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Tianru Jin

cDNAs from these species further revealed that it encodes not only glucagon but also two glucagon-like peptide hormones, namely glucagon-like peptide-1 (GLP-1) and GLP-2 ( Lund et al . 1982 ). Glucagon is produced and released from the pancreatic α

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Sandra Steensels, Matthias Lannoo, Bert Avau, Jorien Laermans, Laurien Vancleef, Ricard Farré, Kristin Verbeke and Inge Depoortere

considered as one of the possible mechanisms for the postsurgical metabolic improvements ( Svane et al. 2015 ). RYGB surgery enhances the secretion of the anorexigenic hormones glucagon-like peptide 1 (GLP1) and peptide YY (PYY), and although more

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Shou-Si Lu, Yun-Li Yu, Hao-Jie Zhu, Xiao-Dong Liu, Li Liu, Yao-Wu Liu, Ping Wang, Lin Xie and Guang-Ji Wang

play is an important role in the regulation of endocrine pancreatic secretion. The intestinal products of the proglucagon gene, glucagon-like peptide-1 (GLP-1), has been shown to contribute significantly to the overall insulin response to oral glucose

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Srividya Vasu, Mary K McGahon, R Charlotte Moffett, Tim M Curtis, J Michael Conlon, Yasser H A Abdel-Wahab and Peter R Flatt

various glucagon-like peptide-1 (GLP-1 mimetics) have been strongly promoted over the past few years ( Kahn et al. 2014 , Irwin & Flatt 2015 ). This approach has several potential advantages over development of small-molecule drugs, providing greater

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Ashley I Taylor, Nigel Irwin, Aine M McKillop, Steven Patterson, Peter R Flatt and Victor A Gault

has examined the plasma stability and satiety effects of xenin, and further characterised the glucose-lowering and insulinotropic effects of xenin both alongside GIP, glucagon-like peptide-1 (GLP1) and neurotensin. Materials and Methods Degradation of

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U Ritzel, U Leonhardt, M Ottleben, A Ruhmann, K Eckart, J Spiess and G Ramadori

Glucagon-like peptide-1 (GLP-1) is the most potent endogenous insulin-stimulating hormone. In the present study the plasma stability and biological activity of a GLP-1 analog, [Ser]GLP-1(7-36)amide, in which the second N-terminal amino acid alanine was replaced by serine, was evaluated in vitro and in vivo. Incubation of GLP-1 with human or rat plasma resulted in degradation of native GLP-1(7-36)amide to GLP-1(9-36)amide, while [Ser]GLP-1(7-36)amide was not significantly degraded by plasma enzymes. Using glucose-responsive HIT-T15 cells, [Ser]GLP-1(7-36)amide showed strong insulinotropic activity, which was inhibited by the specific GLP-1 receptor antagonist exendin-4(9-39)amide. Simultaneous i.v. injection of [Ser]GLP-1(7-36)amide and glucose in rats induced a twofold higher increase in plasma insulin levels than unmodified GLP-1(7-36)amide with glucose and a fivefold higher increase than glucose alone. [Ser]GLP-1(7-36)amide induced a 1.5-fold higher increase in plasma insulin than GLP-1(7-36)amide when given 1 h before i.v. application of glucose. The insulinotropic effect of [Ser]GLP-1(7-36)amide was suppressed by i.v. application of exendin-4(9-39)amide. The present data demonstrate that replacement of the second N-terminal amino acid alanine by serine improves the plasma stability of GLP-1(7-36)amide. The insulinotropic action in vitro and in vivo was not impaired significantly by this modification.

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Petra Kaválková, Miloš Mráz, Pavel Trachta, Jana Kloučková, Anna Cinkajzlová, Zdeňka Lacinová, Denisa Haluzíková, Marek Beneš, Zuzana Vlasáková, Václav Burda, Daniel Novák, Tomáš Petr, Libor Vítek, Terezie Pelikánová and Martin Haluzík

laboratory methods, and LDL cholesterol was calculated in the Department of Biochemistry of the General University Hospital, Prague, Czech Republic. Plasma active GLP1, GIP, leptin and insulin were measured by commercial multiplex assay (Human Metabolic

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Sarah L Craig, Victor A Gault, Gerd Hamscher and Nigel Irwin

relates to preventing degradation and subsequent loss of bioactivity of the endogenous intestinal-derived incretin hormones, glucagon-like peptiede-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) ( Deacon 2019 ). Thus, GLP-1 and GIP

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J Schirra, P Leicht, P Hildebrand, C Beglinger, R Arnold, B Goke and M Katschinski

Twelve patients with non-insulin dependent diabetes mellitus (NIDDM) under secondary failure to sulfonylureas were studied to evaluate the effects of subcutaneous glucagon-like peptide-1(7-36)amide (GLP-1) on (a) the gastric emptying pattern of a solid meal (250 kcal) and (b) the glycemic and endocrine responses to this solid meal and an oral glucose tolerance test (OGTT, 300 kcal). 0.5 nmol/kg of GLP-1 or placebo were subcutaneously injected 20 min after meal ingestion. GLP-1 modified the pattern of gastric emptying by prolonging the time to reach maximal emptying velocity (lag period) which was followed by an acceleration in the post-lag period. The maximal emptying velocity and the emptying half-time remained unaltered. With both meals, GLP-1 diminished the postprandial glucose peak, and reduced the glycemic response during the first two postprandial hours by 54.5% (solid meal) and 32.7% (OGTT) (P < 0.05). GLP-1 markedly stimulated insulin secretion with an effect lasting for 105 min (solid meal) or 150 min (OGTT). The postprandial increase of plasma glucagon was abolished by GLP-1. GLP-1 diminished the postprandial release of pancreatic polypeptide. The initial and transient delay of gastric emptying, the enhancement of postprandial insulin release, and the inhibition of postprandial glucagon release were independent determinants (P < 0.002) of the postprandial glucose response after subcutaneous GLP-1. An inhibition of efferent vagal activity may contribute to the inhibitory effect of GLP-1 on gastric emptying.

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Andreas Nygaard Madsen, Gitte Hansen, Sarah Juel Paulsen, Kirsten Lykkegaard, Mads Tang-Christensen, Harald S Hansen, Barry E Levin, Philip Just Larsen, Lotte Bjerre Knudsen, Keld Fosgerau and Niels Vrang

the novel human GLP-1 analog liraglutide for 28 days. Materials and Methods Animals All experiments were conducted in accordance with internationally accepted principles for the care and use of laboratory animals, and were approved by the Danish