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Adrian Holliday and Andrew Blannin

–tyrosine (PYY) and glucagon-like peptide 1 (GLP-1) have been observed with continuous, high-intensity aerobic bouts of exercise lasting as little as 30 min ( Ueda et al . 2009 a ), and with intermittent exercise bouts yielding energy expenditure values of as

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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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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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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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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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C Herrmann-Rinke, A Vöge, M Hess and B Göke

Abstract

Food ingestion induces a rapid increase in the insulinotropic glucagon-like peptide-1 (GLP-1) in plasma. Paradoxically, GLP-1 originates from the lower intestines and therefore a complex regulation of postprandial GLP-1 secretion must exist. This was addressed in the present study by utilizing an isolated vascularly perfused rat ileum preparation. Peptides and neurotransmitters thought to be candidate mediators triggering GLP-1 secretion were arterially infused and GLP-1 was measured in the venous effluent. Arterial infusion of cholinergic agonists strongly enhanced GLP-1 secretion which was counteracted by the addition of atropine. Histamine, dopamine, 5-hydoxytryptamine, γ-aminobutyric acid, and norepinephrine had no effect. Peptides of the bombesin family were strong stimulants whereas tachykinins, enkephalins, dynorphin, TRH, calcitonin-gene-related peptide and members of the secretin family, vasoactive intestinal peptide, peptide histidine isoleucine and neuropeptide Y, were less effective. The second incretin hormone, gastric inhibitory polypeptide (GIP), was the most potent stimulant of GLP-1 secretion in our study. It enhanced GLP-1 release up to sixfold above basal during the early phase followed by a sustained secretion at 400% above basal. This stimulation remained unaffected by atropine. In conclusion, in addition to luminal stimulation of nutrients, a cholinergic impulse as well as peptidergic mediators (among them possibly GIP and GRP) may have an impact on postprandial GLP-1 secretion from the rat ileum.

Journal of Endocrinology (1995) 147, 25–31