The Integrative Role of CNS Fuel-Sensing Mechanisms in Energy Balance and Glucose Regulation
Abstract
The incidences of both obesity and type 2 diabetes mellitus are rising at epidemic proportions. Despite this, the balance between caloric intake and expenditure is tremendously accurate under most circumstances. Growing evidence suggests that nutrient and hormonal signals converge and directly act on brain centers, leading to changes in fuel metabolism and, thus, stable body weight over time. Growing evidence also suggests that these same signals act on the central nervous system (CNS) to regulate glucose metabolism independently. We propose that this is not coincidental and that the CNS responds to peripheral signals to orchestrate changes in both energy and glucose homeostasis. In this way the CNS ensures that the nutrient demands of peripheral tissues (and likely of the brain itself) are being met. Consequently, dysfunction of the ability of the CNS to integrate fuel-sensing signals may underlie the etiology of metabolic diseases such as obesity and diabetes.
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Central brain-endocrine crosstalk plays a critical role in glucose homeostasis.
“In addition to peripheral GIG interactions, the recently recognized central brain-endocrine crosstalk also plays a critical role in glucose homeostasis [1].”
From A mathematical model of brain glucose homeostasis (2009) · cites this paper as [1]
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- Authors
- Sandoval, D., Cota, D., & Seeley, R. J.
- Affiliations
- University of Cincinnati (US)
- Venue
- Annual Review of Physiology
- Publisher
- Annual Reviews
- Published
- 2008-03-01
- Volume
- 70
- Issue
- 1
- Pages
- 513-535
- ISSN
- 0066-4278 (ISSN-L)
- 1545-1585
- OpenAlex
- W2135960244
- Cited by
- 178
- References
- 167
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 5 · 2023: 6 · 2022: 5 · 2021: 12 · 2020: 9 · 2019: 5 · 2018: 5 · 2017: 7 · 2016: 12 · 2015: 10 · 2014: 7 · 2013: 12 · 2012: 20
- FWCI
- 1.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 075365, R01DK054890, P01DK056863, DK-54890, K01DK075365, DK-56863)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- energy homeostasis, glucose homeostasis, central nervous system, obesity, type 2 diabetes, nutrient signaling, metabolic disorders, brain glucose metabolism
- MeSH terms
- Animals, Blood Glucose, Diabetes Mellitus, Type 2, Energy Metabolism, Humans, Hypothalamus, Obesity, Signal Transduction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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