NDLI: Contribution of glycolytic and mitochondrial pathways in glucose-induced changes in islet respiration and insulin secretion

Content Provider	Springer Nature Link
Author	Ortsäter, Henrik Liss, Per Åkerman, Karl E. Bergsten, Peter
Copyright Year	2002
Abstract	The different roles of glycolytic and mitochondrial pathways in glucose-induced metabolic activation and insulin secretion were studied in islets of Langerhans. Single islets were perifused with 3 mM glucose together with agents affecting the production or consumption of ATP. Subsequently, glucose was raised to 11 mM and the effects of the agents on metabolic and secretory responses were evaluated. Metabolism was monitored continuously with an oxygen-sensitive microelectrode inserted into the islet. Insulin secretion was determined by assaying insulin in perifusate with ELISA. Inhibitors of mitochondrial ATP production reduced the metabolic and secretory response to glucose. When glycolytic ATP production was reduced, initial but not sustained glucose-stimulated insulin release was observed. Inhibition of mitochondrial pyruvate transport reduced the glucose-induced decline in pO2. Although mitochondrial metabolism was eventually similar to normal, insulin release was only 20% of normal. Increased energy expenditure also changed the kinetics of the glucose-induced decline in pO2 and decreased the insulin release by 50%. In conclusion, glucose-induced enhancement of insulin release was only seen when the rise of the sugar concentration triggered a rapid and sustained increase of mitochondrial metabolism. This activation of mitochondrial metabolism required a good metabolic state prior to the glucose challenge.
Starting Page	506
Ending Page	512
Page Count	7
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	444
Issue Number	4
e-ISSN	14322013
Language	English
Publisher	Springer-Verlag
Publisher Date	2002-06-08
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Contribution of glycolytic and mitochondrial pathways in glucose-induced changes in islet respiration and insulin secretion

Anoctamin 1 (Ano1) is required for glucose-induced membrane potential oscillations and insulin secretion by murine β-cells

TRPM5 regulates glucose-stimulated insulin secretion

Immaturity of Glucose-Induced Insulin Secretion in Fetal Rat Islets is Due to Low Glucokinase Activity

Potentiation of Glucose-Induced Insulin Secretion by Fagomine, a Pseudo-Sugar Isolated from Mulberry Leaves

Mitochondrial reactive oxygen species are obligatory signals for glucose-induced insulin secretion.

Difference in Mechanism between Glyceraldehyde- and Glucose-Induced Insulin Secretion from Isolated Rat Pancreatic Islets

Intracerebroventricular infusion of a triglyceride emulsion leads to both altered insulin secretion and hepatic glucose production in rats

Glucose-induced inhibition of insulin secretion

Contribution of glycolytic and mitochondrial pathways in glucose-induced changes in islet respiration and insulin secretion

Similar Documents

Contribution of glycolytic and mitochondrial pathways in glucose-induced changes in islet respiration and insulin secretion

Anoctamin 1 (Ano1) is required for glucose-induced membrane potential oscillations and insulin secretion by murine β-cells

TRPM5 regulates glucose-stimulated insulin secretion

Immaturity of Glucose-Induced Insulin Secretion in Fetal Rat Islets is Due to Low Glucokinase Activity

Potentiation of Glucose-Induced Insulin Secretion by Fagomine, a Pseudo-Sugar Isolated from Mulberry Leaves

Mitochondrial reactive oxygen species are obligatory signals for glucose-induced insulin secretion.

Difference in Mechanism between Glyceraldehyde- and Glucose-Induced Insulin Secretion from Isolated Rat Pancreatic Islets

Intracerebroventricular infusion of a triglyceride emulsion leads to both altered insulin secretion and hepatic glucose production in rats

Glucose-induced inhibition of insulin secretion

Contribution of glycolytic and mitochondrial pathways in glucose-induced changes in islet respiration and insulin secretion