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4221. Postnatal expansion of the pancreatic beta-cell mass is dependent on survivin.
作者: Yuying Jiang.;Wataru Nishimura.;Deborah Devor-Henneman.;Donna Kusewitt.;Haijuan Wang.;Michael P Holloway.;Takehiko Dohi.;Edmond Sabo.;Michael L Robinson.;Dario C Altieri.;Arun Sharma.;Rachel A Altura.
来源: Diabetes. 2008年57卷10期2718-27页
Diabetes results from a deficiency of functional beta-cells due to both an increase in beta-cell death and an inhibition of beta-cell replication. The molecular mechanisms responsible for these effects in susceptible individuals are mostly unknown. The objective of this study was to determine whether a gene critical for cell division and cell survival in cancer cells, survivin, might also be important for beta-cells.
4222. FTO variants are associated with obesity in the Chinese and Malay populations in Singapore.
作者: Jonathan T Tan.;Rajkumar Dorajoo.;Mark Seielstad.;Xue Ling Sim.;Rick Twee-Hee Ong.;Kee Seng Chia.;Tien Yin Wong.;Seang Mei Saw.;Suok Kai Chew.;Tin Aung.;E-Shyong Tai.
来源: Diabetes. 2008年57卷10期2851-7页
Association between genetic variants at the FTO locus and obesity has been consistently observed in populations of European ancestry and inconsistently in non-Europeans. The aim of this study was to examine the effects of FTO variants on obesity and type 2 diabetes in Southeast Asian populations.
4223. Potent inhibition of cicatricial contraction in proliferative vitreoretinal diseases by statins.
作者: Shuhei Kawahara.;Yasuaki Hata.;Takeshi Kita.;Ryoichi Arita.;Muneki Miura.;Shintaro Nakao.;Yasutaka Mochizuki.;Hiroshi Enaida.;Tadahisa Kagimoto.;Yoshinobu Goto.;Ali Hafezi-Moghadam.;Tatsuro Ishibashi.
来源: Diabetes. 2008年57卷10期2784-93页
Despite tremendous progress in vitreoretinal surgery, certain postsurgical complications limit the success in the treatment of proliferative vitreoretinal diseases (PVDs), such as proliferative diabetic retinopathy (PDR) and proliferative vitreoretinopathy (PVR). One of the most significant complications is the cicatricial contraction of proliferative membranes, resulting in tractional retinal detachment and severe vision loss. Novel pharmaceutical approaches are thus urgently needed for the management of these vision-threatening diseases. In the current study, we investigated the inhibitory effects of statins on the progression of PVDs.
4224. Correction of HDL dysfunction in individuals with diabetes and the haptoglobin 2-2 genotype.
作者: Rabea Asleh.;Shany Blum.;Shiri Kalet-Litman.;Jonia Alshiek.;Rachel Miller-Lotan.;Roy Asaf.;Wasseem Rock.;Michael Aviram.;Uzi Milman.;Chen Shapira.;Zaid Abassi.;Andrew P Levy.
来源: Diabetes. 2008年57卷10期2794-800页
Pharmacogenomics is a key component of personalized medicine. The Israel Cardiovascular Events Reduction with Vitamin E Study, a prospective placebo-controlled study, recently demonstrated that vitamin E could dramatically reduce CVD in individuals with diabetes and the haptoglobin (Hp) 2-2 genotype (40% of diabetic individuals). However, because of the large number of clinical trials that failed to demonstrate benefit from vitamin E coupled with the lack of a mechanistic explanation for why vitamin E should be beneficial only in diabetic individuals with the Hp 2-2 genotype, enthusiasm for this pharmacogenomic paradigm has been limited. In this study, we sought to provide such a mechanistic explanation based on the hypothesis that the Hp 2-2 genotype and diabetes interact to promote HDL oxidative modification and dysfunction.
4225. Distinct monocyte gene-expression profiles in autoimmune diabetes.
作者: Roos C Padmos.;Nanette C Schloot.;Huriya Beyan.;Cindy Ruwhof.;Frank J T Staal.;Dick de Ridder.;Henk-Jan Aanstoot.;Wai Kwan Lam-Tse.;Harm de Wit.;Christian de Herder.;Roos C Drexhage.;Barbara Menart.;R David Leslie.;Hemmo A Drexhage.; .
来源: Diabetes. 2008年57卷10期2768-73页
There is evidence that monocytes of patients with type 1 diabetes show proinflammatory activation and disturbed migration/adhesion, but the evidence is inconsistent. Our hypothesis is that monocytes are distinctly activated/disturbed in different subforms of autoimmune diabetes.
4226. Evaluating the role of LPIN1 variation in insulin resistance, body weight, and human lipodystrophy in U.K. Populations.
作者: Katherine A Fawcett.;Neil Grimsey.;Ruth J F Loos.;Eleanor Wheeler.;Allan Daly.;Maria Soos.;Robert Semple.;Holly Syddall.;Cyrus Cooper.;Symeon Siniossoglou.;Stephen O'Rahilly.;Nicholas J Wareham.;Inês Barroso.
来源: Diabetes. 2008年57卷9期2527-33页
Loss of lipin 1 activity causes lipodystrophy and insulin resistance in the fld mouse, and LPIN1 expression and common genetic variation were recently suggested to influence adiposity and insulin sensitivity in humans. We aimed to conduct a comprehensive association study to clarify the influence of common LPIN1 variation on adiposity and insulin sensitivity in U.K. populations and to examine the role of LPIN1 mutations in insulin resistance syndromes.
4227. Physical activity and insulin sensitivity: the RISC study.
作者: Beverley Balkau.;Leila Mhamdi.;Jean-Michel Oppert.;John Nolan.;Alain Golay.;Francesca Porcellati.;Markku Laakso.;Ele Ferrannini.; .
来源: Diabetes. 2008年57卷10期2613-8页
Physical activity is a modifiable risk factor for type 2 diabetes, partly through its action on insulin sensitivity. We report the relation between insulin sensitivity and physical activity measured by accelerometry.
4228. miR-375 targets 3'-phosphoinositide-dependent protein kinase-1 and regulates glucose-induced biological responses in pancreatic beta-cells.
作者: Abdelfattah El Ouaamari.;Nadine Baroukh.;Geert A Martens.;Patricia Lebrun.;Daniel Pipeleers.;Emmanuel van Obberghen.
来源: Diabetes. 2008年57卷10期2708-17页
MicroRNAs are short, noncoding RNAs that regulate gene expression. We hypothesized that the phosphatidylinositol 3-kinase (PI 3-kinase) cascade known to be important in beta-cell physiology could be regulated by microRNAs. Here, we focused on the pancreas-specific miR-375 as a potential regulator of its predicted target 3'-phosphoinositide-dependent protein kinase-1 (PDK1), and we analyzed its implication in the response of insulin-producing cells to elevation of glucose levels.
4229. Cytokine-induced beta-cell death is independent of endoplasmic reticulum stress signaling.
作者: Mia C Akerfeldt.;Jennifer Howes.;Jeng Yie Chan.;Veronica A Stevens.;Nacer Boubenna.;Helen M McGuire.;Cecile King.;Trevor J Biden.;D Ross Laybutt.
来源: Diabetes. 2008年57卷11期3034-44页
Cytokines contribute to beta-cell destruction in type 1 diabetes. Endoplasmic reticulum (ER) stress-mediated apoptosis has been proposed as a mechanism for beta-cell death. We tested whether ER stress was necessary for cytokine-induced beta-cell death and also whether ER stress gene activation was present in beta-cells of the NOD mouse model of type 1 diabetes.
4230. Decreased fetal size is associated with beta-cell hyperfunction in early life and failure with age.
作者: Manu V Chakravarthy.;Yimin Zhu.;Mitchell B Wice.;Trey Coleman.;Kirk L Pappan.;Connie A Marshall.;Michael L McDaniel.;Clay F Semenkovich.
来源: Diabetes. 2008年57卷10期2698-707页
Low birth weight is associated with diabetes in adult life. Accelerated or "catch-up" postnatal growth in response to small birth size is thought to presage disease years later. Whether adult disease is caused by intrauterine beta-cell-specific programming or by altered metabolism associated with catch-up growth is unknown.
4231. Metabolism-independent sugar sensing in central orexin neurons.
作者: J Antonio González.;Lise T Jensen.;Lars Fugger.;Denis Burdakov.
来源: Diabetes. 2008年57卷10期2569-76页
Glucose sensing by specialized neurons of the hypothalamus is vital for normal energy balance. In many glucose-activated neurons, glucose metabolism is considered a critical step in glucose sensing, but whether glucose-inhibited neurons follow the same strategy is unclear. Orexin/hypocretin neurons of the lateral hypothalamus are widely projecting glucose-inhibited cells essential for normal cognitive arousal and feeding behavior. Here, we used different sugars, energy metabolites, and pharmacological tools to explore the glucose-sensing strategy of orexin cells.
4232. Baseline serum 25-hydroxy vitamin d is predictive of future glycemic status and insulin resistance: the Medical Research Council Ely Prospective Study 1990-2000.
作者: Nita G Forouhi.;Jian'an Luan.;Andrew Cooper.;Barbara J Boucher.;Nicholas J Wareham.
来源: Diabetes. 2008年57卷10期2619-25页
Accumulating epidemiological evidence suggests that hypovitaminosis D may be associated with type 2 diabetes and related metabolic risks. However, prospective data using the biomarker serum 25-hydroxyvitamin D [25(OH)D] are limited and therefore examined in the present study.
4233. Reduction of Ptf1a gene dosage causes pancreatic hypoplasia and diabetes in mice.
作者: Akihisa Fukuda.;Yoshiya Kawaguchi.;Kenichiro Furuyama.;Sota Kodama.;Masashi Horiguchi.;Takeshi Kuhara.;Michiya Kawaguchi.;Mami Terao.;Ryuichiro Doi.;Christopher V E Wright.;Mikio Hoshino.;Tsutomu Chiba.;Shinji Uemoto.
来源: Diabetes. 2008年57卷9期2421-31页
Most pancreatic endocrine cells derive from Ptf1a-expressing progenitor cells. In humans, nonsense mutations in Ptf1a have recently been identified as a cause of permanent neonatal diabetes associated with pancreatic agenesis. The death of Ptf1a-null mice soon after birth has not allowed further insight into the pathogenesis of the disease; it is therefore unclear how much pancreatic endocrine function is dependent on Ptf1a in mammals. This study aims to investigate gene-dosage effects of Ptf1a on pancreas development and function in mice.
4234. Neuronatin: a new inflammation gene expressed on the aortic endothelium of diabetic mice.
作者: Nino Mzhavia.;Shuiqing Yu.;Shota Ikeda.;Tehua T Chu.;Ira Goldberg.;Hayes M Dansky.
来源: Diabetes. 2008年57卷10期2774-83页
Identification of arterial genes and pathways altered in obesity and diabetes.
4235. Assessing the combined impact of 18 common genetic variants of modest effect sizes on type 2 diabetes risk.
作者: Hana Lango.; .;Colin N A Palmer.;Andrew D Morris.;Eleftheria Zeggini.;Andrew T Hattersley.;Mark I McCarthy.;Timothy M Frayling.;Michael N Weedon.
来源: Diabetes. 2008年57卷11期3129-35页
Genome-wide association studies have dramatically increased the number of common genetic variants that are robustly associated with type 2 diabetes. A possible clinical use of this information is to identify individuals at high risk of developing the disease, so that preventative measures may be more effectively targeted. Here, we assess the ability of 18 confirmed type 2 diabetes variants to differentiate between type 2 diabetic case and control subjects.
4236. A common nonsynonymous single nucleotide polymorphism in the SLC30A8 gene determines ZnT8 autoantibody specificity in type 1 diabetes.
作者: Janet M Wenzlau.;Yu Liu.;Liping Yu.;Ong Moua.;Kimberly T Fowler.;Sampathkumar Rangasamy.;Jay Walters.;George S Eisenbarth.;Howard W Davidson.;John C Hutton.
来源: Diabetes. 2008年57卷10期2693-7页
Zinc transporter eight (SLC30A8) is a major target of autoimmunity in human type 1A diabetes and is implicated in type 2 diabetes in genome-wide association studies. The type 2 diabetes nonsynonymous single nucleotide polymorphism (SNP) affecting aa(325) lies within the region of highest ZnT8 autoantibody (ZnT8A) binding, prompting an investigation of its relationship to type 1 diabetes.
4237. Evidence for interindividual heterogeneity in the glucose gradient across the human red blood cell membrane and its relationship to hemoglobin glycation.
作者: Paramjit K Khera.;Clinton H Joiner.;Anthony Carruthers.;Christopher J Lindsell.;Eric P Smith.;Robert S Franco.;Yancey R Holmes.;Robert M Cohen.
来源: Diabetes. 2008年57卷9期2445-52页
To determine whether interindividual heterogeneity in the erythrocyte (red blood cell [RBC]) transmembrane glucose gradient might explain discordances between A1C and glycemic control based on measured fructosamine.
4238. Diabetes susceptibility in the Canadian Oji-Cree population is moderated by abnormal mRNA processing of HNF1A G319S transcripts.
作者: Lorna W Harries.;Melissa J Sloman.;Elizabeth A C Sellers.;Andrew T Hattersley.;Sian Ellard.
来源: Diabetes. 2008年57卷7期1978-82页
The G319S HNF1A variant is associated with an increased risk of type 2 diabetes in the Canadian Oji-Cree population. We hypothesized that the variant site at the 3' end of exon 4 might influence splicing and characterized mRNA transcripts to investigate the mutational mechanism underlying this susceptibility to diabetes.
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