ArticleDiabetologia2013
Hydrogen sulfide-induced inhibition of L-type Ca2+ channels and insulin secretion in mouse pancreatic beta cells.
Article in Diabetologia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 66 citations in OpenAlex.
- Microbial and proteomic signatures of type 2 diabetes in an Arab population.Journal of translational medicine · 2024Article
- Hydrogen sulfide and its role in female reproduction.Frontiers in veterinary science · 2024Review
- T-type calcium channel modulation by hydrogen sulfide in neuropathic pain conditions.Frontiers in pharmacology · 2023Review
- Research Progress of HMolecules (Basel, Switzerland) · 2022Review
- Effect of Exogenous Hydrogen Sulfide and Polysulfide Donors on Insulin Sensitivity of the Adipose Tissue.Biomolecules · 2022Article
- Fluidics system for resolving concentration-dependent effects of dissolved gases on tissue metabolism.eLife · 2021Article
- Hydrogen Sulfide Actions in the Vasculature.Comprehensive Physiology · 2021Article
- The Role of HAdvances in experimental medicine and biology · 2021Article
- Hydrogen Sulfide Upregulates Acid-sensing Ion ChannelsFunction (Oxford, England) · 2021Article
- Hydrogen Sulfide and its Interaction with Other Players in Inflammation.Advances in experimental medicine and biology · 2021Article
- Hydrogen sulfide regulates insulin secretion and insulin resistance in diabetes mellitus, a new promising target for diabetes mellitus treatment? A review.Journal of advanced research · 2021Review
- Circadian rhythms and the gut microbiota: from the metabolic syndrome to cancer.Nature reviews. Endocrinology · 2020Review
- Regulation of carbohydrate metabolism by nitric oxide and hydrogen sulfide: Implications in diabetes.Biochemical pharmacology · 2020Review
- Discovery of a Redox Thiol Switch: Implications for Cellular Energy Metabolism.Molecular & cellular proteomics : MCP · 2020Article
- The Role of Host-Generated HFrontiers in cellular and infection microbiology · 2020Review
- ATP-sensitive KPflugers Archiv : European journal of physiology · 2019Article
- Hydrogen sulfide signaling in mitochondria and disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Review
- Hydrogen sulfide inhibits CaAmerican journal of physiology. Endocrinology and metabolism · 2019Article
- Natural Hydrogen Sulfide Donors fromNutrients · 2019Review
- Effects of Hydrogen Sulfide on Carbohydrate Metabolism in Obese Type 2 Diabetic Rats.Molecules (Basel, Switzerland) · 2019Article
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
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisL-type voltage-dependent Ca(2+) channels (VDCCs) in pancreatic beta cells play a critical role in regulating insulin secretion. The gasotransmitter H(2)S is mostly generated from L-cysteine in pancreatic beta cells by cystathionine γ-lyase (CSE) and has been reported to inhibit insulin release by opening ATP-sensitive K(+) channels. However, whether and how H(2)S affects VDCCs in beta cells is unknown.
methodsThe whole-cell patch-clamp technique was used to record VDCCs in beta cells from Cse (also known as Cth)-knockout (KO) and wild-type (WT) mice. Insulin secretion from pancreatic islets and endogenous H(2)S production in pancreas were measured.
resultsThe H(2)S donor NaHS reversibly decreased L-type VDCC current density in a concentration-dependent fashion in WT pancreatic beta cells, and the current density was further inhibited by nifedipine. Furthermore, NaHS inhibited the channel recovery from depolarisation-induced inactivation, but did not shift the current-voltage (I-V) relationship. ACS67, another H(2)S donor, also inhibited L-type VDCCs in beta cells. Inhibiting CSE activity with DL-propargylglycine increased the basal L-channel activity of beta cells from WT mice, but not that of beta cells from Cse-KO mice. Beta cells from Cse-KO mice displayed higher L-type VDCC density than those from WT mice. Insulin secretion from pancreatic islets was elevated in Cse-KO mice compared with WT mice. NaHS dose-dependently inhibited glucose-stimulated insulin secretion, which was further inhibited by nifedipine. Bay K-8644 increased glucose-stimulated insulin secretion, but this was counteracted by NaHS and nifedipine. CONCLUSIONS/
interpretationExogenous and endogenous H(2)S inhibit L-type VDCC activity and pancreatic insulin secretion, constituting a novel mechanism for the regulation of insulin secretion by the CSE/H(2)S system.
Indexed as
Identifiers
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.