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Nguyen Khanh Hoa, Åke Norberg, Rannar Sillard, Dao Van Phan, Nguyen Duy Thuan, Dang Thi Ngoc Dzung, Hans Jörnvall, and Claes-Göran Östenson

-cell K-ATP channel (DeFronzo1999, Brown et al. 2004 ). Glucose-stimulated biphasic insulin secretion involves at least two signaling pathways, the K-ATP channel-dependent and K-ATP channel-independent pathways respectively ( Chow et al. 1995

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Min Joo Kim, Se Hee Min, Seon Young Shin, Mi Na Kim, Hakmo Lee, Jin Young Jang, Sun-Whe Kim, Kyong Soo Park, and Hye Seung Jung

, they were reported to be slightly glucose intolerant ( Harding et al . 2001 ); however, Wang and coworkers found that Perk +/− mice exhibited enhanced insulin secretion during neonatal and juvenile development, resulting in a transient reduction in

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Brit H Boehmer, Peter R Baker II, Laura D Brown, Stephanie R Wesolowski, and Paul J Rozance

Introduction Metabolism of nutrients by the β-cell in the pancreatic islet is key to nutrient-stimulated insulin secretion. This is described by the fuel-mediated hypothesis of insulin release ( Malaisse et al. 1979 ). The fuel

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Bethany P Cummings, Andrew A Bremer, Timothy J Kieffer, David D'Alessio, and Peter J Havel

hyperinsulinemia ( Karlsson et al . 2001 , Nicod et al . 2003 ), which is supported by both clinical studies in humans and studies in rodents demonstrating marked increases in glucose-stimulated insulin secretion during short-term glucocorticoid treatment

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Hideyuki Takahashi, Yohei Kurose, Muneyuki Sakaida, Yoshihiro Suzuki, Shigeki Kobayashi, Toshihisa Sugino, Masayasu Kojima, Kenji Kangawa, Yoshihisa Hasegawa, and Yoshiaki Terashima

role in the regulation of pancreatic insulin secretion. Some studies in rats show that ghrelin stimulates insulin secretion in vivo ( Lee et al. 2002 ) and in vitro ( Date et al. 2002 , Adeghate & Ponery 2002 ). Others show that ghrelin

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F J Steyn, T Y Xie, L Huang, S T Ngo, J D Veldhuis, M J Waters, and C Chen

pulsatile GH secretion and body weight, epididymal fat mass, and circulating levels of leptin and insulin. Parameters of pulsatile GH secretion did not change relative to circulating levels of NEFAs or glucose. We conclude that impaired pulsatile GH

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Salvatore P Mangiafico, Shueh H Lim, Sandra Neoh, Helene Massinet, Christos N Joannides, Joseph Proietto, Sofianos Andrikopoulos, and Barbara C Fam

Introduction Type 2 diabetes (T2D) is characterised by glucose intolerance that is contributed to by both defects in insulin action (in liver and muscle/fat) and insulin secretion. Whether defects in both insulin action and secretion are necessary

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Muhammed Yusuf Ali, Matthew Whiteman, Chian-Ming Low, and Philip K Moore

, Ashcroft & Gribble 1998 ). K ATP channels are therefore crucial in this pathway since they act to link metabolic state of the cell with insulin secretion. Reduced insulin secretion and/or insulin sensitivity results in diabetes mellitus; a complex disease

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Astrid C Hauge-Evans, James Bowe, Zara J Franklin, Zoheb Hassan, and Peter M Jones

identified (reviewed by Moller et al . (2003) ). In pancreatic islets, receptors have been identified on both α- and β-cells ( Strowski et al . 2000 , Cejvan et al . 2003 ) and exogenously administered SST inhibits both insulin and glucagon secretion

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T S McQuaid, M C Saleh, J W Joseph, A Gyulkhandanyan, J E Manning-Fox, J D MacLellan, M B Wheeler, and C B Chan

Introduction Previously, uncoupling protein-2 (UCP2) was identified in islets and shown to be a negative regulator of insulin secretion ( Chan et al. 1999 , 2001 , Hong et al. 2001 , Zhang et al. 2001 ). Ucp2 mRNA and