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      Glucagon-like peptide-1(7-36) amide (GLP-1) enhances insulin-stimulated glucose metabolism in 3T3-L1 adipocytes: one of several potential extrapancreatic sites of GLP-1 action.

      Endocrinology
      3T3 Cells, chemistry, cytology, metabolism, Adipocytes, Animals, Base Sequence, Blotting, Southern, DNA, Complementary, analysis, genetics, Glucagon, Glucagon-Like Peptide 1, Glucagon-Like Peptides, Glucose, Insulin, pharmacology, Kidney, ultrastructure, Mice, Molecular Sequence Data, Muscle, Skeletal, Peptide Fragments, Polymerase Chain Reaction, RNA, Messenger

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          Abstract

          We investigated the effects of glucagon-like peptide-1(7-36) amide, GLP-1, on glucose metabolism in 3T3-L1 adipocytes and we used polymerase chain reaction to search for the presence of GLP-1 receptors in various rat tissues. GLP-1 at 1 nM significantly increased insulin-mediated 2-deoxyglucose uptake by 40% while having no effect on basal uptake. In conjunction with the elevated uptake, the insulin-dependent incorporation of 14C-glucose into fatty acids was also increased. Moreover, neither glycogen synthesis nor insulin binding to its receptor were affected by GLP-1. In addition to the presence of GLP-1 receptor in pancreas we found messenger RNA for this receptor in brain, kidney, heart, fat, skeletal muscle, liver, and intestine. This study indicates that GLP-1, in addition to its well known effect of stimulating insulin secretion, may improve insulin responsiveness by promoting fatty acid synthesis in adipose cells and possibly modulating insulin signaling in other insulin sensitive tissues.

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