ArticleThe EMBO journal2024
TRPC5 controls the adrenaline-mediated counter regulation of hypoglycemia.
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Transient receptor potential canonical (TRPC) channels in diabetes and associated complications.Channels (Austin, Tex.) · 2026Review
- X chromosome-wide association studies for quantitative trait loci based on the mixture of general pedigrees and additional unrelated individuals.Briefings in bioinformatics · 2026Article
- Ideal efficacy photoswitching for chromocontrol of TRPC4/5 channel functions in live tissues.Nature chemical biology · 2026Article
- NaThe Journal of membrane biology · 2026Article
- MOGEDN: small-sample cancer subtype classification with encoder-decoder networks for missing-omics recovery and biomarker discovery.Briefings in bioinformatics · 2025Article
- Physiological functions and pharmacological targeting of transient receptor potential channels.Pharmacological reviews · 2025Review
- Review
- Cellular mechanisms underlying pituitary adenylate cyclase activating polypeptide-stimulated secretion in the adrenal medulla.Biochemical Society transactions · 2024Review
- TRPC5: a new entry to the chromaffin cell's palette of ion channels that control adrenal response to hypoglycemia.The EMBO journal · 2024Article
Corrections and comments
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Authors and funding
40 authors.
Funding
Abstract
Hypoglycemia triggers autonomic and endocrine counter-regulatory responses to restore glucose homeostasis, a response that is impaired in patients with diabetes and its long-term complication hypoglycemia-associated autonomic failure (HAAF). We show that insulin-evoked hypoglycemia is severely aggravated in mice lacking the cation channel proteins TRPC1, TRPC4, TRPC5, and TRPC6, which cannot be explained by alterations in glucagon or glucocorticoid action. By using various TRPC compound knockout mouse lines, we pinpointed the failure in sympathetic counter-regulation to the lack of the TRPC5 channel subtype in adrenal chromaffin cells, which prevents proper adrenaline rise in blood plasma. Using electrophysiological analyses, we delineate a previously unknown signaling pathway in which stimulation of PAC1 or muscarinic receptors activates TRPC5 channels in a phospholipase-C-dependent manner to induce sustained adrenaline secretion as a crucial step in the sympathetic counter response to insulin-induced hypoglycemia. By comparing metabolites in the plasma, we identified reduced taurine levels after hypoglycemia induction as a commonality in TRPC5-deficient mice and HAAF patients.
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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 Socratic graph.