); the British Heart Foundation; and Wellcome. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NHMRC, ARC, the NIHR, or the Department of Health and Social Care. The authors acknowledge the facilities and support of the Sydney Mass Spectrometry Facility (SydneyMS), University of Sydney. Funding Information: We thank Betina Bolmgreen, Nikoline R. Andersen, Jesper B. Birk, and Irene B. Nielsen (Department of Nutrition, Exercise, and Sports) for their skilled technical help in the laboratory. We would like to thank Professor Bente Kiens for scientific discussion, Kasper E. Villumsen and Kim A. Sj\u00F8berg for assistance during the experimental trials, and Le Lene S. Stevner for support on data regulation and protection. This work was funded by a Pfizer, Inc. grant (to D.E.J., J.F.P.W., and C.P.) and a grant from the National Health and Medical Research Council (NHMRC; GNT2011083 to S.J.H., D.E.J., and J.F.P.W.). E.J.N. was supported by an Australian Government Research Training Program Scholarship , the University of Sydney Val Street Scholarship , and the Schmidt Science Fellows, in partnership with the Rhodes Trust . S.J.H. is supported by an NHMRC Investigator Grant ( 2026905 ). D.E.J. is an Australian Research Council (ARC) Laureate Fellow supported by The Novo Nordisk Foundation (no. NN0070370 , NNF082659 , and NNF0079480 to J.F.P.W.) and The University of Sydney University of Copenhagen Partnership Collaboration Awards (to J.F.P.W. and D.E.J.). J.D.O. and M.R.L. were supported by a research grant from the Danish Diabetes and Endocrinology Academy , which is funded by the Novo Nordisk Foundation , grant no. NNF17SA0031406 ; Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research 19K20007 (to K.K.); and the European Foundation for the Study of Diabetes JDS Fellowship Program (to K.K.). B.L.P. is supported by an NHMRC Investigator Grant ( 2009642 ). E.J.N. was supported by core funding from EMBO ( ALTF 1071-2021 ); the British Heart Foundation ( RG/18/13/33946 ); NIHR Cambridge Biomedical Research Centre ( BRC-1215-20014 and NIHR203312 ); Cambridge BHF Centre of Research Excellence ( RE/18/1/34212 ); BHF Chair Award ( CH/12/2/29428 ); Health Data Research UK , which is funded by the UK Medical Research Council ; the Engineering and Physical Sciences Research Council ; the Economic and Social Research Council ; the Department of Health and Social Care (England) ; the Chief Scientist Office of the Scottish Government Health and Social Care Directorates ; the Health and Social Care Research and Development Division (Welsh Government) ; the Public Health Agency (Northern Ireland) ; the British Heart Foundation ; and Wellcome. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NHMRC, ARC, the NIHR, or the Department of Health and Social Care. The authors acknowledge the facilities and support of the Sydney Mass Spectrometry Facility (SydneyMS), University of Sydney . Publisher Copyright: © 2024 The Author(s)

PY - 2024

Y1 - 2024

N2 - Type 2 diabetes is preceded by a defective insulin response, yet our knowledge of the precise mechanisms is incomplete. Here, we investigate how insulin resistance alters skeletal muscle signaling and how exercise partially counteracts this effect. We measured parallel phenotypes and phosphoproteomes of insulin-resistant (IR) and insulin-sensitive (IS) men as they responded to exercise and insulin (n = 19, 114 biopsies), quantifying over 12,000 phosphopeptides in each biopsy. Insulin resistance involves selective and time-dependent alterations to signaling, including reduced insulin-stimulated mTORC1 and non-canonical signaling responses. Prior exercise promotes insulin sensitivity even in IR individuals by “priming” a portion of insulin signaling prior to insulin infusion. This includes MINDY1 S441, which we show is an AKT substrate. We found that MINDY1 knockdown enhances insulin-stimulated glucose uptake in rat myotubes. This work delineates the signaling alterations in IR skeletal muscle and identifies MINDY1 as a regulator of insulin action.

AB - Type 2 diabetes is preceded by a defective insulin response, yet our knowledge of the precise mechanisms is incomplete. Here, we investigate how insulin resistance alters skeletal muscle signaling and how exercise partially counteracts this effect. We measured parallel phenotypes and phosphoproteomes of insulin-resistant (IR) and insulin-sensitive (IS) men as they responded to exercise and insulin (n = 19, 114 biopsies), quantifying over 12,000 phosphopeptides in each biopsy. Insulin resistance involves selective and time-dependent alterations to signaling, including reduced insulin-stimulated mTORC1 and non-canonical signaling responses. Prior exercise promotes insulin sensitivity even in IR individuals by “priming” a portion of insulin signaling prior to insulin infusion. This includes MINDY1 S441, which we show is an AKT substrate. We found that MINDY1 knockdown enhances insulin-stimulated glucose uptake in rat myotubes. This work delineates the signaling alterations in IR skeletal muscle and identifies MINDY1 as a regulator of insulin action.

KW - cell signaling

KW - exercise

KW - insulin

KW - insulin resistance

KW - MINDY1

KW - phosphoproteomics

KW - proteomics

KW - skeletal muscle

U2 - 10.1016/j.cmet.2024.10.020

DO - 10.1016/j.cmet.2024.10.020

M3 - Journal article

C2 - 39577414

AN - SCOPUS:85210363028

SN - 1550-4131

VL - 36

SP - 2542

EP - 2559

JO - Cell Metabolism

JF - Cell Metabolism

IS - 12

ER -