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Cited by 79Regulation of Appetite and ObesityPancreatic function and diabetesNeuroscience of respiration and sleep

Metabolic sensors

Levin, Barry E·2002·Physiology & Behavior
DOI 10.1016/s0031-9384(02)00763-1
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Abstract

Glucose is a critical substrate for brain and organ function. Specialized glucosensing neurons, which are involved in the control of energy homeostasis and neuroendocrine function, are located in specific anatomic locations in the brain. Glucose-excited neurons increase their firing rate when ambient glucose levels rise. This glucosensing capacity appears to be regulated by a combination of glucokinase and an ATP-sensitive K(+) (K(ATP)) channel whose activity is regulated by ATP derived from glucose metabolism. Glucose inhibited neurons decrease their firing rate when glucose levels rise, although it is unclear what mechanism is used to control this function. Neuropeptide Y and proopiomelanocortin neurons in the hypothalamic arcuate nucleus are examples of neurons that are capable of sensing both glucose and a host of other peripheral metabolic signals, possibly by their actions on the K(ATP) channel. These metabolic sensing neurons are intimately involved in energy homeostasis, and it is postulated that glucose is only one of several peripheral metabolic signals involved in this process under physiologic conditions. However, when glucose supply is severely limited, glucose appears to assume primacy as a stimulant of glucosensing in order to activate the counterregulatory and ingestive processes necessary to restore the vital supply of glucose. Thus, the role of glucosensing is postulated to be a relative one that is dependent upon the supply of peripheral glucose.

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  • Hypothalamic neurons have the capacity to sense glucose and free fatty acids simultaneously and to integrate other nutritional and hormonal inputs.

    “and the capacity of hypothalamic neurons to sense glucose and FFA simultaneously and to integrate other nutritional and hormonal inputs ([95](#B95), [99](#B99))”

    From Mitochondrial fatty acid oxidation in obesity (2013) · cites this paper as [99]

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Authors
Levin, B. E.
Affiliations
East Orange VA Medical Center (US)
Corresponding author
Levin, Barry E
ORCID
Levin, Barry E
Venue
Physiology & Behavior
Publisher
Elsevier BV
Published
2002-07
Volume
76
Issue
3
Pages
397-401
ISSN
0031-9384 (ISSN-L)
DOI
10.1016/s0031-9384(02)00763-1
OpenAlex
W2198516513
Cited by
79
References
63
Citations by year
2019: 1 · 2018: 3 · 2017: 2 · 2016: 2 · 2015: 2 · 2014: 4 · 2013: 3 · 2012: 3
FWCI
2.63
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Physiology & Behavior (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
Keywords
glucose detection, energy homeostasis, ATP-sensitive potassium channels, glucokinase, neuropeptide Y neurons, proopiomelanocortin neurons, arcuate nucleus, neuroendocrine regulation, counterregulation
MeSH terms
Animals, Brain Chemistry, Chemoreceptor Cells, Glucokinase, Glucose, Humans, Neurons, Afferent, Potassium Channels, ATP-Binding Cassette Transporters, Potassium Channels, Inwardly Rectifying, KATP Channels

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