ArticleBMC endocrine disorders2004
Nutrient-stimulated insulin secretion in mouse islets is critically dependent on intracellular pH.
Article in BMC endocrine disorders, 2004. 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, 16 citations in OpenAlex.
- pH-Dependence of Glucose-Dependent Activity of Beta Cell Networks in Acute Mouse Pancreatic Tissue Slice.Frontiers in endocrinology · 2022Article
- Electrogenic sodium bicarbonate cotransporter NBCe1 regulates pancreatic β cell function in type 2 diabetes.The Journal of clinical investigation · 2021Article
- Another Consequence of the Warburg Effect? Metabolic Regulation of NaFrontiers in oncology · 2020Review
- The Effects of Systemic and Local Acidosis on Insulin Resistance and Signaling.International journal of molecular sciences · 2018Review
- In scarcity and abundance: metabolic signals regulating cell growth.Physiology (Bethesda, Md.) · 2013Review
- Imaging energy status in live cells with a fluorescent biosensor of the intracellular ATP-to-ADP ratio.Nature communications · 2013Article
- Cytosolic pH is a second messenger for glucose and regulates the PKA pathway through V-ATPase.The EMBO journal · 2010Article
- Dimethyl amiloride improves glucose homeostasis in mouse models of type 2 diabetes.American journal of physiology. Endocrinology and metabolism · 2008Article
- Amiloride derivatives enhance insulin release in pancreatic islets from diabetic mice.BMC endocrine disorders · 2005Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMany mechanistic steps underlying nutrient-stimulated insulin secretion (NSIS) are poorly understood. The influence of intracellular pH (pHi) on insulin secretion is widely documented, and can be used as an investigative tool. This study demonstrates previously unknown effects of pHi-alteration on insulin secretion in mouse islets, which may be utilized to correct defects in insulin secretion.
methodsDifferent components of insulin secretion in mouse islets were monitored in the presence and absence of forced changes in pHi. The parameters measured included time-dependent potentiation of insulin secretion by glucose, and direct insulin secretion by different mitochondrial and non-mitochondrial secretagogues. Islet pHi was altered using amiloride, removal of medium Cl-, and changing medium pH. Resulting changes in islet pHi were monitored by confocal microscopy using a pH-sensitive fluorescent indicator. To investigate the underlying mechanisms of the effects of pHi-alteration, cellular NAD(P)H levels were measured using two-photon excitation microscopy (TPEM). Data were analyzed using Student's t test.
resultsTime-dependent potentiation, a function normally absent in mouse islets, can be unmasked by a forced decrease in pHi. The optimal range of pHi for NSIS is 6.4-6.8. Bringing islet pHi to this range enhances insulin secretion by all mitochondrial fuels tested, reverses the inhibition of glucose-stimulated insulin secretion (GSIS) by mitochondrial inhibitors, and is associated with increased levels of cellular NAD(P)H.
conclusionsPharmacological alteration of pHi is a potential means to correct the secretory defect in non-insulin dependent diabetes mellitus (NIDDM), since forcing islet pHi to the optimal range enhances NSIS and induces secretory functions that are normally absent.
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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.