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4141. Development of selective axonopathy in adult sensory neurons isolated from diabetic rats: role of glucose-induced oxidative stress.
作者: Elena Zherebitskaya.;Eli Akude.;Darrell R Smith.;Paul Fernyhough.
来源: Diabetes. 2009年58卷6期1356-64页
Reactive oxygen species (ROS) are pro-oxidant factors in distal neurodegeneration in diabetes. We tested the hypothesis that sensory neurons exposed to type 1 diabetes would exhibit enhanced ROS and oxidative stress and determined whether this stress was associated with abnormal axon outgrowth.
4142. Genetic variation in KCNQ1 associates with fasting glucose and beta-cell function: a study of 3,734 subjects comprising three ethnicities living in Singapore.
作者: Jonathan T Tan.;Siti Nurbaya.;Daphne Gardner.;Sandra Ye.;E Shyong Tai.;Daniel P K Ng.
来源: Diabetes. 2009年58卷6期1445-9页
The potassium voltage-gated channel, KQT-like subfamily, member 1 (KCNQ1) has been found through a genome-wide association study to be a strong candidate for conferring susceptibility to type 2 diabetes in East Asian and European populations. Our objective was to describe the association between polymorphisms at the KCNQ1 locus with insulin resistance, beta-cell function, and other type 2 diabetes-related traits in a sample of Chinese, Malays, and Asian Indians living in Singapore.
4143. Genome-wide association scan for diabetic nephropathy susceptibility genes in type 1 diabetes.
作者: Marcus G Pezzolesi.;G David Poznik.;Josyf C Mychaleckyj.;Andrew D Paterson.;Michelle T Barati.;Jon B Klein.;Daniel P K Ng.;Grzegorz Placha.;Luis H Canani.;Jacek Bochenski.;Daryl Waggott.;Michael L Merchant.;Bozena Krolewski.;Lucia Mirea.;Krzysztof Wanic.;Pisut Katavetin.;Masahiko Kure.;Pawel Wolkow.;Jonathon S Dunn.;Adam Smiles.;William H Walker.;Andrew P Boright.;Shelley B Bull.; .;Alessandro Doria.;John J Rogus.;Stephen S Rich.;James H Warram.;Andrzej S Krolewski.
来源: Diabetes. 2009年58卷6期1403-10页
Despite extensive evidence for genetic susceptibility to diabetic nephropathy, the identification of susceptibility genes and their variants has had limited success. To search for genes that contribute to diabetic nephropathy, a genome-wide association scan was implemented on the Genetics of Kidneys in Diabetes collection.
4144. Interrogating type 2 diabetes genome-wide association data using a biological pathway-based approach.
作者: John R B Perry.;Mark I McCarthy.;Andrew T Hattersley.;Eleftheria Zeggini.; .;Michael N Weedon.;Timothy M Frayling.
来源: Diabetes. 2009年58卷6期1463-7页
Recent genome-wide association studies have resulted in a dramatic increase in our knowledge of the genetic loci involved in type 2 diabetes. In a complementary approach to these single-marker studies, we attempted to identify biological pathways associated with type 2 diabetes. This approach could allow us to identify additional risk loci.
4149. Age-dependent decline in beta-cell proliferation restricts the capacity of beta-cell regeneration in mice.
作者: Shuen-Ing Tschen.;Sangeeta Dhawan.;Tatyana Gurlo.;Anil Bhushan.
来源: Diabetes. 2009年58卷6期1312-20页
The aim of this study was to elucidate whether age plays a role in the expansion or regeneration of beta-cell mass.
4150. Dynamic changes in pancreatic endocrine cell abundance, distribution, and function in antigen-induced and spontaneous autoimmune diabetes.
作者: Klaus Pechhold.;Xiaolong Zhu.;Victor S Harrison.;Janet Lee.;Sagarika Chakrabarty.;Kerstin Koczwara.;Oksana Gavrilova.;David M Harlan.
来源: Diabetes. 2009年58卷5期1175-84页
Insulin deficiency in type 1 diabetes and in rodent autoimmune diabetes models is caused by beta-cell-specific killing by autoreactive T-cells. Less is known about beta-cell numbers and phenotype remaining at diabetes onset and the fate of other pancreatic endocrine cellular constituents.
4151. Genetic variation in the multidrug and toxin extrusion 1 transporter protein influences the glucose-lowering effect of metformin in patients with diabetes: a preliminary study.
作者: Matthijs L Becker.;Loes E Visser.;Ron H N van Schaik.;Albert Hofman.;André G Uitterlinden.;Bruno H Ch Stricker.
来源: Diabetes. 2009年58卷3期745-9页
Metformin, an oral glucose-lowering drug, is taken up in hepatocytes by the organic cation transporter (OCT) 1 and in renal epithelium by OCT2. In these cells, the multidrug and toxin extrusion (MATE) 1 protein, encoded by the SLC47A1 gene, is responsible for the excretion of metformin into the bile and urine, respectively. We studied the effect of single nucleotide polymorphisms (SNPs) in the SLC47A1 gene on the A1C-lowering effect of metformin.
4152. Type 2 diabetes risk alleles are associated with reduced size at birth.
作者: Rachel M Freathy.;Amanda J Bennett.;Susan M Ring.;Beverley Shields.;Christopher J Groves.;Nicholas J Timpson.;Michael N Weedon.;Eleftheria Zeggini.;Cecilia M Lindgren.;Hana Lango.;John R B Perry.;Anneli Pouta.;Aimo Ruokonen.;Elina Hyppönen.;Chris Power.;Paul Elliott.;David P Strachan.;Marjo-Riitta Järvelin.;George Davey Smith.;Mark I McCarthy.;Timothy M Frayling.;Andrew T Hattersley.
来源: Diabetes. 2009年58卷6期1428-33页
Low birth weight is associated with an increased risk of type 2 diabetes. The mechanisms underlying this association are unknown and may represent intrauterine programming or two phenotypes of one genotype. The fetal insulin hypothesis proposes that common genetic variants that reduce insulin secretion or action may predispose to type 2 diabetes and also reduce birth weight, since insulin is a key fetal growth factor. We tested whether common genetic variants that predispose to type 2 diabetes also reduce birth weight.
4153. Changes in insulin sensitivity and insulin release in relation to glycemia and glucose tolerance in 6,414 Finnish men.
作者: Alena Stancáková.;Martin Javorský.;Teemu Kuulasmaa.;Steven M Haffner.;Johanna Kuusisto.;Markku Laakso.
来源: Diabetes. 2009年58卷5期1212-21页
We evaluated insulin sensitivity and insulin secretion across the entire range of fasting (FPG) and 2-h plasma glucose (PG), and we investigated the differences in insulin sensitivity and insulin release in different glucose tolerance categories.
4154. Degradation of cAMP-responsive element-binding protein by the ubiquitin-proteasome pathway contributes to glucotoxicity in beta-cells and human pancreatic islets.
作者: Safia Costes.;Brigitte Vandewalle.;Cécile Tourrel-Cuzin.;Christophe Broca.;Nathalie Linck.;Gyslaine Bertrand.;Julie Kerr-Conte.;Bernard Portha.;François Pattou.;Joel Bockaert.;Stéphane Dalle.
来源: Diabetes. 2009年58卷5期1105-15页
In type 2 diabetes, chronic hyperglycemia is detrimental to beta-cells, causing apoptosis and impaired insulin secretion. The transcription factor cAMP-responsive element-binding protein (CREB) is crucial for beta-cell survival and function. We investigated whether prolonged exposure of beta-cells to high glucose affects the functional integrity of CREB.
4155. Genetic deficiency of Itgb2 or ItgaL prevents autoimmune diabetes through distinctly different mechanisms in NOD/LtJ mice.
作者: John D Glawe.;D Ross Patrick.;Meng Huang.;Christopher D Sharp.;Shayne C Barlow.;Christopher G Kevil.
来源: Diabetes. 2009年58卷6期1292-301页
Insulitis is an important pathological feature of autoimmune diabetes; however, mechanisms governing the recruitment of diabetogenic T-cells into pancreatic islets are poorly understood. Here, we determined the importance of leukocyte integrins beta(2)(Itgb2) and alphaL (ItgaL) in developing insulitis and frank diabetes.
4156. Medium-chain fatty acids improve cognitive function in intensively treated type 1 diabetic patients and support in vitro synaptic transmission during acute hypoglycemia.
作者: Kathleen A Page.;Anne Williamson.;Namyi Yu.;Ewan C McNay.;James Dzuira.;Rory J McCrimmon.;Robert S Sherwin.
来源: Diabetes. 2009年58卷5期1237-44页
We examined whether ingestion of medium-chain triglycerides could improve cognition during hypoglycemia in subjects with intensively treated type 1 diabetes and assessed potential underlying mechanisms by testing the effect of beta-hydroxybutyrate and octanoate on rat hippocampal synaptic transmission during exposure to low glucose.
4157. Muscle microvascular dysfunction in central obesity is related to muscle insulin insensitivity but is not reversed by high-dose statin treatment.
作者: Geraldine F Clough.;Magdalena Turzyniecka.;Lara Walter.;Andrew J Krentz.;Sarah H Wild.;Andrew J Chipperfield.;John Gamble.;Christopher D Byrne.
来源: Diabetes. 2009年58卷5期1185-91页
To test the hypotheses that decreased insulin-mediated glucose disposal in muscle is associated with a reduced muscle microvascular exchange capacity (Kf) and that 6 months of high-dose statin therapy would improve microvascular function in people with central obesity.
4158. Interleukin-21 is required for the development of type 1 diabetes in NOD mice.
作者: Andrew P R Sutherland.;Tom Van Belle.;Andrea L Wurster.;Akira Suto.;Monia Michaud.;Dorothy Zhang.;Michael J Grusby.;Matthias von Herrath.
来源: Diabetes. 2009年58卷5期1144-55页
Interleukin (IL)-21 is a type 1 cytokine that has been implicated in the pathogenesis of type 1 diabetes via the unique biology of the nonobese diabetic (NOD) mouse strain. The aim of this study was to investigate a causal role for IL-21 in type 1 diabetes.
4159. GPR119 is essential for oleoylethanolamide-induced glucagon-like peptide-1 secretion from the intestinal enteroendocrine L-cell.
Intestinal L-cells secrete the incretin glucagon-like peptide-1 (GLP-1) in response to ingestion of nutrients, especially long-chain fatty acids. The Galphas-coupled receptor GPR119 binds the long-chain fatty acid derivate oleoylethanolamide (OEA), and GPR119 agonists enhance GLP-1 secretion. We therefore hypothesized that OEA stimulates GLP-1 release through a GPR119-dependent mechanism.
4160. Inhibition of contraction-stimulated AMP-activated protein kinase inhibits contraction-stimulated increases in PAS-TBC1D1 and glucose transport without altering PAS-AS160 in rat skeletal muscle.
Phosphorylation of two members of the TBC1 domain family of proteins, Akt substrate of 160 kDa (AS160, also known as TBC1D4) and TBC1D1, has been implicated in the regulation of glucose transport in skeletal muscle. Insulin-stimulated phosphorylation (measured using the phospho-Akt substrate [PAS] antibody) of AS160 and TBC1D1 appears to occur in an Akt-dependent manner, but the kinases responsible for contraction-stimulated PAS-AS160 and PAS-TBC1D1 remain unclear. AMP-activated protein kinase (AMPK) and Akt, both activated by contraction, can each phosphorylate AS160 and TBC1D1 in cell-free assays.
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