Effect of substitution of a permeable weak acid for the permissive role of glucose in amino acid-induced electrical activity in B-cells.

  title={Effect of substitution of a permeable weak acid for the permissive role of glucose in amino acid-induced electrical activity in B-cells.},
  author={Caroline S. Pace and Kelly T. Goldsmith},
  volume={119 6},
The amino acids L-leucine, L-isoleucine, and L-arginine require a subthreshold concentration of glucose to elicit insulin release and electrical activity from B-cells. There is evidence suggesting that protons couple the metabolism of glucose to the functional response of B-cells. In view of this, a permeable weak acid, sulfamerazine, was used to determine if the generation of intracellular protons could account for the permissive action of glucose. Addition of 10 mM sulfamerazine elicited… 


Findings support the view that a decrease in the H+-sensitive K+-permeability is responsible for the physiological depolarization observed when raising the glucose concentration in the medium.

Diphenylhydantoin suppresses glucose-induced insulin release by decreasing cytoplasmic H+ concentration in pancreatic islets.

DPH inhibits glucose-induced insulin secretion not only by inhibiting mitochondrial ATP production, but also by reducing Ca2+ efficacy in the exocytotic system through its alkalizing effect on cytoplasm.

Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.

Recent advances in understanding of the β-cell transcriptome, electrical activity, and insulin exocytosis are reviewed and models of how the different ion channels contribute to their electrical activity and insulin secretion are provided, and how these processes become perturbed in T2DM are discussed.

Physiological effects of nutrients on insulin release by pancreatic beta cells

Understanding the subjacent mechanisms of each nutrient on β-cells can help to unravel the effects of mixed variables and complexity in the context of β-cell pathology.



Effects of amino acids on membrane potential and 86Rb+ fluxes in pancreatic beta-cells.

It is proposed that leucine, ketoisocaproate, and BCH, as glucose, depolarize beta-cells by decreasing their potassium permeability, whereas arginine acts differently.

Amiloride-sensitive regulation of intracellular pH in B-cells: activation by glucose.

Electrical and Secretory Manifestations of Glucose and Amino Acid Interactions in Rat Pancreatic Islets

Data show that glucose plays a pre-eminent role as regulator of islet cell function, governing the efficacy of amino acids as β-cells stimulants.

Effects of glucose and other modifiers of insulin release on the oxidative metabolism of amino acids in micro-dissected pancreatic islets.

It is suggested that the effects of glucose on the oxidation of alanine and leucine were mediated by metabolism of the sugar, and that amino acids do not act as insulin secretagogues by serving as fuels for the beta-cells.

Stimulus-secretion coupling in beta-cells: modulation by pH.

It is evident that pH modulates the electrical events and cationic fluxes and ultimately influences the transduction of information to the mechanisms controlling the secretory process in the beta-cell.

The stimulus-secretion coupling of amino acid-induced insulin release. II. Sensitivity to K+, NH4+ and H+ of leucine-stimulated islets.

In the islets exposed to L-leucine, an alteration in the islet content of NH4+ and possibly H+ interferes with the normal coupling between metabolic and secretory events.

Effect of glucose on the intracellular pH of pancreatic islet cells.

It is concluded that, in contrast with previous assumptions, glucose increases intracellular pH in the islet cells and may be coupled to the glucose metabolism and associated with triggering of insulin release.

Potassium permeability activated by intracellular calcium ion concentration in the pancreatic beta‐cell.

It is proposed that the membrane potential of the beta‐cell in the absence of glucose is predominantly controlled by the [Ca2+]i‐activated PK, and further suggested that this permeability to K controls the level for glucose stimulation and leads to the generation of the burst pattern.

Pancreatic beta-cell electrical activity: the role of anions and the control of pH.

Amiloride, a specific blocker of the transmembrane sodium proton exchange, has been used to demonstrate that this mechanism is also operative in the beta-cell membrane in the control of pHi and to explain many of the effects observed in this study.

Lowering of pHi inhibits Ca2+-activated K+ channels in pancreatic B-cells

The patch-clamp method is used to study identified rat B-cells and it is shown that the B-cell GK(Ca) channel is activated by membrane depolarization as well as by cytoplasmic Ca2+, while it is inhibited by acidification of the cytopLasmic membrane surface.