ReviewLife sciences2012
Critical metabolic roles of β-cell M3 muscarinic acetylcholine receptors.
Review in Life sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Antipsychotic-induced changes in blood levels of leptin in schizophrenia: a meta-analysis.Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2015Pooled it
- The thiazolidinedione drug troglitazone inhibits Gq signaling through direct binding to the Gq alpha subunit through inhibition of GDP release.Molecular pharmacology · 2025Article
- Comparative in vitro and in silico evaluation of the toxic effects of metformin and/or ascorbic acid, new treatment options in the treatment of Melasma.Toxicology research · 2025Article
- Post-Bariatric Hypoglycemia: an Impaired Metabolic Response to a Meal.Obesity surgery · 2024Article
- The Role of Muscarinic Acetylcholine Receptor MInternational journal of molecular sciences · 2024Review
- GRK2 regulates GLP-1R-mediated early phase insulin secretion in vivo.BMC biology · 2021Article
- SPARC promotes insulin secretion through down-regulation of RGS4 protein in pancreatic β cells.Scientific reports · 2020Article
- Teaching an Old Drug New Tricks: Agonism, Antagonism, and Biased Signaling of Pilocarpine through M3 Muscarinic Acetylcholine Receptor.Molecular pharmacology · 2017Article
- Regulator of G-protein signaling Gβ5-R7 is a crucial activator of muscarinic M3 receptor-stimulated insulin secretion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Single nucleotide polymorphisms and genotypes of transient receptor potential ion channel and acetylcholine receptor genes from isolated B lymphocytes in myalgic encephalomyelitis/chronic fatigue syndrome patients.The Journal of international medical research · 2016Article
- The effect of vagal nerve blockade using electrical impulses on glucose metabolism in nondiabetic subjects.Diabetes, metabolic syndrome and obesity : targets and therapy · 2014Article
- Second generation antipsychotic-induced type 2 diabetes: a role for the muscarinic M3 receptor.CNS drugs · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Muscarinic acetylcholine (ACh) receptors (mAChRs; M(1)-M(5)) regulate the activity of an extraordinarily large number of important physiological processes. We and others previously demonstrated that pancreatic β-cells are endowed with M(3) mAChRs which are linked to G proteins of the G(q) family. The activation of these receptors by ACh or other muscarinic agonists leads to the augmentation of glucose-induced insulin release via multiple mechanisms. Interestingly, in humans, ACh acting on human β-cell mAChRs is released from adjacent α-cells which express both choline acetyltransferase (ChAT) and the vesicular acetylcholine transporter (vAChT), indicative of the presence of a non-neuronal cholinergic system in human pancreatic islets. In order to shed light on the physiological roles of β-cell M(3) receptors, we recently generated and analyzed various mutant mouse models. Specifically, we carried out studies with mice which overexpressed M(3) receptors or mutant M(3) receptors in pancreatic β-cells or which selectively lacked M(3) receptors or M(3)-receptor-associated proteins in pancreatic β-cells. Our findings indicate that β-cell M(3) receptors play a key role in maintaining proper insulin release and whole body glucose homeostasis and that strategies aimed at enhancing signaling through β-cell M(3) receptors may prove useful to improve β-cell function for the treatment of type 2 diabetes (T2D).
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What OpenQuestion holds
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.