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      Glucose-sensing in glucagon-like peptide-1-secreting cells.

      Diabetes
      Action Potentials, drug effects, Adenosine Triphosphate, physiology, Animals, Cell Line, Cell Membrane, Diazoxide, pharmacology, Electric Conductivity, Glucagon, secretion, Glucagon-Like Peptide 1, Glucokinase, metabolism, Glucose, Glycosyltransferases, Hypoglycemic Agents, Membrane Proteins, Peptide Fragments, Potassium Channels, Potassium Channels, Inwardly Rectifying, Protein Precursors, Repressor Proteins, Reverse Transcriptase Polymerase Chain Reaction, Saccharomyces cerevisiae Proteins, Tolbutamide

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          Abstract

          Glucagon-like peptide-1 (GLP-1) is released from intestinal L-cells in response to carbohydrate and fat in the diet. Despite the interest in GLP-1 as an antidiabetic agent, very little is known about the mechanism of stimulus-secretion coupling in L-cells. We investigated the electrophysiological events underlying glucose-induced GLP-1 release in the GLP-1-secreting cell line, GLUTag. Cells were studied using perforated-patch and standard whole-cell patch clamp recordings. GLUTag cells were largely quiescent and hyperpolarized in the absence of glucose. Increasing the glucose concentration between 0 and 20 mmol/l decreased the membrane conductance, caused membrane depolarization, and triggered the generation of action potentials. Action potentials were also triggered by tolbutamide (500 micro mol/l) and were suppressed by diazoxide (340 micro mol/l) or the metabolic inhibitor azide (3 mmol/l), suggesting an involvement of K(ATP) channels. Large tolbutamide-sensitive washout currents developed in standard whole-cell recordings, confirming the presence of K(ATP) channels. RT-PCR detected the K(ATP) channel subunits Kir6.2 and SUR1 and glucokinase. GLP-1 secretion was also stimulated by glucose over the concentration range 0-25 mmol/l and by tolbutamide. Our results suggest that glucose triggers GLP-1 release through closure of K(ATP) channels and action potential generation.

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