Coupling factors in nutrient-induced insulin release

  title={Coupling factors in nutrient-induced insulin release},
  author={W. Malaisse and F. Malaisse-Lagae and A. Sener},
table insulinoma. Cooperativity and discrimination of anomers. Diabetes 32 (1983) 1146 1151. 82 Miwa, I., Okuda, J., Niki, H., and Niki, A., Uptake of radioactive D-glucose anomers by pancreatic islets. J. Biochem. 78 (1975) 1109-1111. 83 Montague, M., and Taylor, K.W., Islet-cell metabolism during insulin release. Effects of glucose, citrate, octanoate, tolbutamide, glucagon and theophylline. Biochem. J. 115 (1969) 257-262. 84 Morrison, A. D., Winegrad, A.I., Fink, C.J., and Lacy, P.E… Expand
Stimulus-secretion coupling in the pancreatic B-cell: Concluding remarks
Mechanisms of the electrical activity induced by glucose and tolbutamide in pancreatic fl-cells as caused by sulfonylurea derivatives, in: Pharmacology and the Future of Man. Expand
Adenine nucleotide pattern in rat pancreatic islets exposed to nutrient secretagogues
The results of this study argue against the monolithic view that the adenine nucleotide pattern in islet cells represents the sole coupling factor between metabolic and more distal events in the process of nutrient-stimulated insulin release. Expand
Inosine partially mimics the effects of glucose on ionic fluxes, electrical activity, and insulin release in mouse pancreatic B-cells
Inosine metabolism in B-cells induces insulin release by triggering the same sequence of events as glucose metabolism: a decrease of K+ permeability of the B-cell membrane, leading to depolarization and activation of voltage-dependent Ca channels. Expand
Stimulation of insulin release by an organic calcium agonist
It is concluded that the gating of Ca-channels, as presumably provoked by the calcium-agonist, simulates the stimulant action of glucose upon both Ca influx into and insulin release from the pancreatic islets. Expand
Fatty acid metabolism and insulin secretion in pancreatic beta cells
Arguments in support of the important roles of NEFA, LC-CoA, and their esterified derivatives in affecting insulin secretion in both normal and pathological states are presented. Expand
Expression of novel organic cation/carnitine transporter (OCTN2) in the mouse pancreas.
The possibility of carnitine uptake in the pancreatic A-cells through OCTN2 is suggested and the presence of carn itine transporter(s) other than OCTn2 in the B-cell is implied. Expand
Time-correlation between membrane depolarization and intracellular calcium in insulin secreting BRIN-BD11 cells: studies using FLIPR.
It is concluded that membrane depolarization of beta cells by glucose stimulation is not immediately followed by elevation of [Ca(2+)](i) and other metabolic events are involved in glucose induced stimulus-secretion coupling. Expand
Associations of the -344 T>C and the 3097 G>A polymorphisms of CYP11B2 gene with hypertension, type 2 diabetes, and metabolic syndrome in a French population.
The -344 T>C and 3097 G>A polymorphisms in the CYP11B2 are associated with T2D, hypertension and the MetS in European subjects with gender variations and significant associations between haplotype combinations and the prevalence or incidence of the three diseases were found. Expand
Nutrient metabolism in islet cells


The stimulus-secretion coupling of glucose-induced insulin release. Does glycolysis control calcium transport in the B-cell?
It is concluded that glycolysis usually exerts a tight control on the rate constant for Ca2+ transport across the B-cell membrane. Expand
The stimulus-secretion coupling of glucose-induced insulin release. Cationic and secretory effects of menadione in the endocrine pancreas.
It is concluded that menadione impairs the insulinotropic action of glucose and other nutrients by impeding the remodelling of cationic fluxes normally provoked by these secretagogues in islet cells. Expand
The stimulus-secretion coupling of glucose-induced insulin release: effect of aminooxyacetate upon nutrient-stimulated insulin secretion.
It is suggested that a transfer of reducing equivalents to extramitochondrial sites participates in the process of insulin release, whether the latter involves the oxidation of exogenous or endogenous nutrients. Expand
The stimulus-secretion coupling of glucose-induced insulin release. Thiol: disulfide balance in pancreatic islets.
The view that a glucose-induced reduction of disulphide bridges to sulphydryl groups participates in the stimulus-secretion coupling of nutrient-induced insulin release is supported. Expand
Metabolic control of potassium permeability in pancreatic islet cells.
  • J. Henquin
  • Chemistry, Medicine
  • The Biochemical journal
  • 1980
The results clearly establish the importance of the metabolic degradation of glucose and other substrates for the control of the K(+) permeability in pancreatic islet cells and support the concept that a decrease in the K-cell permeability represents a major step of the B-cell response to physiological stimulation. Expand
The stimulus-secretion coupling of glucose-induced insulin release. Metabolic effects of menadione in isolated islets.
When insulinotropic nutrients are oxidized in the B-cell, the increased availability of reduced pyridine nucleotides could modify the affinity for cations of native ionophoretic systems, eventually leading to the accumulation of calcium up to a level sufficient to trigger insulin release. Expand
Interrelationship between chloride fluxes in pancreatic islets and insulin release.
  • J. Sehlin
  • Chemistry, Medicine
  • The American journal of physiology
  • 1978
The role of Cl- in the function of pancreatic beta-cells was studied by using islets of noninbred ob/ob mice and it is suggested that Cl- is nonpassively distributed across the beta-cell plasma membrane. Expand
The stimulus--secretion coupling 4-methyl-2-oxopentanoate-induced insulin release.
It is proposed that changes in the redox state of NADP and Ca transport may serve as mediators in the stimulus-secretion coupling mechanism of insulin release induced by 4-methyl-2-oxopentanoate. Expand
Interrelationship of islet metabolism, adenosine triphosphate content and insulin release.
Results provide further evidence of a close association between the metabolic activity of exogenous substrates and their ability to initiate insulin release and Glucoreceptor models are formulated in the light of these observations. Expand
A possible role of intracellular and membrane thiols of rat pancreatic islets in calcium uptake and insulin release.
The present data collected from isolated pancreatic islets have several implications, including that the reduced state of the intracellular glutathione to GSSG ratio, which causes the superficial thiol to remain in the reduction state, constitutes a prerequisite for glucose-stimulated 45Ca uptake and insulin release. Expand