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Cited by 30Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesPancreatic function and diabetes

The Brain-Gut-Islet Connection

Open access
Woods, Stephen C., Benoit, Stephen C., Clegg, Deborah J.·2006·Diabetes
DOI 10.2337/db06-s015
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Abstract

Peptide signals from the pancreatic islets and the gastrointestinal tract influence the regulation of energy homeostasis by the brain, and the brain in turn influences the secretions of both the islets and the gut. This article focuses on how insulin interacts with the brain to influence food intake, blood glucose, and cognitive behavior. Insulin is secreted in response to changes of ambient glucose, and the levels achieved are directly proportional to body adiposity. Hence, insulin, like leptin, is an adiposity signal. An increased insulin signal in the mediobasal hypothalamus indicates that ample or excess energy is available in the body and elicits responses that limit food intake and reduce hepatic glucose secretion. Increased insulin (and leptin as well) locally within the brain complements other signals that indicate a surfeit of energy in the body, including satiety signals generated by the gut during meals, glucose, and some fatty acids. There is compelling evidence that overlapping intracellular signaling pathways within the mediobasal hypothalamus mediate the overall catabolic response to these diverse metabolic signals. Insulin receptors are also densely expressed in the hippocampus, and insulin acts there to facilitate learning and memory. The function of insulin receptors in other brain areas is poorly understood. Obesity and/or the consumption of diets high in fat render the brain as well as the body insulin resistant. In the hypothalamus, this is manifest as a reduced ability of insulin to reduce food intake and body weight, and in the hippocampus, it is manifest as a reduced ability of insulin to improve learning and/or memory.

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  • The central brain-endocrine crosstalk, mainly the glucosensor-hypothalamus-liver-pancreas link, modifies peripheral GIG interactions to control brain glucose homeostasis.

    “The latter, mainly consisting of the glucosensor-hypothalamus-liver-pancreas link [17,30], modifies the peripheral GIG interactions in order to control brain glucose homeostasis, as shown in Fig. 1.”

    From A mathematical model of brain glucose homeostasis (2009) · cites this paper as [30]

    The section “Insulin Regulates Energy Homeostasis in the Hypothalamus” describes pancreatic insulin signaling in the hypothalamus reducing liver glucose output and blood glucose. The opening discussion also describes reciprocal brain–gut–islet signaling. Neither passage characterizes that system as mainly a glucosensor–hypothalamus–liver–pancreas link or says it controls glucose homeostasis specifically in the brain; the reported outcome is blood glucose regulation. (LLM, conf=0.85)

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Research works printed but not linked: 1

  1. Dourish CT, Cooper SJ, Iversen SD, Iversen LL, Eds. Oxford, U.K., Oxford University Press, 1992, p. 166 -182

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Related

Authors
Woods, S. C., Benoit, S. C., & Clegg, D. J.
Affiliations
University of Cincinnati (US)
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
2006-12-01
Volume
55
Issue
Supplement_2
Pages
S114-S121
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/db06-s015
OpenAlex
W2021047329
Cited by
30
References
157
Citations by year
2024: 1 · 2021: 2 · 2018: 2 · 2017: 1 · 2016: 2 · 2015: 3 · 2013: 6 · 2012: 3
FWCI
1.39
Type
journal article
Language
en
Open access
Locations
Diabetes (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
pancreatic islets, insulin signaling, hypothalamus, food intake regulation, energy homeostasis, leptin, adiposity signals, hippocampus, insulin resistance, obesity, learning and memory, blood glucose regulation

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