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4161. Activation of insulin-reactive CD8 T-cells for development of autoimmune diabetes.
作者: F Susan Wong.;Lai Khai Siew.;Gwen Scott.;Ian J Thomas.;Stephen Chapman.;Christophe Viret.;Li Wen.
来源: Diabetes. 2009年58卷5期1156-64页
We have previously reported a highly diabetogenic CD8 T-cell clone, G9C8, in the nonobese diabetic (NOD) mouse, specific to low-avidity insulin peptide B15-23, and cells responsive to this antigen are among the earliest islet infiltrates. We aimed to study the selection, activation, and development of the diabetogenic capacity of these insulin-reactive T-cells.
4162. Accelerated postnatal growth increases lipogenic gene expression and adipocyte size in low-birth weight mice.
作者: Elvira Isganaitis.;Jose Jimenez-Chillaron.;Melissa Woo.;Alice Chow.;Jennifer DeCoste.;Martha Vokes.;Manway Liu.;Simon Kasif.;Ann-Marie Zavacki.;Rebecca L Leshan.;Martin G Myers.;Mary-Elizabeth Patti.
来源: Diabetes. 2009年58卷5期1192-200页
To characterize the hormonal milieu and adipose gene expression in response to catch-up growth (CUG), a growth pattern associated with obesity and diabetes risk, in a mouse model of low birth weight (LBW).
4163. Mechanisms of podocyte injury in diabetes: role of cytochrome P450 and NADPH oxidases.
作者: Assaad A Eid.;Yves Gorin.;Bridget M Fagg.;Rita Maalouf.;Jeffrey L Barnes.;Karen Block.;Hanna E Abboud.
来源: Diabetes. 2009年58卷5期1201-11页
We investigated the role of cytochrome P450 of the 4A family (CYP4A), its metabolites, and NADPH oxidases both in reactive oxygen species (ROS) production and apoptosis of podocytes exposed to high glucose and in OVE26 mice, a model of type 1 diabetes.
4164. Hyperglycemia induces a dynamic cooperativity of histone methylase and demethylase enzymes associated with gene-activating epigenetic marks that coexist on the lysine tail.
作者: Daniella Brasacchio.;Jun Okabe.;Christos Tikellis.;Aneta Balcerczyk.;Prince George.;Emma K Baker.;Anna C Calkin.;Michael Brownlee.;Mark E Cooper.;Assam El-Osta.
来源: Diabetes. 2009年58卷5期1229-36页
Results from the Diabetes Control Complications Trial (DCCT) and the subsequent Epidemiology of Diabetes Interventions and Complications (EDIC) Study and more recently from the U.K. Prospective Diabetes Study (UKPDS) have revealed that the deleterious end-organ effects that occurred in both conventional and more aggressively treated subjects continued to operate >5 years after the patients had returned to usual glycemic control and is interpreted as a legacy of past glycemia known as "hyperglycemic memory." We have hypothesized that transient hyperglycemia mediates persistent gene-activating events attributed to changes in epigenetic information.
4165. Loss-of-function mutation in myostatin reduces tumor necrosis factor alpha production and protects liver against obesity-induced insulin resistance.
Insulin resistance develops in tandem with obesity. Ablating myostatin (Mstn) prevents obesity, so we investigated if Mstn deficiency could improve insulin sensitivity. A loss-of-function mutation (Mstn(Ln)) in either one or both alleles of the Mstn gene shows how Mstn deficiency protects whole-body insulin sensitivity.
4166. Kinetics of GLUT4 trafficking in rat and human skeletal muscle.
作者: Håkan K R Karlsson.;Alexander V Chibalin.;Heikki A Koistinen.;Jing Yang.;Francoise Koumanov.;Harriet Wallberg-Henriksson.;Juleen R Zierath.;Geoffrey D Holman.
来源: Diabetes. 2009年58卷4期847-54页
In skeletal muscle, insulin stimulates glucose transport activity three- to fourfold, and a large part of this stimulation is associated with a net translocation of GLUT4 from an intracellular compartment to the cell surface. We examined the extent to which insulin or the AMP-activated protein kinase activator AICAR can lead to a stimulation of the exocytosis limb of the GLUT4 translocation pathway and thereby account for the net increase in glucose transport activity.
4167. Functional targets of the monogenic diabetes transcription factors HNF-1alpha and HNF-4alpha are highly conserved between mice and humans.
作者: Sylvia F Boj.;Joan Marc Servitja.;David Martin.;Martin Rios.;Iannis Talianidis.;Roderic Guigo.;Jorge Ferrer.
来源: Diabetes. 2009年58卷5期1245-53页
The evolutionary conservation of transcriptional mechanisms has been widely exploited to understand human biology and disease. Recent findings, however, unexpectedly showed that the transcriptional regulators hepatocyte nuclear factor (HNF)-1alpha and -4alpha rarely bind to the same genes in mice and humans, leading to the proposal that tissue-specific transcriptional regulation has undergone extensive divergence in the two species. Such observations have major implications for the use of mouse models to understand HNF-1alpha- and HNF-4alpha-deficient diabetes. However, the significance of studies that assess binding without considering regulatory function is poorly understood.
4168. High glucose suppresses epidermal growth factor receptor/phosphatidylinositol 3-kinase/Akt signaling pathway and attenuates corneal epithelial wound healing.
Patients with diabetes are at an increased risk for developing corneal complications and delayed wound healing. This study investigated the effects of high glucose on epidermal growth factor receptor (EGFR) signaling and on epithelial wound healing in the cornea.
4169. Do non-HLA genes influence development of persistent islet autoimmunity and type 1 diabetes in children with high-risk HLA-DR,DQ genotypes?
作者: Andrea K Steck.;Weiming Zhang.;Teodorica L Bugawan.;Katherine J Barriga.;Alan Blair.;Henry A Erlich.;George S Eisenbarth.;Jill M Norris.;Marian J Rewers.
来源: Diabetes. 2009年58卷4期1028-33页
Specific alleles of non-HLA genes INS, CTLA-4, and PTPN22 have been associated with type 1 diabetes. We examined whether some of these alleles influence development of islet autoimmunity or progression from persistent islet autoimmunity to type 1 diabetes in children with high-risk HLA-DR,DQ genotypes.
4170. Breast-feeding modifies the association of PPARgamma2 polymorphism Pro12Ala with growth in early life: the Generation R Study.
作者: Dennis O Mook-Kanamori.;Eric A P Steegers.;Andre G Uitterlinden.;Henriëtte A Moll.;Cornelia M van Duijn.;Albert Hofman.;Vincent W V Jaddoe.
来源: Diabetes. 2009年58卷4期992-8页
We examined whether the PPARgamma2 Ala12 allele influences growth in early life and whether this association is modified by breast-feeding.
4171. Prenatal stress or high-fat diet increases susceptibility to diet-induced obesity in rat offspring.
作者: Kellie L K Tamashiro.;Chantelle E Terrillion.;Jayson Hyun.;James I Koenig.;Timothy H Moran.
来源: Diabetes. 2009年58卷5期1116-25页
Perturbations to the prenatal environment have been associated with the development of adult chronic disease, findings that gave rise to the "Barker Hypothesis" or the "developmental origins of adult disease" concept. In this study, we used an animal model to determine the metabolic consequences of maternal prenatal stress and high-fat feeding on the developing offspring.
4172. Liver-specific loss of lipolysis-stimulated lipoprotein receptor triggers systemic hyperlipidemia in mice.
作者: Prachiti Narvekar.;Mauricio Berriel Diaz.;Anja Krones-Herzig.;Ulrike Hardeland.;Daniela Strzoda.;Sigrid Stöhr.;Marcus Frohme.;Stephan Herzig.
来源: Diabetes. 2009年58卷5期1040-9页
In mammals, proper storage and distribution of lipids in and between tissues is essential for the maintenance of energy homeostasis. In contrast, aberrantly high levels of triglycerides in the blood ("hypertriglyceridemia") represent a hallmark of the metabolic syndrome and type 2 diabetes. As hypertriglyceridemia has been identified as an important risk factor for cardiovascular complications, in this study we aimed to identify molecular mechanisms in aberrant triglyceride elevation under these conditions.
4173. Protective effect of perindopril on diabetic retinopathy is associated with decreased vascular endothelial growth factor-to-pigment epithelium-derived factor ratio: involvement of a mitochondria-reactive oxygen species pathway.
作者: Zhi Zheng.;Haibing Chen.;Genjie Ke.;Ying Fan.;Haidong Zou.;Xiaodong Sun.;Qing Gu.;Xun Xu.;Patrick C P Ho.
来源: Diabetes. 2009年58卷4期954-64页
This study aimed to verify whether the decreased vascular endothelial growth factor (VEGF)-to-pigment epithelium-derived factor (PEDF) ratio can serve as an indicator for the protective effect of angiotensin-converting enzyme inhibitors (ACEIs) on diabetic retinopathy (DR) and to investigate the role of mitochondrial reactive oxygen species (ROS) in the downregulated VEGF-to-PEDF ratio.
4174. Weight loss may reverse blunted sympathetic neural responsiveness to glucose ingestion in obese subjects with metabolic syndrome.
作者: Nora E Straznicky.;Gavin W Lambert.;Mariee T McGrane.;Kazuko Masuo.;Tye Dawood.;Paul J Nestel.;Nina Eikelis.;Markus P Schlaich.;Murray D Esler.;Florentia Socratous.;Reena Chopra.;Elisabeth A Lambert.
来源: Diabetes. 2009年58卷5期1126-32页
The purpose of this study was to examine the effects of weight loss on sympathetic nervous system responsiveness to glucose ingestion in obese subjects with metabolic syndrome, in whom such responses are reportedly blunted.
4175. Interleukin-6 attenuates insulin-mediated increases in endothelial cell signaling but augments skeletal muscle insulin action via differential effects on tumor necrosis factor-alpha expression.
作者: Derek Y C Yuen.;Renee M Dwyer.;Vance B Matthews.;Lei Zhang.;Brian G Drew.;Bronwyn Neill.;Bronwyn A Kingwell.;Michael G Clark.;Stephen Rattigan.;Mark A Febbraio.
来源: Diabetes. 2009年58卷5期1086-95页
The cytokine interleukin-6 (IL-6) stimulates AMP-activated protein kinase (AMPK) and insulin signaling in skeletal muscle, both of which result in the activation of endothelial nitric oxide synthase (eNOS). We hypothesized that IL-6 promotes endothelial cell signaling and capillary recruitment in vivo, contributing to increased glucose uptake.
4176. Specific local cardiovascular changes of Nepsilon-(carboxymethyl)lysine, vascular endothelial growth factor, and Smad2 in the developing embryos coincide with maternal diabetes-induced congenital heart defects.
作者: Pauline A M Roest.;Daniël G M Molin.;Casper G Schalkwijk.;Liesbeth van Iperen.;Parri Wentzel.;Ulf J Eriksson.;Adriana C Gittenberger-de Groot.
来源: Diabetes. 2009年58卷5期1222-8页
Embryos exposed to a diabetic environment in utero have an increased risk to develop congenital heart malformations. The mechanism behind the teratogenicity of diabetes still remains enigmatic. Detrimental effects of glycation products in diabetic patients have been well documented. We therefore studied a possible link between glycation products and the development of congenital cardiovascular malformations. Furthermore, we investigated other possible mechanisms involved in this pathogenesis: alterations in the levels of vascular endothelial growth factor (VEGF) or phosphorylated Smad2 (the latter can be induced by both glycation products and VEGF).
4177. MicroRNAs induced during adipogenesis that accelerate fat cell development are downregulated in obesity.
We investigated the regulation and involvement of microRNAs (miRNAs) in fat cell development and obesity.
4178. Munc18c depletion selectively impairs the sustained phase of insulin release.
The Sec1/Munc18 protein Munc18c has been implicated in Syntaxin 4-mediated exocytosis events, although its purpose in exocytosis has remained elusive. Given that Syntaxin 4 functions in the second phase of glucose-stimulated insulin secretion (GSIS), we hypothesized that Munc18c would also be required and sought insight into the possible mechanism(s) using the islet beta-cell as a model system.
4179. Imatinib mesylate reduces endoplasmic reticulum stress and induces remission of diabetes in db/db mice.
作者: Myoung Sook Han.;Kun Wook Chung.;Hyae Gyeong Cheon.;Sang Dal Rhee.;Chang-Hwan Yoon.;Moon-Kyu Lee.;Kwang-Won Kim.;Myung-Shik Lee.
来源: Diabetes. 2009年58卷2期329-36页
Imatinib has been reported to induce regression of type 2 diabetes in chronic leukemia patients. However, the mechanism of diabetes amelioration by imatinib is unknown, and it is uncertain whether imatinib has effects on type 2 diabetes itself without other confounding diseases like leukemia. We studied the effect of imatinib on diabetes in db/db mice and investigated possible mechanism's underlying improved glycemic control by imatinib.
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