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F Bertuzzi, C Berra, C Socci, A M Davalli, G Calori, M Freschi, L Piemonti, P De Nittis, G Pozza, and A E Pontiroli


It has been shown that peripheral glucagon secreting cells (A-cells) are lost during most of the isolation procedures employed for pig islets. Loss of A-cells decreases intra-islet glucagon levels and cAMP levels in B-cells and might reduce glucose-induced insulin release. This study was designed to test this hypothesis, by evaluating the effects of culture of porcine islets with exogenous glucagon on insulin secretion and on insulin and cAMP content in islets. Islets were isolated from adult 2-year old Large White pigs using an automated method. The number of A-cells was calculated by immunostaining for glucagon in islets before and after isolation and a significant decrease in A-cells was observed. After an overnight culture, islets were cultured for 48 h in a standard medium (CMRL 1066, 10% foetal calf serum, 1% antibiotics, 1% glutamine) alone or in the presence of glucagon at two different concentrations (1·0 and 10·0 μm); exposure to glucagon was either continuous or alternated with periods of incubation in CMRL 1066 alone. After the 48-h culture in standard medium, the islet glucagon response to arginine was almost negligible and significantly lower than that observed in human islets. After culture, islet insulin response to glucose, and islet insulin and cAMP content were evaluated; continuous exposure to glucagon did not produce any significant effect on either insulin secretion or insulin and cAMP content; in contrast, discontinuous exposure to glucagon induced a significant improvement in insulin release, proportional to glucagon concentrations (integrated insulin release: −13·8 ±20·12 pg/islet/20 min in control islets, 111·0±50·73 and 144·7± 47·54 pg/islet/20 min in islets exposed to 1·0 and 10·0 μg glucagon respectively; n=10, P=0·01). Intracellular insulin and cAMP content of islets cultured in different culture media were not different. In conclusion, discontinuous exposure of isolated pig islets to exogenous glucagon induced a significant increase in glucose-induced insulin release which was not associated with an increase in cAMP content. The fact that even in the presence of glucagon the secretory activity of pig islets was lower than the reported activity of human or rat islets suggests that glucagon is only one of the factors involved in the poor insulin responsiveness of pig islets.

Journal of Endocrinology (1995) 147, 87–93

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Hongbin Liu, Anthony E Dear, Lotte B Knudsen, and Richard W Simpson

protected from the development of biochemical abnormalities associated with endothelial cell dysfunction and development of atherosclerosis ( Eitzman et al . 2000 , Mao et al . 2004 ). Liraglutide, an acylated glucagon-like peptide-1 (GLP-1) analogue, has

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Hongbin Liu, Yunshan Hu, Richard W Simpson, and Anthony E Dear

Introduction Glucagon-like peptide-1 (GLP-1), an incretin first identified in 1984, has been proposed as a potential candidate target for therapy in the treatment of type 2 diabetes ( Nauck et al . 1993 , Edwards 2005 ). GLP-1, the product of the

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Patrice D Cani, Catherine A Daubioul, Brigitte Reusens, Claude Remacle, Grégory Catillon, and Nathalie M Delzenne

( Reimer & McBurney 1996 , Cani et al. 2004 ). In the intestine, the post-translational modification of the proglucagon gene by prohormone convertase 1 (PC1) leads to the production of glucagon-like peptide-1(7–36) amide (GLP-1(7–36) amide) which, among

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L Bai, G Meredith, and B E Tuch

Introduction Glucagon-like peptide-1 (GLP-1) is a peptide secreted from the gut in response to food. It acts directly on β cells, enhancing the effect of glucose in stimulating insulin secretion from these cells. When administered to

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Neville H McClenaghan, Peter R Flatt, and Andrew J Ball

-cell desensitisation compared with sulphonylureas may occur following prolonged exposure to nateglinide ( Ball et al. 2004 b ). In vivo , insulin secretion can be stimulated by glucagon-like peptide-1 (GLP-1), a hormone of the enteroinsular axis, released

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Hong Lan, Galya Vassileva, Aaron Corona, Li Liu, Hana Baker, Andrei Golovko, Susan J Abbondanzo, Weiwen Hu, Shijun Yang, Yun Ning, Robert A Del Vecchio, Frederique Poulet, Maureen Laverty, Eric L Gustafson, Joseph A Hedrick, and Timothy J Kowalski

fall into two major categories: drugs that improve insulin sensitivity, and those that increase insulin secretion from β-cells. Agents that enhance insulin secretion in a glucose-dependent manner, such as glucagon-like peptide-1 (GLP-1) mimetics (e

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A L Pierce, J T Dickey, L Felli, P Swanson, and W W Dickhoff

hormones may modulate the effect of Gh on liver Igf2 production in fishes. To test this hypothesis, we examined basal and Gh-dependent effects of insulin, glucagon, dexamethasone (Dex), and triiodothyronine (T 3 ) on igf2 gene expression in primary

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B D Green, N Irwin, V A Gault, C J Bailey, F P M O’Harte, and P R Flatt

Introduction The incretin hormone glucagon-like peptide-1 (GLP-1) has potent insulinotropic effects on pancreatic β-cells, and further promotes glucose lowering by enhancing glucose uptake and glyconeogenesis in peripheral tissues

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Patricia Vázquez, Isabel Roncero, Enrique Blázquez, and Elvira Alvarez

Introduction Glucagon-like peptide-1(7–36)amide (GLP-1) is an intestinal peptide synthesised in L-cells. It is also produced in the brain ( Jin et al. 1988 , Kreymann et al. 1989 ), where it exerts some effects on