The glucose-dependent insulinotropic polypeptide (GIP) regulates body weight and food intake via CNS-GIPR signaling
Uncertainty exists as to whether the glucose-dependent insulinotropic polypeptide receptor (GIPR) should be activated or inhibited for the treatment of obesity. Gipr was recently demonstrated in hypothalamic feeding centers, but the physiological relevance of CNS Gipr remains unknown. Here we show t...
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| Published in | Cell metabolism Vol. 33; no. 4; pp. 833 - 844.e5 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
06.04.2021
Cell Press |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1550-4131 1932-7420 1932-7420 |
| DOI | 10.1016/j.cmet.2021.01.015 |
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| Abstract | Uncertainty exists as to whether the glucose-dependent insulinotropic polypeptide receptor (GIPR) should be activated or inhibited for the treatment of obesity. Gipr was recently demonstrated in hypothalamic feeding centers, but the physiological relevance of CNS Gipr remains unknown. Here we show that HFD-fed CNS-Gipr KO mice and humanized (h)GIPR knockin mice with CNS-hGIPR deletion show decreased body weight and improved glucose metabolism. In DIO mice, acute central and peripheral administration of acyl-GIP increases cFos neuronal activity in hypothalamic feeding centers, and this coincides with decreased body weight and food intake and improved glucose handling. Chronic central and peripheral administration of acyl-GIP lowers body weight and food intake in wild-type mice, but shows blunted/absent efficacy in CNS-Gipr KO mice. Also, the superior metabolic effect of GLP-1/GIP co-agonism relative to GLP-1 is extinguished in CNS-Gipr KO mice. Our data hence establish a key role of CNS Gipr for control of energy metabolism.
[Display omitted]
•CNS-Gipr KO mice are protected from diet-induced obesity and glucose intolerance•Acyl-GIP increases cFOS neuronal activity in key hypothalamic feeding centers•Acyl-GIP effects on body weight and food intake are absent/blunted in CNS-mGipr KO mice•GLP-1/GIP dual-agonism loses superior potency over GLP-1 in CNS-mGipr KO mice.
Zhang et al. report that CNS GIPR plays a significant role in regulating food intake. They show that treatment with acyl-GIP or with a GLP-1/GIP dual-agonist lowers body weight and food intake in wild-type mice but shows blunted efficacy in CNS-Gipr KO mice. |
|---|---|
| AbstractList | Uncertainty exists as to whether the glucose-dependent insulinotropic polypeptide receptor (GIPR) should be activated or inhibited for the treatment of obesity. Gipr was recently demonstrated in hypothalamic feeding centers, but the physiological relevance of CNS Gipr remains unknown. Here we show that HFD-fed CNS-
Gipr
KO mice and humanized
(h)GIPR
knockin mice with CNS-
hGIPR
deletion show decreased body weight and improved glucose metabolism. In DIO mice, acute central and peripheral administration of acyl-GIP increases cFos neuronal activity in hypothalamic feeding centers, and this coincides with decreased body weight and food intake and improved glucose handling. Chronic central and peripheral administration of acyl-GIP lowers body weight and food intake in wild-type mice, but shows blunted/absent efficacy in CNS-
Gipr
KO mice. Also, the superior metabolic effect of GLP-1/GIP co-agonism relative to GLP-1 is extinguished in CNS-
Gipr
KO mice. Our data hence establish a key role of CNS Gipr for control of energy metabolism.
•
CNS-
Gipr
KO mice are protected from diet-induced obesity and glucose intolerance
•
Acyl-GIP increases cFOS neuronal activity in key hypothalamic feeding centers
•
Acyl-GIP effects on body weight and food intake are absent/blunted in
CNS-mGipr
KO mice
•
GLP-1/GIP dual-agonism loses superior potency over GLP-1 in
CNS-mGipr
KO mice.
Zhang et al. report that CNS GIPR plays a significant role in regulating food intake. They show that treatment with acyl-GIP or with a GLP-1/GIP dual-agonist lowers body weight and food intake in wild-type mice but shows blunted efficacy in CNS-Gipr KO mice. Uncertainty exists as to whether the glucose-dependent insulinotropic polypeptide receptor (GIPR) should be activated or inhibited for the treatment of obesity. Gipr was recently demonstrated in hypothalamic feeding centers, but the physiological relevance of CNS Gipr remains unknown. Here we show that HFD-fed CNS-Gipr KO mice and humanized (h)GIPR knockin mice with CNS-hGIPR deletion show decreased body weight and improved glucose metabolism. In DIO mice, acute central and peripheral administration of acyl-GIP increases cFos neuronal activity in hypothalamic feeding centers, and this coincides with decreased body weight and food intake and improved glucose handling. Chronic central and peripheral administration of acyl-GIP lowers body weight and food intake in wild-type mice, but shows blunted/absent efficacy in CNS-Gipr KO mice. Also, the superior metabolic effect of GLP-1/GIP co-agonism relative to GLP-1 is extinguished in CNS-Gipr KO mice. Our data hence establish a key role of CNS Gipr for control of energy metabolism.Uncertainty exists as to whether the glucose-dependent insulinotropic polypeptide receptor (GIPR) should be activated or inhibited for the treatment of obesity. Gipr was recently demonstrated in hypothalamic feeding centers, but the physiological relevance of CNS Gipr remains unknown. Here we show that HFD-fed CNS-Gipr KO mice and humanized (h)GIPR knockin mice with CNS-hGIPR deletion show decreased body weight and improved glucose metabolism. In DIO mice, acute central and peripheral administration of acyl-GIP increases cFos neuronal activity in hypothalamic feeding centers, and this coincides with decreased body weight and food intake and improved glucose handling. Chronic central and peripheral administration of acyl-GIP lowers body weight and food intake in wild-type mice, but shows blunted/absent efficacy in CNS-Gipr KO mice. Also, the superior metabolic effect of GLP-1/GIP co-agonism relative to GLP-1 is extinguished in CNS-Gipr KO mice. Our data hence establish a key role of CNS Gipr for control of energy metabolism. Uncertainty exists as to whether the glucose-dependent insulinotropic polypeptide receptor (GIPR) should be activated or inhibited for the treatment of obesity. Gipr was recently demonstrated in hypothalamic feeding centers, but the physiological relevance of CNS Gipr remains unknown. Here we show that HFD-fed CNS-Gipr KO mice and humanized (h)GIPR knockin mice with CNS-hGIPR deletion show decreased body weight and improved glucose metabolism. In DIO mice, acute central and peripheral administration of acyl-GIP increases cFos neuronal activity in hypothalamic feeding centers, and this coincides with decreased body weight and food intake and improved glucose handling. Chronic central and peripheral administration of acyl-GIP lowers body weight and food intake in wild-type mice, but shows blunted/absent efficacy in CNS-Gipr KO mice. Also, the superior metabolic effect of GLP-1/GIP co-agonism relative to GLP-1 is extinguished in CNS-Gipr KO mice. Our data hence establish a key role of CNS Gipr for control of energy metabolism. Uncertainty exists as to whether the glucose-dependent insulinotropic polypeptide receptor (GIPR) should be activated or inhibited for the treatment of obesity. Gipr was recently demonstrated in hypothalamic feeding centers, but the physiological relevance of CNS Gipr remains unknown. Here we show that HFD-fed CNS-Gipr KO mice and humanized (h)GIPR knockin mice with CNS-hGIPR deletion show decreased body weight and improved glucose metabolism. In DIO mice, acute central and peripheral administration of acyl-GIP increases cFos neuronal activity in hypothalamic feeding centers, and this coincides with decreased body weight and food intake and improved glucose handling. Chronic central and peripheral administration of acyl-GIP lowers body weight and food intake in wild-type mice, but shows blunted/absent efficacy in CNS-Gipr KO mice. Also, the superior metabolic effect of GLP-1/GIP co-agonism relative to GLP-1 is extinguished in CNS-Gipr KO mice. Our data hence establish a key role of CNS Gipr for control of energy metabolism. [Display omitted] •CNS-Gipr KO mice are protected from diet-induced obesity and glucose intolerance•Acyl-GIP increases cFOS neuronal activity in key hypothalamic feeding centers•Acyl-GIP effects on body weight and food intake are absent/blunted in CNS-mGipr KO mice•GLP-1/GIP dual-agonism loses superior potency over GLP-1 in CNS-mGipr KO mice. Zhang et al. report that CNS GIPR plays a significant role in regulating food intake. They show that treatment with acyl-GIP or with a GLP-1/GIP dual-agonist lowers body weight and food intake in wild-type mice but shows blunted efficacy in CNS-Gipr KO mice. |
| Author | Salinno, Ciro Mowery, Stephanie A. DiMarchi, Richard D. Perez-Tilve, Diego Herzig, Stephan Augustin, Robert Holleman, Cassie Lynn Sehrer, Laura Legutko, Beata Müller, Timo D. Medina, Marta Tarquis Drucker, Daniel J. Wolfrum, Christian Liu, Xue Jastroch, Martin Caceres, Cristina Garcia Malogajski, Emilija Stemmer, Kerstin Hofmann, Susanna Knerr, Patrick J. Lutter, Dominik Zhang, Qian Tschöp, Matthias H. Luippold, Gerd Harger, Alexandra Bakhti, Mostafa Feuchtinger, Annette Kulaj, Konxhe Lickert, Heiko Keipert, Susanne Blutke, Andreas Finan, Brian Colldén, Gustav Delessa, Challa Tenagne Kleinert, Maximilian Grandl, Gerald |
| Author_xml | – sequence: 1 givenname: Qian surname: Zhang fullname: Zhang, Qian organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 2 givenname: Challa Tenagne surname: Delessa fullname: Delessa, Challa Tenagne organization: Institute of Food, Nutrition and Health, Department of Health Sciences and Technology (D-HEST), ETH Zürich, Zurich, Switzerland – sequence: 3 givenname: Robert surname: Augustin fullname: Augustin, Robert organization: Cardiometabolic Diseases Research Department, Boehringer Ingelheim Pharma GmbH and Co., KG, Biberach/Riss, Germany – sequence: 4 givenname: Mostafa surname: Bakhti fullname: Bakhti, Mostafa organization: German Center for Diabetes Research (DZD), Neuherberg, Germany – sequence: 5 givenname: Gustav surname: Colldén fullname: Colldén, Gustav organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 6 givenname: Daniel J. surname: Drucker fullname: Drucker, Daniel J. organization: Lunenfeld-Tanenbaum Research Institute, Mt. Sinai Hospital, University of Toronto, Toronto, ON M5G 1X5, Canada – sequence: 7 givenname: Annette surname: Feuchtinger fullname: Feuchtinger, Annette organization: Research Unit Analytical Pathology, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 8 givenname: Cristina Garcia surname: Caceres fullname: Caceres, Cristina Garcia organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 9 givenname: Gerald surname: Grandl fullname: Grandl, Gerald organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 10 givenname: Alexandra surname: Harger fullname: Harger, Alexandra organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 11 givenname: Stephan surname: Herzig fullname: Herzig, Stephan organization: German Center for Diabetes Research (DZD), Neuherberg, Germany – sequence: 12 givenname: Susanna surname: Hofmann fullname: Hofmann, Susanna organization: German Center for Diabetes Research (DZD), Neuherberg, Germany – sequence: 13 givenname: Cassie Lynn surname: Holleman fullname: Holleman, Cassie Lynn organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 14 givenname: Martin surname: Jastroch fullname: Jastroch, Martin organization: Department of Molecular Biosciences, The Wenner-Gren Institute, The Arrhenius Laboratories F3, Stockholm University, Stockholm, Sweden – sequence: 15 givenname: Susanne surname: Keipert fullname: Keipert, Susanne organization: Department of Molecular Biosciences, The Wenner-Gren Institute, The Arrhenius Laboratories F3, Stockholm University, Stockholm, Sweden – sequence: 16 givenname: Maximilian surname: Kleinert fullname: Kleinert, Maximilian organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 17 givenname: Patrick J. surname: Knerr fullname: Knerr, Patrick J. organization: Novo Nordisk Research Center Indianapolis, Indianapolis, IN 46241, USA – sequence: 18 givenname: Konxhe surname: Kulaj fullname: Kulaj, Konxhe organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 19 givenname: Beata surname: Legutko fullname: Legutko, Beata organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 20 givenname: Heiko surname: Lickert fullname: Lickert, Heiko organization: German Center for Diabetes Research (DZD), Neuherberg, Germany – sequence: 21 givenname: Xue surname: Liu fullname: Liu, Xue organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 22 givenname: Gerd surname: Luippold fullname: Luippold, Gerd organization: Cardiometabolic Diseases Research Department, Boehringer Ingelheim Pharma GmbH and Co., KG, Biberach/Riss, Germany – sequence: 23 givenname: Dominik surname: Lutter fullname: Lutter, Dominik organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 24 givenname: Emilija surname: Malogajski fullname: Malogajski, Emilija organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 25 givenname: Marta Tarquis surname: Medina fullname: Medina, Marta Tarquis organization: German Center for Diabetes Research (DZD), Neuherberg, Germany – sequence: 26 givenname: Stephanie A. surname: Mowery fullname: Mowery, Stephanie A. organization: Novo Nordisk Research Center Indianapolis, Indianapolis, IN 46241, USA – sequence: 27 givenname: Andreas surname: Blutke fullname: Blutke, Andreas organization: Research Unit Analytical Pathology, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 28 givenname: Diego surname: Perez-Tilve fullname: Perez-Tilve, Diego organization: Department of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH, USA – sequence: 29 givenname: Ciro surname: Salinno fullname: Salinno, Ciro organization: German Center for Diabetes Research (DZD), Neuherberg, Germany – sequence: 30 givenname: Laura surname: Sehrer fullname: Sehrer, Laura organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 31 givenname: Richard D. surname: DiMarchi fullname: DiMarchi, Richard D. organization: Department of Chemistry, Indiana University, Bloomington, IN 47405, USA – sequence: 32 givenname: Matthias H. surname: Tschöp fullname: Tschöp, Matthias H. organization: German Center for Diabetes Research (DZD), Neuherberg, Germany – sequence: 33 givenname: Kerstin surname: Stemmer fullname: Stemmer, Kerstin organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany – sequence: 34 givenname: Brian surname: Finan fullname: Finan, Brian organization: Novo Nordisk Research Center Indianapolis, Indianapolis, IN 46241, USA – sequence: 35 givenname: Christian surname: Wolfrum fullname: Wolfrum, Christian organization: Institute of Food, Nutrition and Health, Department of Health Sciences and Technology (D-HEST), ETH Zürich, Zurich, Switzerland – sequence: 36 givenname: Timo D. surname: Müller fullname: Müller, Timo D. email: timo.mueller@helmholtz-muenchen.de organization: Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, Neuherberg, Germany |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33571454$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-194271$$DView record from Swedish Publication Index |
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| Title | The glucose-dependent insulinotropic polypeptide (GIP) regulates body weight and food intake via CNS-GIPR signaling |
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