ArticleEndocrinology2010
Beneficial metabolic effects caused by persistent activation of beta-cell M3 muscarinic acetylcholine receptors in transgenic mice.
Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 42 citations in OpenAlex.
- Double transgenic neonatal porcine islets as an alternative source for beta cell replacement therapy.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Mitofusins Mfn1 and Mfn2 Are Required to Preserve Glucose- but Not Incretin-Stimulated β-Cell Connectivity and Insulin Secretion.Diabetes · 2022Article
- Quercetin prevents insulin dysfunction in hypertensive animals.Journal of diabetes and metabolic disorders · 2022Article
- The beneficial effects of a muscarinic agonist on pancreatic β-cells.Scientific reports · 2019Article
- Muscarinic Receptor Type-3 in Hypertension and Cholinergic-Adrenergic Crosstalk: Genetic Insights and Potential for New Antihypertensive Targets.The Canadian journal of cardiology · 2019Article
- Inhibition of cholinergic potentiation of insulin secretion from pancreatic islets by chronic elevation of glucose and fatty acids: Protection by casein kinase 2 inhibitor.Molecular metabolism · 2017Article
- Transgenic Expression of Glucagon-Like Peptide-1 (GLP-1) and Activated Muscarinic Receptor (M3R) Significantly Improves Pig Islet Secretory Function.Cell transplantation · 2017Article
- Gene Editing, Gene Therapy, and Cell Xenotransplantation: Cell Transplantation Across Species.Current transplantation reports · 2017Review
- CK2 acts as a potent negative regulator of receptor-mediated insulin release in vitro and in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Muscarinic acetylcholine receptors: novel opportunities for drug development.Nature reviews. Drug discovery · 2014Review
- Muscarinic control of MIN6 pancreatic β cells is enhanced by impaired amino acid signaling.The Journal of biological chemistry · 2014Article
- Employing novel animal models in the design of clinically efficacious GPCR ligands.Current opinion in cell biology · 2014Review
- Nervous glucose sensing regulates postnatal β cell proliferation and glucose homeostasis.The Journal of clinical investigation · 2014Article
- Second generation antipsychotic-induced type 2 diabetes: a role for the muscarinic M3 receptor.CNS drugs · 2013Review
- Muscarinic receptors as model targets and antitargets for structure-based ligand discovery.Molecular pharmacology · 2013Article
- Minireview: Novel aspects of M3 muscarinic receptor signaling in pancreatic β-cells.Molecular endocrinology (Baltimore, Md.) · 2013Review
- Critical metabolic roles of β-cell M3 muscarinic acetylcholine receptors.Life sciences · 2012Review
- Spinophilin as a novel regulator of M3 muscarinic receptor-mediated insulin release in vitro and in vivo.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Early postnatal low-protein nutrition, metabolic programming and the autonomic nervous system in adult life.Nutrition & metabolism · 2012Article
- Targeted deletion of one or two copies of the G protein β subunit Gβ5 gene has distinct effects on body weight and behavior in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Previous studies have shown that β-cell M(3) muscarinic acetylcholine receptors (M3Rs) play a key role in maintaining blood glucose homeostasis by enhancing glucose-dependent insulin release. In this study, we tested the hypothesis that long-term, persistent activation of β-cell M3Rs can improve glucose tolerance and ameliorate the metabolic deficits associated with the consumption of a high-fat diet. To achieve the selective and persistent activation of β-cell M3Rs in vivo, we generated transgenic mice that expressed the Q490L mutant M3R in their pancreatic β-cells (β-M3-Q490L Tg mice). The Q490L point mutation is known to render the M3R constitutively active. The metabolic phenotypes of the transgenic mice were examined in several in vitro and in vivo metabolic tests. In the presence of 15 mm glucose and the absence of M3R ligands, isolated perifused islets prepared from β-M3-Q490L Tg mice released considerably more insulin than wild-type control islets. This effect could be completely blocked by incubation of the transgenic islets with atropine (10 μm), an inverse muscarinic agonist, indicating that the Q490L mutant M3R exhibited ligand-independent signaling (constitutive activity) in mouse β-cells. In vivo studies showed that β-M3-Q490L Tg mice displayed greatly improved glucose tolerance and increased serum insulin levels as well as resistance to diet-induced glucose intolerance and hyperglycemia. These results suggest that chronic activation of β-cell M3Rs may represent a useful approach to boost insulin output in the long-term treatment of type 2 diabetes.
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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.