Cell metabolism

How a gut hormone controls body weight and eating through brain signaling

Updated

Abstract

HFD-fed CNS-Gipr KO mice show decreased body weight and improved glucose metabolism.

  • The physiological relevance of GIPR in the central nervous system remains unclear.
  • Acute administration of acyl-GIP increases neuronal activity in hypothalamic feeding centers, which is linked to reduced body weight and food intake.
  • Chronic administration of acyl-GIP decreases body weight and food intake in wild-type mice but is less effective in CNS-Gipr KO mice.
  • The enhanced metabolic effect of GLP-1/GIP co-agonism compared to GLP-1 alone is not observed in CNS-Gipr KO mice.
  • CNS Gipr appears to play a crucial role in regulating energy metabolism.

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Funding

Competing interests

Declaration of interests M.H.T. is a member of the scientific advisory board of ERX Pharmaceuticals, Cambridge, MA. He was a member of the Research Cluster Advisory Panel (ReCAP) of the Novo Nordisk Foundation between 2017 and 2019. He attended a scientific advisory board meeting of the Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, in 2016. He received funding for his research projects from Novo Nordisk (2016–2020) and Sanofi-Aventis (2012–2019). He was a consultant for Bionorica SE (2013–2017), Menarini Ricerche S.p.A. (2016), and Bayer Pharma AG Berlin (2016). As former Director of the Helmholtz Diabetes Center and the Institute for Diabetes and Obesity at Helmholtz Zentrum München (2011–2018), and since 2018, as CEO of Helmholtz Zentrum München, he has been responsible for collaborations with a multitude of companies and institutions worldwide. In this capacity, he discussed potential projects with and has signed/signs contracts for his institute(s) and for the staff for research funding and/or collaborations with industry and academia worldwide, including, but not limited to, pharmaceutical corporations like Boehringer Ingelheim, Eli Lilly, Novo Nordisk, Medigene, Arbormed, BioSyngen, and others. In this role, he was/is further responsible for commercial technology transfer activities of his institute(s), including diabetes-related patent portfolios of Helmholtz Zentrum München as, e.g., WO/2016/188932 A2 or WO/2017/194499 A1. M.H.T. confirms that to the best of his knowledge none of the above funding sources were involved in the preparation of this paper. T.D.M. and K.S. receive research funding from Novo Nordisk, but these funds are unrelated to the here described work. D.J.D. has received speaking and consulting fees from Merck and Novo Nordisk Inc. and consulting fees from Forkhead Biopharmaceuticals and Kallyope Inc. R.D.D. is a co-inventor on intellectual property owned by Indiana University and licensed to Novo Nordisk. He was previously employed by Novo Nordisk. P.J.K., S.A.M., and B.F. are current employees of Novo Nordisk.
PubMed

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