Hexose metabolism in pancreatic islets: Effect of D-glucose on the mitochondrial redox state

1995 ◽  
Vol 142 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Remedios Ramirez ◽  
Abdullah Sener ◽  
Willy J. Malaisse
Keyword(s):  
Pancreatic Islets ◽  
Redox State ◽  
Mitochondrial Redox State ◽  
Hexose Metabolism

Disturbed mitochondrial redox state and tissue energy charge in cholestasis

2021 ◽  
Author(s):  
Vahid Ghanbarinejad ◽  
Mohammad M. Ommati ◽  
Zhipeng Jia ◽  
Omid Farshad ◽  
Akram Jamshidzadeh ◽  
...  
Keyword(s):  
Redox State ◽  
Energy Charge ◽  
Mitochondrial Redox State

scholarly journals Rapid and delayed effects of epidermal growth factor on gluconeogenesis

1993 ◽  
Vol 294 (3) ◽  
pp. 865-872 ◽  
Author(s):  
C Soler ◽  
M Soley
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Redox State ◽  
Metabolic Flux ◽  
Isolated Hepatocytes ◽  
Delayed Effect ◽  
Delayed Effects ◽  
Mitochondrial Redox State ◽  
Glucose Synthesis ◽  
Epidermal Growth

Most reports on the effects of epidermal growth factor (EGF) on gluconeogenesis have indicated that such effects depend on the substrate used and are only observable after a lag time of 30-40 min. Recently, an immediate and transient effect of EGF on glucose synthesis was described in a perfused liver system. Here we extend the study of the effect of EGF on gluconeogenesis to isolated hepatocytes from fasted rats. The delayed effect of EGF on gluconeogenesis was studied by adding the substrate 40 min after the peptide. Under these conditions EGF increased glucose synthesis from pyruvate, decreased it when the substrate was lactate or glycerol and did not modify gluconeogensis from fructose or dihydroxyacetone. EGF did not affect the metabolic flux through glycolysis, determined as the production of lactate+pyruvate from 30 mM glucose. Furthermore, EGF did not modify the metabolic flux through pyruvate kinase, determined as the production of lactate+pyruvate from 1 mM dihydroxyacetone. The differing effects of EGF on gluconeogenesis depending on the substrate used can be explained by the effects of EGF on the cytosolic redox state (measured as the lactate/pyruvate ratio). About 20 min after the addition of EGF, the mitochondrial redox state (measured as the 3-hydroxybutyrate/acetoacetate ratio) decreased. This effect of EGF was blocked by ammonium, which also abolished the effect of the peptide on gluconeogenesis. Thus the effect of EGF at the mitochondrial level appears to be necessary for its effects on gluconeogenesis. Taken together, our results indicate that the delayed effects of EGF on gluconeogenesis are secondary to the effects of the peptide at both the mitochondrial and cytosolic levels. In addition to these delayed effects, we observed that EGF rapidly and transiently stimulated glucose synthesis from lactate, decreased the cytosolic redox state and increased oxygen consumption. All of these rapid effects required the presence of extracellular calcium and disappeared in the presence of rotenone, suggesting that this rapid effect of EGF on gluconeogenesis is secondary to the stimulation of mitochondrial respiration.

scholarly journals NCLX, but not Letm1, mediates matrix Ca2+ extrusion and modulates the mitochondrial redox state during HeLa cell stimulation

2012 ◽  
Vol 1817 ◽  
pp. S86-S87
Author(s):  
Umberto De Marchi ◽  
Jaime Santo-Domingo ◽  
Israel Sekler ◽  
Andreas Wiederkehr ◽  
Nicolas Demaurex
Keyword(s):  
Hela Cell ◽  
Redox State ◽  
Cell Stimulation ◽  
Mitochondrial Redox State

Hexose metabolism in pancreatic islets. Regulation of aerobic glycolysis and pyruvate decarboxylation

1991 ◽  
Vol 23 (9) ◽  
pp. 955-959 ◽  
Author(s):  
Willy J. Malaisse ◽  
Joanne Rasschaert ◽  
Ignacio Conget ◽  
Abdullah Sener
Keyword(s):  
Pancreatic Islets ◽  
Aerobic Glycolysis ◽  
Hexose Metabolism

scholarly journals IMAGING REDOX STATE HETEROGENEITY WITHIN INDIVIDUAL EMBRYONIC STEM CELL COLONIES

2011 ◽  
Vol 04 (03) ◽  
pp. 279-288 ◽  
Author(s):  
HE N. XU ◽  
RUSSELL C. ADDIS ◽  
DAVIDA F. GOINGS ◽  
SHOKO NIOKA ◽  
BRITTON CHANCE ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Embryonic Stem Cell ◽  
Redox State ◽  
Embryonic Stem ◽  
Reduced Form ◽  
Significant Heterogeneity ◽  
Imaging Data ◽  
Mitochondrial Redox State ◽  
Reduced State

Redox state mediates embryonic stem cell (ESC) differentiation and thus offers an important complementary approach to understanding the pluripotency of stem cells. NADH redox ratio (NADH/(Fp + NADH)), where NADH is the reduced form of nicotinamide adenine dinucleotide and Fp is the oxidized flavoproteins, has been established as a sensitive indicator of mitochondrial redox state. In this paper, we report our redox imaging data on the mitochondrial redox state of mouse ESC (mESC) colonies and the implications thereof. The low-temperature NADH/Fp redox scanner was employed to image mESC colonies grown on a feeder layer of gamma-irradiated mouse embryonic fibroblasts (MEFs) on glass cover slips. The result showed significant heterogeneity in the mitochondrial redox state within individual mESC colonies (size: ~200–440 μm), exhibiting a core with a more reduced state than the periphery. This more reduced state positively correlates with the expression pattern of Oct4, a well-established marker of pluripotency. Our observation is the first to show the heterogeneity in the mitochondrial redox state within a mESC colony, suggesting that mitochondrial redox state should be further investigated as a potential new biomarker for the stemness of embryonic stem cells.

scholarly journals Direct assessment of renal mitochondrial redox state using hyperpolarized 13 C‐acetoacetate

2018 ◽  
Vol 79 (4) ◽  
pp. 1862-1869 ◽  
Author(s):  
Cornelius Morze ◽  
Michael A. Ohliger ◽  
Irene Marco‐Rius ◽  
David M. Wilson ◽  
Robert R. Flavell ◽  
...  
Keyword(s):  
Redox State ◽  
Direct Assessment ◽  
Mitochondrial Redox State

Hexose metabolism in pancreatic islets

1987 ◽  
Vol 49 (2-3) ◽  
pp. 219-225 ◽  
Author(s):  
Marie-Hélǹe Giroix ◽  
Abdullah Sener ◽  
Willy J. Malaisse
Keyword(s):  
Pancreatic Islets ◽  
Hexose Metabolism
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