Ca2+, NAD(P)H and membrane potential changes in pancreatic beta-cells by methyl succinate: comparison with glucose.

Ca2+, NAD(P)H and membrane potential changes in pancreatic beta-cells by methyl succinate: comparison with glucose. Research Abstract Details 

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Ca2+, NAD(P)H and membrane potential changes in pancreatic beta-cells by methyl succinate: comparison with glucose. Abstract Text:

Emma Heart,Gordon C Yaney,Richard F Corkey,Vera Schultz,Esthere Luc,Lihan Liu,Jude T Deeney,Orian Shirihai,Keith Tornheim,Peter J S Smith,Barbara E Corkey,

The present study was undertaken to determine the main metabolic secretory signals generated by the mitochondrial substrate MeS (methyl succinate) compared with glucose in mouse and rat islets and to understand the differences. Glycolysis and mitochondrial metabolism both have key roles in the stimulation of insulin secretion by glucose. Both fuels elicited comparable oscillatory patterns of Ca2+ and changes in plasma and mitochondrial membrane potential in rat islet cells and clonal pancreatic beta-cells (INS-1). Saturation of the Ca2+ signal occurred between 5 and 6 mM MeS, while secretion reached its maximum at 15 mM, suggesting operation of a K(ATP)-channel-independent pathway. Additional responses to MeS and glucose included elevated NAD(P)H autofluorescence in INS-1 cells and islets and increases in assayed NADH and NADPH and the ATP/ADP ratio. Increased NADPH and ATP/ADP ratios occurred more rapidly with MeS, although similar levels were reached after 5 min of exposure to each fuel, whereas NADH increased more with MeS than with glucose. Reversal of MeS-induced cell depolarization by Methylene Blue completely inhibited MeS-stimulated secretion, whereas basal secretion and KCl-induced changes in these parameters were not affected. MeS had no effect on secretion or signals in the mouse islets, in contrast with glucose, possibly due to a lack of malic enzyme. The data are consistent with the common intermediates being pyruvate, cytosolic NADPH or both, and suggest that cytosolic NADPH production could account for the more rapid onset of MeS-induced secretion compared with glucose stimulation.

Ca2+, NAD(P)H and membrane potential changes in pancreatic beta-cells by methyl succinate: comparison with glucose. Publishing Authors By Initials

E Heart,GC Yaney,RF Corkey,V Schultz,E Luc,L Liu,JT Deeney,O Shirihai,K Tornheim,PJ Smith,BE Corkey,

For similar organic chemicals: carboxylic acids: acids, acyclic: dicarboxylic acids: succinic acids: succinic acid: succinates research abstracts see: organic chemicals: carboxylic acids: acids, acyclic: dicarboxylic acids: succinic acids: succinic acid: succinates research

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Ca2+, NAD(P)H and membrane potential changes in pancreatic beta-cells by methyl succinate: comparison with glucose. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Biochemical journal

VOLUME: 403

Page Numbers: 197-205

Journal Abbreviation: Biochem. J.

ISSN: 1470-8728

DAY: 1

MONTH: Apr

YEAR: 2007

Ca2+, NAD(P)H and membrane potential changes in pancreatic beta-cells by methyl succinate: comparison with glucose. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2984726

Ca2+, NAD(P)H and membrane potential changes in pancreatic beta-cells by methyl succinate: comparison with glucose. Keywords Mesh Terms:

KEYWORDS: Succinates

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Ca2+, NAD(P)H and membrane potential changes in pancreatic beta-cells by methyl succinate: comparison with glucose. Information

Substance Name: Calcium

Registry Number: 7440-70-2

Grant and Affiliation Information for Ca2+, NAD(P)H and membrane potential changes in pancreatic beta-cells by methyl succinate: comparison with glucose.

AFFILIATION: Obesity Research Center, Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA.

Country: England

AGENCY: United States NHLBI

GRANT: T32 HL-07224

ACRONYM: HL

MEDLINETA: Biochem J

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