ReviewActa physiologica (Oxford, England)2010
Glucose-induced inhibition: how many ionic mechanisms?
Review in Acta physiologica (Oxford, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 29 citations in OpenAlex.
- Modulation of olfactory-driven behavior by metabolic signals: role of the piriform cortex.Brain structure & function · 2019Article
- Peripheral and central glucose sensing in hypoglycemic detection.Physiology (Bethesda, Md.) · 2014Review
- Lateral hypothalamus as a sensor-regulator in respiratory and metabolic control.Physiology & behavior · 2013Review
- Orexin neurons as conditional glucosensors: paradoxical regulation of sugar sensing by intracellular fuels.The Journal of physiology · 2011Article
- Neuropeptide Y cells represent a distinct glucose-sensing population in the lateral hypothalamus.Endocrinology · 2011Article
- Multiple hypothalamic circuits sense and regulate glucose levels.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Review
- Glucose stimulation of hypothalamic MCH neurons involves K(ATP) channels, is modulated by UCP2, and regulates peripheral glucose homeostasis.Cell metabolism · 2010Article
- Electrophysiological identification of glucose-sensing neurons in rat nodose ganglia.The Journal of physiology · 2010Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sensing of sugar by specialized 'glucose-inhibited' cells helps organisms to counteract swings in their internal energy levels. Evidence from several cell types in both vertebrates and invertebrates suggests that this process involves sugar-induced stimulation of plasma membrane K(+) currents. However, the molecular composition and the mechanism of activation of the underlying channel(s) remain controversial. In mouse hypothalamic neurones and neurosecretory cells of the crab Cancer borealis, glucose stimulates K(+) currents displaying leak-like properties. Yet knockout of some of the candidate 'leak' channel subunits encoded by the KCNK gene family so far failed to abolish glucose inhibition of hypothalamic cells. Moreover, in other tissues, such as the carotid body, glucose-stimulated K(+) channels appear to be not leak-like but voltage-gated, suggesting that glucose-induced inhibition may engage multiple types of K(+) channels. Other mechanisms of glucose-induced inhibition, such as hyperpolarization mediated by opening of Cl(-) channels and depolarization block caused by closure of K(ATP) channels have also been proposed. Here we review known ionic and pharmacological features of glucose-induced inhibition in different cell types, which may help to identify its molecular correlates.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.