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Te Du, Liu Yang, Xu Xu, Xiaofan Shi, Xin Xu, Jian Lu, Jianlu Lv, Xi Huang, Jing Chen, Heyao Wang, Jiming Ye, Lihong Hu, and Xu Shen

& Nolan 2006 ). As such, β-cell dysfunction is one of the key contributors to T2DM. Pathologically, pancreatic β-cell dysfunction involves a combination of decreased β-cell mass and impaired insulin secretion ( Prentki & Nolan 2006 ). The mass of β

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B Maiztegui, M I Borelli, M A Raschia, H Del Zotto, and J J Gagliardino

. 2003 ). Evidence in the literature has shown that glucokinase (GK) activity plays a pivotal role upon islet glucose metabolism and insulin secretion. As opposed to other hexokinases (HK), GK kinetics shows a cooperative glucose dependence (Hill

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Liselotte Fransson, Stephanie Franzén, Victoria Rosengren, Petra Wolbert, Åke Sjöholm, and Henrik Ortsäter

evaluation using insulin ELISA (Mercodia). Islet isolation and glucose-stimulated insulin secretion Pancreatic glands were excised and islets were isolated by collagenase digestion. Islets used for chaperone expression were lysed directly after isolation and

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Ivonne Gisèle Makom Ndifossap, Francesca Frigerio, Marina Casimir, Florence Ngueguim Tsofack, Etienne Dongo, Pierre Kamtchouing, Théophile Dimo, and Pierre Maechler

). Despite these promising in vivo studies, cellular and molecular mechanisms responsible for hypoglycaemic effects of the plant have not been investigated. Blood glucose control depends on the normal regulation of insulin secretion from the pancreatic β

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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

monster) ( Conlon et al. 2006 ). This peptide has been shown to stimulate insulin secretion and exert a range of glucoregulatory actions in a fashion similar to incretin hormone, GLP-1 ( Parkes et al. 2013 ). Subsequently, long-acting GLP-1 mimetics

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K K Sidhu, R C Fowkes, R H Skelly, and J M Burrin

the synthesis and secretion of insulin in a glucose-dependent manner. Indeed, GLP-1 has turned out to be the most potent and efficacious regulatory stimulator of insulin secretion discovered so far ( Fehmann et al. 1995 ). These beneficial effects

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It has been reported that hypoglycin and hypoglycin-like compounds, including 4-pentenoic acid, inhibit fatty acid oxidation and gluconeogenesis as well as inducing profound hypoglycaemia (Bressler, Corredor & Brendel, 1969). A vinyl group separated by two carbon atoms from the carboxyl group is apparently a structural requirement for biological effects (Corredor, Brendel & Bressler, 1967), valeric acid, the saturated analogue of 4-pentenoic acid, being inactive. In the course of investigations on insulin secretion in ruminants we observed that valerate is a very potent insulin secretogogue (Horino, Machlin, Hertelendy & Kipnis, 1968). In this communication evidence is presented which shows that 4-pentenoic acid is also a potent stimulant of insulin secretion in the sheep and, contrary to observations in non-ruminants, it can induce hyperglycaemia and inhibit lipolysis.

Four castrated male sheep (35–50 kg) were infused through a polyethylene catheter inserted into a jugular vein after a 24-h fast. Two animals received I

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Hyo-Eun Kim, Sung-E Choi, Soo-Jin Lee, Ji-Hyun Lee, Youn-Jung Lee, Sang Sun Kang, Jaesun Chun, and Yup Kang

Introduction Secretion of insulin from pancreatic β-cells is an essential prerequisite to maintaining an appropriate level of blood glucose. For appropriate glucose-stimulated insulin secretion (GSIS) to occur, all steps, from glucose sensing to

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Rahman M Hafizur, Randa Babiker, Sakina Yagi, Sidra Chishti, Nurul Kabir, and M Iqbal Choudhary

between the effects of G. alata and Gb, it can be suggested that the mode of action of G. alata extract might be mediated by an enhanced insulin secretion. This assumption was confirmed by our biochemical examination, which revealed enhanced insulin

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S B Richardson, T Laya, and M VanOoy


Arginine vasopressin (VP) activates phospholipase C (PLC) and stimulates insulin secretion and inositol phosphate (insP) production in mouse islets and clonal hamster beta cells (HIT). The insulin response to VP is reportedly dependent on extracellular glucose and there is evidence that glucose also activates PLC. The interactions of VP and glucose have been further examined in HIT cells. Glucose stimulated insulin secretion but not insP production and VP stimulated both insulin secretion and insP production in the absence of extracellular glucose. However, in the presence of glucose the insulin and insP responses to VP were potentiated. The phorbol ester, tetradecanoylphorbol acetate (TPA), which activates protein kinase C (PKC), stimulated basal insulin secretion but inhibited insP production. In the presence of submaximal concentrations of VP, 100 nmol/l TPA inhibited VP-stimulated inositol monophosphate production and there was no additivity of stimulated insulin secretion. With a maximal (10 nmol/l) concentration of VP, TPA caused additive insulin secretion and insP levels were stimulated above baseline. Twenty-four hour preincubation with TPA to down-regulate PKC did not inhibit the insulin response to VP. We conclude that extracellular glucose does not activate PLC and is not required for VP-stimulated insulin secretion although it potentiates VP-stimulated insulin secretion and insP production.

Journal of Endocrinology (1995) 145, 221–226