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Ahter D Sanlioglu, Bahri Karacay, Mustafa Kemal Balci, Thomas S Griffith and Salih Sanlioglu

related to insulin secretion pathways rather than insulin sensitivity. As single-marker GWAS may generally overlook the potential interaction of multiple genes responsible for the development of disease phenotype, pathway-based GWAS analysis was conducted

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Narudee Kashemsant and Catherine B Chan

available for conversion of ADP to ATP ( Schrauwen & Hesselink 2002 ). Overexpression of UCP2 inhibits glucose-stimulated insulin secretion ( Chan et al. 1999 , 2001 , Hong et al. 2001 ), whereas its absence promotes enhanced insulin release ( Zhang

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Weijuan Shao, Vivian Szeto, Zhuolun Song, Lili Tian, Zhong-Ping Feng, M Cristina Nostro and Tianru Jin

INS-1 832/13. We have also compared the effect of adenovirus-mediated TCF7L2DN expression and siRNA-mediated Isl1 knockdown on β-cell gene expression, as well as high glucose (HG) and HG plus GLP-1 stimulated insulin secretion. Our observations have

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Qi Cheng, Violeta D Beltran, Stanley M H Chan, Jeremy R Brown, Alan Bevington and Terence P Herbert

Introduction The branched-chain amino acids (BCAA), leucine, isoleucine and valine, are essential amino acids that play an important role in glucose homeostasis. In vitro , leucine stimulates insulin secretion ( Newsholme et al. 2007 ) and

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S Lortz, S Lenzen and I Mehmeti

Forward: 5′-GCGTCCACCCGCGAGTACAA-3′ Reverse: 5′-TTGCAATGCCGGAGCCGTT-3′ Peptidylprolyl isomerase A (cyclophilin A) Ppia Forward: 5′-TTGCAGACGCCGCTGTCTCTT-3′ Reverse: 5′-TGGAACTTTGTCTGCAAACAGCTCG-3′ Quantification of glucose-induced insulin secretion

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Gerald Thiel, Isabelle Müller and Oliver G Rössler

channel activation and insulin secretion. TRPM2 is activated by H 2 O 2 and reactive oxygen species. Accordingly, TRPM2 function has been correlated with β-cell apoptosis ( Hara et al . 2002 ). TRPM2-deficient mice have higher basal glucose levels and an

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Zhipeng Li, Zhaoshui Shangguan, Yijie Liu, Jihua Wang, Xuejun Li, Shuyu Yang and Suhuan Liu

– the main form of β-cell death in the two forms of the disease ( Cnop et al . 2005 ). Current therapeutic approaches are mainly focused on increasing serum insulin levels by direct insulin administration or other agents that promote insulin secretion

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Eugenio D’Amico, Hongxiang Hui, Nasif Khoury, Umberto Di Mario and Riccardo Perfetti

impaired insulin secretion ( Patty et al. 2002 ) and β-cells apoptosis induced by the administration of immunosuppressive drugs (ISD) ( Drachenberg et al. 1999 ). For any type of immunossuppression after transplantation, a balance is sought

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Magdalene O Wilson, Kathleen T Scougall, Jarupa Ratanamart, Elizabeth A McIntyre and James A M Shaw

the muscle following plasmid injection ( Martinenghi et al. 2002 , Croze & Prud’homme 2003 ). Therapeutic applicability of this approach will be critically dependent on a mechanism for attaining regulated insulin secretion in addition to

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Kay E Garnett, Philip Chapman, Julie A Chambers, Ian D Waddell and David S W Boam

remain unknown. Chronic exposure to high glucose and elevated free fatty acid levels, observed in humans and in animal models of T2D is detrimental to β-cell function, resulting in blunted glucose-induced insulin secretion and increased levels of