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R Buettner, K G Parhofer, M Woenckhaus, C E Wrede, L A Kunz-Schughart, J Schölmerich, and L C Bollheimer

the column than short-chain fatty acids or unsaturated fatty acids. Internal standards are used for identification and quantification. Insulin secretion analysis from pancreatic islets ex vivo Pancreatic islets were

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Holger Steinbrenner, Anna-Lena Hotze, Bodo Speckmann, Antonio Pinto, Helmut Sies, Matthias Schott, Margret Ehlers, Werner A Scherbaum, and Sven Schinner

Introduction Insulin resistance is a hallmark in the pathogenesis of type 2 diabetes mellitus (T2DM). Pancreatic β-cells have the capacity to compensate for insulin resistance by a reactive increase in insulin secretion over a long period. However

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Inês Cebola and Lorenzo Pasquali

most prevalent form accounting for >90% of all causes of diabetes. T2D is characterized by decreased insulin sensitivity and defective insulin secretion. The resulting elevated blood glucose levels eventually lead to microvascular damage, making T2D a

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Qingling Huang, Elena Timofeeva, and Denis Richard

(VMH). Numerous data argue for a role of the VMH in control of FI and insulin secretion ( King et al. 1984 , Dube et al. 1999 ). There is evidence that the CRF 2 R is responsible for the anorectic effects of CRF ( Vaughan et al. 1995 ). The CRF 2

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Jan Christiansen, Astrid M Kolte, Thomas v O Hansen, and Finn C Nielsen

glucose response and insulin secretion. Both processes are influenced by a series of different pathways under control of both environmental and genetic factors (for review see Kahn 1994 ). Among these, physical inactivity, obesity, the gut microbiome and

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Sushi Jiang, Hening Zhai, Danjie Li, Jiana Huang, Heng Zhang, Ziru Li, Weizhen Zhang, and Geyang Xu

mechanisms ( Baggio & Drucker 2007 ). Postprandial GLP1 levels peak within 15–30 min of nutrient consumption. GLP1, a potent antihyperglycemic hormone, induces glucose-dependent stimulation of insulin secretion, whereas suppresses glucagon secretion

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Marie Schaeffer, David J Hodson, Chrystel Lafont, and Patrice Mollard

.3883490 . Kjems LL Ravier MA Jonas JC Henquin JC 2002 Do oscillations of insulin secretion occur in the absence of cytoplasmic Ca 2+ oscillations in beta-cells? Diabetes 51 ( Suppl 1 ) S177 – S182 . doi:10.2337/diabetes.51.2007.S177

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Kenichi Kanai, Shinsaku Aramata, Sayo Katakami, Kunio Yasuda, and Kohsuke Kataoka

et al . 2006 , Wang et al . 2007 ). In Mafa knockout mice, islets are normal at birth, but β-cells exhibit a deficiency in glucose-stimulated insulin secretion over time and show progressive degeneration by 8–12 weeks of age ( Zhang et al . 2005

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Kira Meyerovich, Fernanda Ortis, and Alessandra K Cardozo

activation of the non-canonical pathway in islets leading to p52 and RelB expression and impaired insulin secretion (adapted from Meyerovich et al . (2016 a ) ). βTrCP, beta-transducin repeats-containing protein; IL-1β, interleukin-1β; IκB, inhibitory κB

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Marija Trajkovic-Arsic, Evdokia Kalideris, and Jens T Siveke

the autocrine regulation of insulin secretion. Early mouse studies demonstrated that a β-cell-specific IR knockout leads to development of progressive glucose intolerance, smaller islets, and decreased insulin content as well as a delay in acute