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4261. Exenatide sensitizes insulin-mediated whole-body glucose disposal and promotes uptake of exogenous glucose by the liver.
作者: Dan Zheng.;Viorica Ionut.;Vahe Mooradian.;Darko Stefanovski.;Richard N Bergman.
来源: Diabetes. 2009年58卷2期352-9页
Recent progress suggests that exenatide, a mimetic of glucagon-like peptide-1 (GLP-1), might lower glycemia independent of increased beta-cell response or reduced gastrointestinal motility. We aimed to investigate whether exenatide stimulates glucose turnover directly in insulin-responsive tissues dependent or independent of insulinemia.
4262. Glucose and pharmacological modulators of ATP-sensitive K+ channels control [Ca2+]c by different mechanisms in isolated mouse alpha-cells.
作者: Nicolas Quoix.;Rui Cheng-Xue.;Laurine Mattart.;Ziad Zeinoun.;Yves Guiot.;Mélanie C Beauvois.;Jean-Claude Henquin.;Patrick Gilon.
来源: Diabetes. 2009年58卷2期412-21页
We studied how glucose and ATP-sensitive K(+) (K(ATP)) channel modulators affect alpha-cell [Ca(2+)](c).
4263. Association analysis of variation in/near FTO, CDKAL1, SLC30A8, HHEX, EXT2, IGF2BP2, LOC387761, and CDKN2B with type 2 diabetes and related quantitative traits in Pima Indians.
作者: Rong Rong.;Robert L Hanson.;Daniel Ortiz.;Christopher Wiedrich.;Sayuko Kobes.;William C Knowler.;Clifton Bogardus.;Leslie J Baier.
来源: Diabetes. 2009年58卷2期478-88页
In recent genome-wide association studies, variants in CDKAL1, SLC30A8, HHEX, EXT2, IGF2BP2, CDKN2B, LOC387761, and FTO were associated with risk for type 2 diabetes in Caucasians. We investigated the association of these single nucleotide polymorphisms (SNPs) and some additional tag SNPs with type 2 diabetes and related quantitative traits in Pima Indians.
4264. Plasma ceramides are elevated in obese subjects with type 2 diabetes and correlate with the severity of insulin resistance.
作者: Jacob M Haus.;Sangeeta R Kashyap.;Takhar Kasumov.;Renliang Zhang.;Karen R Kelly.;Ralph A Defronzo.;John P Kirwan.
来源: Diabetes. 2009年58卷2期337-43页
To quantitate plasma ceramide subspecies concentrations in obese subjects with type 2 diabetes and relate these plasma levels to the severity of insulin resistance. Ceramides are a putative mediator of insulin resistance and lipotoxicity, and accumulation of ceramides within tissues in obese and diabetic subjects has been well described.
4265. Macrophage content in subcutaneous adipose tissue: associations with adiposity, age, inflammatory markers, and whole-body insulin action in healthy Pima Indians.
作者: Emilio Ortega Martinez de Victoria.;Xiaoyuan Xu.;Juraj Koska.;Ann Marie Francisco.;Michael Scalise.;Anthony W Ferrante.;Jonathan Krakoff.
来源: Diabetes. 2009年58卷2期385-93页
In severely obese individuals and patients with diabetes, accumulation and activation of macrophages in adipose tissue has been implicated in the development of obesity-associated complications, including insulin resistance. We sought to determine whether in a healthy population, adiposity, sex, age, or insulin action is associated with adipose tissue macrophage content (ATMc) and/or markers of macrophage activation.
4266. Overexpression of SIRT1 protects pancreatic beta-cells against cytokine toxicity by suppressing the nuclear factor-kappaB signaling pathway.
作者: Ji-Hyun Lee.;Mi-Young Song.;Eun-Kyung Song.;Eun-Kyung Kim.;Woo Sung Moon.;Myung-Kwan Han.;Jin-Woo Park.;Kang-Beom Kwon.;Byung-Hyun Park.
来源: Diabetes. 2009年58卷2期344-51页
SIRT1, a class III histone/protein deacetylase, is known to interfere with the nuclear factor-kappaB (NF-kappaB) signaling pathway and thereby has an anti-inflammatory function. Because of the central role of NF-kappaB in cytokine-mediated pancreatic beta-cell damage, we postulated that SIRT1 might work in pancreatic beta-cell damage models.
4267. Amylase alpha-2A autoantibodies: novel marker of autoimmune pancreatitis and fulminant type 1 diabetes.
作者: Toyoshi Endo.;Soichi Takizawa.;Shoichiro Tanaka.;Masashi Takahashi.;Hideki Fujii.;Terumi Kamisawa.;Tetsuro Kobayashi.
来源: Diabetes. 2009年58卷3期732-7页
The pathogenesis of autoimmune pancreatitis (AIP) and fulminant type 1 diabetes remains unclear, although it is known that immune-mediated processes severely compromise the endocrine and exocrine functions in both diseases.
4268. Recovery of endogenous beta-cell function in nonhuman primates after chemical diabetes induction and islet transplantation.
作者: Rita Bottino.;Angela Criscimanna.;Anna Casu.;Jing He.;Dirk J Van der Windt.;William A Rudert.;Carla Giordano.;Massimo Trucco.
来源: Diabetes. 2009年58卷2期442-7页
To describe the ability of nonhuman primate endocrine pancreata to reestablish endogenous insulin production after chemical beta-cell destruction.
4269. Exendin-4 improves glycemic control, ameliorates brain and pancreatic pathologies, and extends survival in a mouse model of Huntington's disease.
作者: Bronwen Martin.;Erin Golden.;Olga D Carlson.;Paul Pistell.;Jie Zhou.;Wook Kim.;Brittany P Frank.;Sam Thomas.;Wayne A Chadwick.;Nigel H Greig.;Gillian P Bates.;Kirupa Sathasivam.;Michel Bernier.;Stuart Maudsley.;Mark P Mattson.;Josephine M Egan.
来源: Diabetes. 2009年58卷2期318-28页
The aim of this study was to find an effective treatment for the genetic form of diabetes that is present in some Huntington's disease patients and in Huntington's disease mouse models. Huntington's disease is a neurodegenerative disorder caused by a polyglutamine expansion within the huntingtin protein. Huntington's disease patients exhibit neuronal dysfunction/degeneration, chorea, and progressive weight loss. Additionally, they suffer from abnormalities in energy metabolism affecting both the brain and periphery. Similarly to Huntington's disease patients, mice expressing the mutated human huntingtin protein also exhibit neurodegenerative changes, motor dysfunction, perturbed energy metabolism, and elevated blood glucose levels.
4270. Somatostatin secreted by islet delta-cells fulfills multiple roles as a paracrine regulator of islet function.
作者: Astrid C Hauge-Evans.;Aileen J King.;Danielle Carmignac.;Carolyn C Richardson.;Iain C A F Robinson.;Malcolm J Low.;Michael R Christie.;Shanta J Persaud.;Peter M Jones.
来源: Diabetes. 2009年58卷2期403-11页
Somatostatin (SST) is secreted by islet delta-cells and by extraislet neuroendocrine cells. SST receptors have been identified on alpha- and beta-cells, and exogenous SST inhibits insulin and glucagon secretion, consistent with a role for SST in regulating alpha- and beta-cell function. However, the specific intraislet function of delta-cell SST remains uncertain. We have used Sst(-/-) mice to investigate the role of delta-cell SST in the regulation of insulin and glucagon secretion in vitro and in vivo.
4271. A single-nucleotide polymorphism in a methylatable Foxa2 binding site of the G6PC2 promoter is associated with insulin secretion in vivo and increased promoter activity in vitro.
The G6PC2 gene encoding islet-specific glucose-6-phosphatase related protein (IGRP) has a common promoter variant, rs573225 (-231G/A), located within a Foxa binding site. We tested the cis-regulatory effects of rs573225 on promoter activity and its association with insulin response to oral glucose.
4272. Idd loci synergize to prolong islet allograft survival induced by costimulation blockade in NOD mice.
作者: Julie Mangada.;Todd Pearson.;Michael A Brehm.;Linda S Wicker.;Laurence B Peterson.;Leonard D Shultz.;David V Serreze.;Aldo A Rossini.;Dale L Greiner.
来源: Diabetes. 2009年58卷1期165-73页
NOD mice model human type 1 diabetes and are used to investigate tolerance induction protocols for islet transplantation in a setting of autoimmunity. However, costimulation blockade-based tolerance protocols have failed in prolonging islet allograft survival in NOD mice.
4273. Slc11a1 enhances the autoimmune diabetogenic T-cell response by altering processing and presentation of pancreatic islet antigens.
作者: Yang D Dai.;Idania G Marrero.;Philippe Gros.;Habib Zaghouani.;Linda S Wicker.;Eli E Sercarz.
来源: Diabetes. 2009年58卷1期156-64页
Efforts to map non-major histocompatibility complex (MHC) genes causing type 1 diabetes in NOD mice identified Slc11a1, formerly Nramp1, as the leading candidate gene in the Idd5.2 region. Slc11a1 is a membrane transporter of bivalent cations that is expressed in late endosomes and lysosomes of macrophages and dendritic cells (DCs). Because DCs are antigen-presenting cells (APCs) known to be critically involved in the immunopathogenic events leading to type 1 diabetes, we hypothesized that Slc11a1 alters the processing or presentation of islet-derived antigens to T-cells.
4274. Xenin, a gastrointestinal peptide, regulates feeding independent of the melanocortin signaling pathway.
Xenin, a 25-amino acid peptide, was initially isolated from human gastric mucosa. Plasma levels of xenin rise after a meal in humans, and administration of xenin inhibits feeding in rats and chicks. However, little is known about the mechanism by which xenin regulates food intake. Signaling pathways including leptin and melanocortins play a pivotal role in the regulation of energy balance. Therefore, we addressed the hypothesis that xenin functions as a satiety factor by acting through the melanocortin system or by interacting with leptin.
4275. All-trans retinoic acid inhibits type 1 diabetes by T regulatory (Treg)-dependent suppression of interferon-gamma-producing T-cells without affecting Th17 cells.
作者: Yang-Hau Van.;Wen-Hui Lee.;Serina Ortiz.;Mi-Heon Lee.;Han-Jun Qin.;Chih-Pin Liu.
来源: Diabetes. 2009年58卷1期146-55页
All-trans retinoic acid (ATRA), a potent derivative of vitamin A, can regulate immune responses. However, its role in inducing immune tolerance associated with the prevention of islet inflammation and inhibition of type 1 diabetes remains unclear.
4276. Methyltransferase Set7/9 maintains transcription and euchromatin structure at islet-enriched genes.
作者: Tye G Deering.;Takeshi Ogihara.;Anthony P Trace.;Bernhard Maier.;Raghavendra G Mirmira.
来源: Diabetes. 2009年58卷1期185-93页
The activation of beta-cell genes, particularly of those encoding preproinsulin, requires an appropriate euchromatin (or "open") DNA template characterized by hypermethylation of Lys4 of histone H3. We hypothesized that this modification is maintained in islet beta-cells by the action of the histone methyltransferase Set7/9.
4277. Regulation of calcium-permeable TRPV2 channel by insulin in pancreatic beta-cells.
作者: Etsuko Hisanaga.;Masahiro Nagasawa.;Kohjiro Ueki.;Rohit N Kulkarni.;Masatomo Mori.;Itaru Kojima.
来源: Diabetes. 2009年58卷1期174-84页
Calcium-permeable cation channel TRPV2 is expressed in pancreatic beta-cells. We investigated regulation and function of TRPV2 in beta-cells.
4278. Hypoxia decreases insulin signaling pathways in adipocytes.
作者: Claire Regazzetti.;Pascal Peraldi.;Thierry Grémeaux.;Rosanna Najem-Lendom.;Issam Ben-Sahra.;Mireille Cormont.;Frédéric Bost.;Yannick Le Marchand-Brustel.;Jean-François Tanti.;Sophie Giorgetti-Peraldi.
来源: Diabetes. 2009年58卷1期95-103页
Obesity is characterized by an overgrowth of adipose tissue that leads to the formation of hypoxic areas within this tissue. We investigated whether this phenomenon could be responsible for insulin resistance by studying the effect of hypoxia on the insulin signaling pathway in adipocytes.
4279. Site-specific GlcNAcylation of human erythrocyte proteins: potential biomarker(s) for diabetes.
作者: Zihao Wang.;Kyoungsook Park.;Frank Comer.;Linda C Hsieh-Wilson.;Christopher D Saudek.;Gerald W Hart.
来源: Diabetes. 2009年58卷2期309-17页
O-linked N-acetylglucosamine (O-GlcNAc) is upregulated in diabetic tissues and plays a role in insulin resistance and glucose toxicity. Here, we investigated the extent of GlcNAcylation on human erythrocyte proteins and compared site-specific GlcNAcylation on erythrocyte proteins from diabetic and normal individuals.
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