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Cell. 2017 Feb 23;168(5):758-774. doi: 10.1016/j.cell.2017.01.025.

Gut-Brain Cross-Talk in Metabolic Control.

Author information

1
Institute for Diabetes and Obesity, Helmholtz Diabetes Center & German Center for Diabetes Research (DZD), Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), 85764 Neuherberg, Germany; Division of Metabolic Diseases, Department of Medicine, Technische Universität München, 80333 Munich, Germany.
2
Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, Cincinnati, OH 45220, USA.
3
Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70803, USA.
4
Departments of Surgery, Internal Medicine, and Nutritional Sciences at the University of Michigan, Ann Arbor, MI 48109, USA.
5
Institute for Diabetes and Obesity, Helmholtz Diabetes Center & German Center for Diabetes Research (DZD), Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), 85764 Neuherberg, Germany; Division of Metabolic Diseases, Department of Medicine, Technische Universität München, 80333 Munich, Germany. Electronic address: tschoep@helmholtz-muenchen.de.

Abstract

Because human energy metabolism evolved to favor adiposity over leanness, the availability of palatable, easily attainable, and calorically dense foods has led to unprecedented levels of obesity and its associated metabolic co-morbidities that appear resistant to traditional lifestyle interventions. However, recent progress identifying the molecular signaling pathways through which the brain and the gastrointestinal system communicate to govern energy homeostasis, combined with emerging insights on the molecular mechanisms underlying successful bariatric surgery, gives reason to be optimistic that novel precision medicines that mimic, enhance, and/or modulate gut-brain signaling can have unprecedented potential for stopping the obesity and type 2 diabetes pandemics.

KEYWORDS:

appetite; bariatric surgery; brain; diabetes; energy balance; gut; metabolic syndrome; obesity; pharmacology; satiety

PMID:
28235194
PMCID:
PMC5839146
DOI:
10.1016/j.cell.2017.01.025
[Indexed for MEDLINE]
Free PMC Article

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