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Jakob Bondo Hansen, Laila Romagueira Bichara Dos Santos, Ying Liu, Kacey J Prentice, Frederik Teudt, Morten Tonnesen, Jean-Christophe Jonas, Michael B Wheeler and Thomas Mandrup-Poulsen

). Additionally, human and rodent beta-cells accumulate iron in conditions of increased circulating iron, as seen in hereditary hemochromatosis and transfusional iron overload, promoting islet apoptosis, decreased islet mass and impaired insulin secretion due to

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Sumaira Z Hasnain, Johannes B Prins and Michael A McGuckin

insulin and has distinct biological effects. The importance of decreased proteolytic processing of insulin in T2D is discussed later in the review. β-cell insulin secretion, depicted schematically in Fig. 1 , is regulated by sensing glucose at

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Z Ma, D F J Ketelhuth, T Wirström, T Ohki, M J Forteza, H Wang, V Grill, C B Wollheim and A Björklund

( Mosmann 1983 ) refer to Supplementary data. Apoptosis was quantified with a cell death detection ELISA plus kit (Roche Applied Bioscience) according to manufacturer’s instruction. Insulin secretion and cellular content Cells Cells were seeded

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Carlos Larqué, Myrian Velasco, Francisco Barajas-Olmos, Neyvis García-Delgado, Juan Pablo Chávez-Maldonado, Jazmín García-Morales, Lorena Orozco and Marcia Hiriart

-cell-related genes. However, these cells show a lower glucose-stimulated insulin secretion (GSIS) response or transcriptome differences compared with completely developed, normal beta-cells ( D’Amour et al . 2006 , Hrvatin et al . 2014 , Narayanan et al . 2014

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Seisuke Sato, Hitomi Imachi, Jingya Lyu, Yumi Miyai, Kensaku Fukunaga, Tao Dong, Tomohiro Ibata, Toshihiro Kobayashi, Takuo Yoshimoto, Fumi Kikuchi, Kazuko Yonezaki, Nao Yamaji, Hisakazu Iwama and Koji Murao

TNF-α played a role in impaired secretion of insulin, which frequently occurs in type 2 diabetes ( Donath et al. 2003 ). In pancreatic β-cells, TNF-α alone inhibited glucose-stimulated insulin secretion (GSIS) ( Zhang & Kim 1995 , Dunger et al

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D Gill, K J Brocklehurst, H W G Brown and D M Smith

Introduction Glucokinase (GK) exists as two isoforms that have independent tissue-specific promoters. In the pancreatic β-cell, GK acts as a glucose sensor and contributes to the regulation of glucose-stimulated insulin secretion (GSIS). The

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Rui Takahashi, Hisamitsu Ishihara, Kazuma Takahashi, Akira Tamura, Suguru Yamaguchi, Takahiro Yamada, Hideki Katagiri and Yoshitomo Oka

with AdCMV-eGFP at an m.o.i. of 900 resulted in reduced glucose (20 mM)-stimulated insulin secretion when compared with that in non-infected islets (data not shown), as was noted previously ( Rao et al. 2005 ). In contrast, a more than fourfold

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Sofia A Rahman, Azizun Nessa and Khalid Hussain

Introduction Congenital hyperinsulinism (CHI) refers to a group of disorders characterised by dysregulated insulin secretion from pancreatic β-cells. As insulin is the key hormone involved in the regulation of the blood glucose level, its

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Guoying Chang, Rui Yang, Yanan Cao, Aifang Nie, Xuefan Gu and Huiwen Zhang

from intracellular stores. The resulting rise in [Ca 2+ ] i then triggers insulin secretory granule (ISG) exocytosis. Abnormalities in intracellular Ca 2+ signals have been associated with impaired insulin secretion in both rodent and human pancreatic

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Neil W Salter, Sudharsana R Ande, Hoa K Nguyen, B L Grégoire Nyomba and Suresh Mishra

-stimulated insulin secretion (GSIS) and exhibit a phenotype similar to maturity onset diabetes of the young (MODY), a group of autosomal dominant, single-gene disorders that cause diabetes in young adults or children ( Bernassola et al . 2002 ). The genetic