CS Olofsson, S Collins, M Bengtsson, L Eliasson, A … - Diabetes, 2007 - Am Diabetes Assoc Mouse β-cells cultured at 15 mmol/l glucose for 72 h had reduced ATP-sensitive K + (K ATP )
channel activity (−30%), increased voltage-gated Ca 2+ currents, higher intracellular free Ca
2+ concentration ([Ca 2+ ] i ; +160%), more exocytosis (monitored by capacitance ... Cited by 10 - Related articles - BL Direct - All 5 versions
- ►duke.edu [PDF] CT Ferrara - dukespace.lib.duke.edu Page 1. Metabolic Pathways of Type 2 Diabetes Intersection of Genetics, Transcriptomics,
and Metabolite Profiling by Christine Therese Ferrara Department of Pharmacology
and Cancer Biology Duke University Date:_____ Approved: ... Related articles - View as HTML - All 3 versions
E Renström, P Rorsman - Pancreatic Beta Cell in Health and Disease, 2007 - Springer Summary. Insulin is stored in secretory granules within the pancreatic beta cell. The release
of insulin requires the fusion of the secretory granule with the plasma membrane and the discharge
of the granule contents into the extracellular space. Insulin secretion follows a ... Related articles - All 2 versions
周晓磊， 陈玉涛， 薛承锐 - 中国老年保健医学, 2009 - journal.shouxi.net 【Abstract】 Objective To observe the proteic expression of pancreatic KATP channels SUR1 in
diabetes rats，and the Intervention of nateglinide and Danshensu on the changes. Methods Wistar
rats were fed high glucose/fat feedstuff and injected STZ into vena caudalis to induce ... Related articles - Cached - All 3 versions
C Soekmadji, P Thorn - Proceedings of the Australian Physiological Society, 2009 - apps.org.au 2. In the classical model of secretion each fused vesicle releases the entirety of its content in
an all-or-none manner. In this way the secretory output of a cell is controlled by regulating the
numbers of fused vesicles. The realization that post-fusion events can control secretory ... Related articles - Cached - All 3 versions
V Poitout - Current Opinion in Endocrinology, Diabetes and …, 2002 - journals.lww.com Fatty acids have positive and negative effects on pancreatic β-cell function. In the short term,
they act as potentiators of insulin release, whereas in the long term, they impair insulin
secretion. The metabolic fate of fatty acids in the β-cell is determined by the concomitant ... Cited by 12 - Related articles - BL Direct - All 3 versions
G Fontés, M Semache, DK Hagman, C Tremblay, R … - Diabetes, 2009 - ncbi.nlm.nih.gov Objective: Prolonged exposure of pancreatic beta cells to simultaneously elevated levels of fatty
acids and glucose (glucolipotoxicity) impairs insulin gene transcription. However, the intracellular
signalling pathways mediating these effects are mostly unknown. This study was aimed to ... Cited by 1 - Related articles - All 3 versions
J Cantley, JG Burchfield, GL Pearson, C Schmitz- … - Diabetes, 2009 - Am Diabetes Assoc Results: The enhanced GSIS could not be explained by increased expression of another PKC
isoform or by alterations in glucose stimulated Ca 2+ influx. Instead an up-regulation of the amplifying
pathways of GSIS in lipid-cultured PKCεKO β-cells was revealed under conditions in ... Cited by 2 - Related articles - All 3 versions
- ►nih.gov C Evans-Molina, RD Robbins, T Kono, SA … - Molecular and Cellular …, 2009 - Am Soc Microbiol The nuclear receptor peroxisome proliferator-activated receptor (PPAR- ) is an important target
in diabetes therapy, but its direct role, if any, in the restoration of islet function has remained
controversial. To identify potential molecular mechanisms of PPAR- in the islet, we treated ... Cited by 2 - Related articles - All 4 versions
