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Hongmei Lang, Zhihua Ai, Zhiqing You, Yong Wan, Wei Guo, Jie Xiao and Xiaolan Jin

, Zhang et al . 2015 ). Type 2 diabetes (T2D) is characterized by reduced insulin secretion from pancreatic β-cells and insulin resistance at the target cells, which result in increased blood glucose levels ( Kahn 2001 ). It has been reported that

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Joong Kwan Kim, Yongchul Lim, Jung Ok Lee, Young-Sun Lee, Nam Hee Won, Hyun Kim and Hyeon Soo Kim

the most physiologically relevant, and it promotes insulin secretion by inducing multiple signaling pathways, including the triggering and amplifying pathways ( Henquin 2000 ). The results of a previous study indicated that arginine methylation of the

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Jessica Sabourin and Florent Allagnat

Introduction Insulin secretion is driven by electrical activity and oscillations of intracellular Ca 2+ concentration ([Ca 2+ ] i ) in pancreatic β-cells. The main driver of insulin secretion is plasma glucose; glucose metabolism produces ATP

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Yu-Feng Zhao, Li Wang, Dingjun Zha, Li Qiao, Lianjun Lu, Jun Yu, Ping Qu, Qiang Sun, Jianhua Qiu and Chen Chen

. There are only reports showing that GW9508 potentiated glucose-stimulated insulin secretion (GSIS) in insulinoma cell lines such as MIN6 cells and INS-1E cells ( Briscoe et al . 2006 , Yang et al . 2010 ). And it was shown that GW9508 does not

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Pamela Petrocchi-Passeri, Cheryl Cero, Alessandro Cutarelli, Claudio Frank, Cinzia Severini, Alessandro Bartolomucci and Roberta Possenti

Introduction Impaired insulin secretion and insulin resistance play major roles in the development of type 2 diabetes (T2D). The most important regulators of insulin secretion are plasma nutrients, among which glucose is the most effective; however

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James E P Brown, David J Onyango, Manjunath Ramanjaneya, Alex C Conner, Snehal T Patel, Simon J Dunmore and Harpal S Randeva

elucidated. This study therefore aimed to clarify the actions of visfatin in the pancreatic β-cell by investigating not only its effects on insulin secretion and insulin receptor phosphorylation, but also its regulation of the expression of a panel of

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Marloes Dekker Nitert, Cecilia L F Nagorny, Anna Wendt, Lena Eliasson and Hindrik Mulder

. 2004 , Taylor et al . 2005 ). Ca 2 + currents that can be inhibited by ω-conotoxin GVIA, which is known to block Ca V 2.2, have been reported in rat β-cells, but their role in insulin secretion is controversial ( Satin et al . 1995 , Sher et al

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Quinn Dufurrena, Nils Bäck, Richard Mains, Louis Hodgson, Herbert Tanowitz, Prashant Mandela, Betty Eipper and Regina Kuliawat

volumes were adjusted in proportion to any changes of cell lysate volume. In vivo secretion studies Relevant cellular processes for insulin secretion can be regulated differently in males and females ( Mauvais-Jarvis 2015 , Roubtsova et al

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Sufang Chen, Wei Wei, Minjie Chen, Xiaobo Qin, Lianglin Qiu, Li Zhang, Yuhao Zhang, Qi Cao and Zhekang Ying

obesity-dependent manner too. Furthermore, several studies have shown that TNFα reduces insulin secretion by cultured pancreatic β cell lines such as INS-1 ( Zhang & Kim 1995 ) and HIT-T15 ( Tsiotra et al . 2001 ), suggesting that in addition to insulin

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A. M. Band, P. M. Jones and S. L. Howell

ABSTRACT

There is growing evidence that arachidonic acid (AA) and/or its metabolites may be involved in the control of insulin secretion. We have now investigated the effect of AA on insulin secretion from rat islets, and the possible involvement of protein kinase C (PKC) in this process. Exogenous AA stimulated insulin secretion from intact islets at a substimulatory concentration of glucose (2 mm), but did not further enhance glucose-induced (20 mm) insulin secretion. AA-induced insulin secretion was temperature dependent. The secretory responses seen at 37°C were totally abolished by reducing the incubation temperature to ≤34°C. AA-induced insulin secretion was not dependent upon extracellular Ca2+ and was potentiated by omission of Ca2+ or bovine serum albumin from the media. PKC in rat islets can thus be stimulated by AA, but the stimulation of PKC is not required for AA-induced insulin secretion.