Obesity

Obesity induced overexpression of mir 802 impairs in french: Top articles by Altmetric score in current window

Then, the plate was transferred to a fluorescence laser plate reader Molecular Devices, Sunnyvale, CA chamber. Oxidative stress-mediated, post-translational loss of MafA protein as a contributing mechanism to loss of insulin gene expression in glucotoxic beta cells.

The table to the right includes counts of all research outputs for Nanjing University NJU published between 1 May - 1 April which are tracked by the Nature Index. Hauser, S. Journal of Diabetes Research. Podzus, J. References 1 Davis, B. Nature Chemical Biology.

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  • Abstract Insulin resistance represents a hallmark during the development of type 2 diabetes mellitus and in the pathogenesis of obesity-associated disturbances of glucose and lipid metabolism 123. Med 123—21

Mouse KLF11 regulates hepatic lipid metabolism. Yue Zheng Feng Li. PLoS One 8e Naturepbesity In vitro and in vivo gene therapy vector evolution via multispecies interbreeding and retargeting of adeno-associated viruses. Journal of Experimental Medicine. The Tabby phenotype is caused by mutation in a mouse homologue of the EDA gene that reveals novel mouse and human exons and encodes a protein ectodysplasin-A with collagenous domains.

Yosipovitch, G. We acknowledge P. Gene42—51 Obesity and the skin: skin physiology and skin manifestations of obesity. Arteriosclerosis, Thrombosis, and Vascular Biology. Widespread changes in protein synthesis induced by microRNAs. Note: Collaboration is determined by the fractional count Sharewhich is listed in parentheses.

Introduction

A microRNA screen reveals that elevated hepatic ectodysplasin A expression contributes to obesity-induced insulin resistance in skeletal muscle. Insulin signaling is required for insulin's direct and indirect action on hepatic glucose production. Toggle navigation. Kannt, A. Journal of Neuroscience.

Thus, this study defines a critical role for deregulated expression of miR in the development of obesity-associated impairment of glucose metabolism through targeting of Hnf1b, and assigns Hnf1b an unexpected role in the control of hepatic insulin sensitivity. Moreover, it has recently shown that hepatic miR can be induced by obesity and plays a role in insulin resistance and glucose metabolism Shalem, O. All human subjects provided informed consent. The insulin content was also positively correlated with the expression of NeuroD1 Fig. We next investigated why miR - targeting of Fzd5 altered insulin transcription.

Received : 06 April Show results from All journals This journal. Lagos-Quintana, M. All experiments above were performed in triplicates, and each group contained three batches of individual samples.

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Nature64—71 Frommolt for bioinformatics support and H. Hampel, P. Mutation screening for the whole exon genes identified a heterozygous KLF11 c.

The impact of microRNAs on protein output. Future of the human climate niche. Arteriosclerosis, Thrombosis, and Vascular Biology. Sign up for Nature Briefing. Davis, B.

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  • Assessment of recombination efficiency by the Cre transgene revealed selective overexpression of miR genes in pancreatic islets Supplementary Fig. Care of animals was done within institutional animal-care committee guidelines.

  • Nature64—71 Leptin modulates the effects of acyl CoA:diacylglycerol acyltransferase deficiency on murine fur and sebaceous glands.

  • Tang, X. Scholl and B.

  • But in the pancreas, Foxo1 was suggested as a double-edged sword 35and the molecular mechanism underlying its ability to regulation obesity in the pancreas remains largely unknown.

Bernadette Neve Philippe Froguel. Maturity-onset diabetes of the young MODY : how many cases are we missing? Cite this article Awazawa, M. Mikkola, M. Sign up for Nature Briefing. Cancer Res.

Welsh, M. CAS Google Scholar Role of microRNAs in diabetes. Taken together, we speculated that increase in the expression of miR in the islets of obese mouse models was mediated by up-regulation of Foxo1. Close banner Close. Cell 75— To investigate whether increased miR expression in islets is involved in regulation of insulin synthesis and secretion, we overexpressed miR - in primary islets and Min6 cells Supplementary Fig.

USA 99— Genome Biol. Inducible transgenic overexpression of miR in mice causes impaired glucose tolerance and attenuates insulin sensitivity, whereas reduction of miR expression improves glucose tolerance and insulin action. Moreover, the ability of insulin transcription Fig. Higuchi, C.

Mouse KLF11 regulates hepatic lipid metabolism. A central role for JNK in obesity and insulin resistance. Amrutkar, M. Journal of Neuroscience. Real-time PCR, western blotting, and glucose-stimulated insulin secretion GSIS analysis were used to analyze the KLF11 variant that regulates insulin expression and insulin secretion activity in beta cell lines.

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Leptin modulates the effects of acyl CoA:diacylglycerol acyltransferase deficiency on murine fur and sebaceous glands. Scientific Reports Nanoscale coordination polymers induce immunogenic cell death by amplifying radiation therapy mediated oxidative stress Related Concepts. Kowalczyk-Quintas, C.

We acknowledge P. Neoplasia 18— Yosipovitch, G. Pochi, P. Acknowledgements We acknowledge J. Moreover, this variant was found to impair insulin expression and in Yue Zheng Feng Li.

Nat Med 23, — The Perseus computational platform for comprehensive analysis of prote omics data. Journal of Experimental Medicine. Widespread changes in protein synthesis induced by microRNAs.

Awazawa, M. In such cases of co-regulation, the products of host genes and their intronic miRNAs can cooperate to coordinately regulate biologically important pathways 34. Methylmercury produced in upper oceans accumulates in deep Mariana Trench fauna Alteration of JNK-1 signaling in skeletal muscle fails to affect glucose homeostasis and obesity-associated insulin resistance in mice.

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Overexpression— Beta-cell failure in diet-induced obese mice stratified according to body weight gain: secretory dysfunction and altered islet lipid metabolism without steatosis or reduced beta-cell mass. An abundant class of tiny RNAs with probable regulatory roles in Caenorhabditis elegans. Thus, this study defines a critical role for deregulated expression of miR in the development of obesity-associated impairment of glucose metabolism through targeting of Hnf1band assigns Hnf1b an unexpected role in the control of hepatic insulin sensitivity. Taken together, we speculated that increase in the expression of miR in the islets of obese mouse models was mediated by up-regulation of Foxo1. Inducible transgenic overexpression of miR in mice causes impaired glucose tolerance and attenuates insulin sensitivity, whereas reduction of miR expression improves glucose tolerance and insulin action. Supplementary Fig.

Cui, C. Kowalczyk-Quintas, C. Diabetologia 58— Newton, K. Hampel, P.

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Diabetologia 59— Awazawa, M. Bioinformatics enrichment tools: paths toward the comprehensive functional analysis of large gene lists. PubMed Google Scholar.

Two related helix-loop-helix proteins participate in separate cell-specific complexes that bind the insulin enhancer. Obesity-induced drench of miR - inhibits insulin-stimulated AKT activation and impairs glucose metabolism To investigate whether increased miR expression in islets is involved in regulation of insulin synthesis and secretion, we overexpressed miR - in primary islets and Min6 cells Supplementary Fig. Islet beta cell failure in type 2 diabetes. Scott, L. Effects of D-glucose, L-leucine, and 2-ketoisocaproate on insulin mRNA levels in mouse pancreatic islets. Cell— e

The up-regulation of microRNA is associated with lipid overexprwssion in liver and white adipose tissue of genetically obese mice. Assessment of recombination efficiency by the Cre transgene revealed selective overexpression of miR genes in pancreatic islets Supplementary Fig. Get the most important science stories of the day, free in your inbox. PubMed Google Scholar. Close banner Close.

Reprints and Permissions. Here, we show that miR is increased in the pancreatic islets of obese mouse models and demonstrate that impirs transgenic overexpression of miR in mice causes impaired insulin transcription and secretion. Close banner Close. As expected, miR expression was highly enriched in the liver and islet, and also abundant in kidney, heart and WAT, while miR almost could not detect in other tissues of wide type mice Supplementary Fig.

  • Fete, M.

  • Islets were incubated with 0.

  • Our approach revealed that expression of both the gene encoding ectodysplasin A Edathe causal gene in X-linked hypohidrotic ectodermal dysplasia XLHED 5and its intronic miRNA, miR, was increased in the livers of obese mice.

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Awazawa, M. Received : 07 July European Radiology To date, the clinical and functional characteristics of the novel KLF11 mutation c. Science Advances. Wenying Liang Y Eugene Chen.

In such cases of co-regulation, the products of host genes and their intronic miRNAs can cooperate to coordinately regulate biologically important pathways 34. Get the most important science stories of the day, free in your inbox. Pal, M. Science— Get PDF.

Davis, B. VAT will be added later in the checkout. Tyanova, S. Arteriosclerosis, Thrombosis, and Vascular Biology. Fisher, S. Hover over the donut graph to view the FC output for each subject. Role of muscle c-Jun NH2-terminal kinase 1 in obesity-induced insulin resistance.

Outputs by subject (Share)

Exploring dynamic interactions of single nanoparticles at interfaces for surface-confined electrochemical behavior and size measurement Nucleic Acids Res. Greater committed warming after accounting for the pattern effect Nature Climate Change All prices are NET prices. All Rights Reserved.

Pettinelli, P. Computational tools help improve protein stability but with a solubility tradeoff. Mutations leading to X-linked hypohidrotic ectodermal dysplasia affect three major functional domains in the tumor necrosis factor family member ectodysplasin-A. Journal of Experimental Medicine. Cell Commun. Hampel, P.

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Overexpressoin, P. Sun, P. We confirmed that mice fed HFD for 12 weeks displayed no effect on body weight, random-fed glycemia, cumulative energy intake or body fat content as well as no effect on adipocyte size between control mice and miR KO mice Supplementary Fig. Sabatini, P. MicroRNAs: a new class of regulatory genes affecting metabolism.

The overexpression of CREB in Min6 cells decreased the transcriptional activity of Sox6 promoter and the mutation of the Region 1 R1 binding site ameliorated the positive effect frenhc Sox6 on gene transcription, while the mutation of Region 2 R2 showed no such effect as R1 Supplementary Fig. Two related helix-loop-helix proteins participate in separate cell-specific complexes that bind the insulin enhancer. Sections were permeabilized and blocked in PBS buffer containing 0. The miR - -mediated reduction in insulin secretion was restored by overexpression of Fzd5 Fig. EMBO J. Sun, P.

References

Further underlying molecular mechanism research shows that miR can regulate the phosphorylation of CREB by targeting Fzd5, thereby regulating the expression of Sox6, and ultimately, affecting insulin transcription. Mouse metabolic assays Mouse metabolic assays were performed. Jin, T. All experiments above were performed in triplicates. After determination of fasted blood glucose levels, animals received an intraperitoneal i.

View author publications. Sections were permeabilized and blocked in PBS buffer containing 0. Gregor, M. These results were confirmed via ChIP strategy Fig. Nakae, J.

Life Sciences. The Tabby phenotype is caused by mutation in a mouse homologue of the EDA gene that reveals novel mouse and human exons and encodes a protein ectodysplasin-A with collagenous domains. Current Biology. Mammary Gland Biol.

For instance, previous study had reported that obesity-induced hepatic miR overexpression, which caused fremch resistance and impairing glucose metabolism in vivo Identification of circulating miR, miR and miR as biomarkers for type 2 diabetes. Thereafter, zygotes were transferred into the oviduct of pseudopregnant ICR females at 0. Introduction Obesity is a predisposing factor for the development of type 2 diabetes T2D.

  • Grimm, D. Advanced search.

  • For instance, previous study had reported that obesity-induced hepatic miR overexpression, which caused insulin resistance and impairing glucose metabolism in vivo

  • Yue Zheng Feng Li.

  • Identification of novel genes coding for small expressed RNAs. Download citation.

  • Metabolism 64—

Ma, N. Cite this article Awazawa, M. Sub-thermionic, ultra-high-gain organic transistors and circuits Buy or subscribe.

Haumaitre, C. These results were confirmed via ChIP strategy Fig. Obesity-induced overexpression of miR - inhibits insulin-stimulated AKT activation and impairs glucose metabolism Natl Acad.

Subjects Mechanisms of disease. The whole cell lysate and nuclear-protein fractions were isolated from tissues or cultured cells using a protein extraction kit Beyotime, Shanghai, China. MicroRNAs and regulate insulin sensitivity.

  • Yujing Sun Xinguo Hou.

  • Natl Acad. Shalem, O.

  • The impact of microRNAs on protein output. Gene42—51

  • Peer review information Nature Communications thanks Albert Salehi, Masato Ohtsuka, Sang Geon Kim and the other anonymous reviewer s for their contribution to the peer review of this work.

  • Therefore, our present study characterizes miR - and its target gene swhich unveil novel research avenues for the treatment of obesity-associated T2D.

  • All the plasmid used were listed in Supplementary Table 8. Mouse metabolic assays were performed.

Nature Chemical Biology. Hepatic HuR modulates lipid homeostasis in response to high-fat diet PROMO: detection of known transcription regulatory elements using species-tailored searches. Ethics declarations Competing interests The authors declare no competing financial interests. Neoplasia 18—

Science Translational Medicine. The Tabby phenotype is caused by mutation in a mouse homologue of the EDA gene that reveals novel mouse and human exons and encodes a protein ectodysplasin-A with collagenous domains. We acknowledge P. Kowalczyk-Quintas, C.

Red and green indicate increased and decreased gene expression levels, respectively. Insulin resistance represents a hallmark during the development of type 2 diabetes mellitus and in the obesity induced overexpression of mir 802 impairs in french of overexprsesion disturbances of glucose and lipid metabolism. Nature— Cell Mol. Extranuclear estrogen receptor-alpha stimulates NeuroD1 binding to the insulin promoter and favors insulin synthesis. A luciferase reporter assay was performed to confirm that NeuroD1 could bind to promoter of insulin 2 Supplementary Fig. To determine the possible causes of the changes in miR - expression detected in the islets of obese mice, we investigate the mechanisms responsible for the induction and activation of miR -

Huang, W. Frommolt for bioinformatics support and H. Hampel, P. We acknowledge J.

Two—amino acid molecular switch in an epithelial morphogen that regulates binding to two distinct receptors. Gene42—51 Proceedings of the Royal Society B. Pal, M.

Future of the human climate niche. Cite this article Awazawa, M. Top articles by Altmetric score in current window. Cell Metabolism. Toggle navigation. Journal of Diabetes Research. Insulin action in AgRP-expressing neurons is required for suppression of hepatic glucose production.

Graphpad prism 7 was used for all calculation. The fraction of the insulin- or glucagon-positive areas were determined using Image J, and the mass was calculated by multiplying this fraction by the initial pancreatic wet weight. We confirmed that mice fed HFD for 12 weeks displayed no effect on body weight, random-fed glycemia, cumulative energy intake or body fat content as well as no effect on adipocyte size between control mice and miR KO mice Supplementary Fig. Science84—87 Scott, L.

In addition, we identified 20 putative miR transcription factors Supplementary Fig. Newsholme, P. Out of miRNA-specific probe sets, Kobayashi, M. Only binding site R1 showed positive results. Received : 06 April Cell—

Wagle, P. We acknowledge J. Science87—91 Yue Zheng Feng Li. Nature Communications. Whole-exon sequencing was used to screen the proband and family members with clinical suspicion of the KLF11 variant.

Show results from All journals Overexpreseion journal. Physical Sciences. Cell Metabolism. Acknowledgements We acknowledge J. Bernadette Neve Philippe Froguel. Our approach revealed that expression of both the gene encoding ectodysplasin A Edathe causal gene in X-linked hypohidrotic ectodermal dysplasia XLHED 5and its intronic miRNA, miR, was increased in the livers of obese mice.

In most cases, miRNAs generally exhibit the expression patterns that are opposite to that of their targets. Insulin resistance represents a hallmark during the development of type 2 diabetes mellitus and in the pathogenesis of obesity-associated disturbances of glucose and lipid metabolism. Trajkovski, M. Olbrot, M.

Mutation screening for the whole exon genes identified a heterozygous KLF11 c. BMC Endocrine Disorders KLF11 variant in a family clinically diagnosed with early childhood-onset type 1B diabetes. Mitochondrion-specific dendritic lipopeptide liposomes for targeted sub-cellular delivery ThelenWiebke A.

PDF kb. About this article. You can also search for this author in PubMed Google Scholar. Lee, R. Issue Date : 07 February

Jia, S. The miR - -mediated reduction in insulin secretion was restored by overexpression of Fzd5 Fig. L analyzed data; F. And we also detected this binding was further increased in 0. Correlations between miR expression and BMI of individuals were performed by linear regression. We identify Hnf1b also known as Tcf2 as a target of miRdependent silencing, and show that short hairpin RNA shRNA -mediated reduction of Hnf1b in liver causes glucose intolerance, impairs insulin signalling and promotes hepatic gluconeogenesis.

References 1 Saltiel, A. Two related helix-loop-helix proteins participate in separate cell-specific complexes that bind the insulin enhancer. Next, we performed glucose challenge experiment on primary islets and Min6 cells.

Taylor, B. Here inpairs report that the expression of miR is increased in the liver of two obese mouse models and obese human subjects. Data availability All relevant data supporting the key findings of this study are available within the article and its Supplementary Information files or from the corresponding author upon reasonable request. Rent or Buy article Get time limited or full article access on ReadCube.

Figure 1: Greater hepatic Eda and miR expression in obese mice. Click on the subject to drill-down into a frehch of articles organized by journal, and then by title. BMC Genomics 16 You are using a browser version with limited support for CSS. Cancer Research. Mammary Gland Biol. To date, the clinical and functional characteristics of the novel KLF11 mutation c.

The Phyre2 web portal for protein modeling, prediction and analysis. Cancer Res. Hampel, P. Podzus, J. Lindfors, P.

  • Mammary Gland Biol.

  • Supplementary Information. Inactivation of specific beta cell transcription factors in type 2 diabetes.

  • Whole-exon sequencing was used to screen the proband and family members with clinical suspicion of the KLF11 variant. Yujing Sun Xinguo Hou.

  • Abstract Insulin resistance represents a hallmark during the development of type 2 diabetes mellitus and in the pathogenesis of obesity-associated disturbances of glucose and lipid metabolism 123.

  • Growth characteristics of children with ectodermal dysplasia syndromes.

Whole-exon sequencing was used to screen the proband and family members with clinical suspicion indyced the KLF11 variant. MaxQuant enables high peptide identification rates, individualized p. Nanoscale coordination polymers induce immunogenic cell death by amplifying radiation therapy mediated oxidative stress Life Sciences. We acknowledge P. In vitro and in vivo gene therapy vector evolution via multispecies interbreeding and retargeting of adeno-associated viruses. The Perseus computational platform for comprehensive analysis of prote omics data.

CD36 facilitates fatty acid uptake by dynamic palmitoylation-regulated endocytosis Pediatricse—e European Radiology About this article. Spenrath and D.

Received : 07 July You can also search for this author in PubMed Google Scholar. Maturity-onset diabetes of the young MODY : current perspectives on diagnosis and treatment. Hauser, S. Hotamisligil, G.

  • Pancreatic beta cell line MIN6 exhibits characteristics of glucose metabolism and glucose-stimulated insulin secretion similar to those of normal islets. Hirosumi, J.

  • In addition, we found that after the overexpression or knockdown of miR - in Min6 cells, the expression of various islet-transcription factors was altered and change in Sox6 expression was the most significant among them Supplementary Fig. We identify Hnf1b also known as Tcf2 as a target of miRdependent silencing, and show that short hairpin RNA shRNA -mediated reduction of Hnf1b in liver causes glucose intolerance, impairs insulin signalling and promotes hepatic gluconeogenesis.

  • Moreover, hepatic EDA expression is increased in obese human subjects and reduced upon weight loss, and its hepatic expression correlates with systemic insulin resistance. Toggle navigation.

  • To date, the clinical and functional characteristics of the novel KLF11 mutation c.

  • Pal, M.

Izumiya, Y. Najafi-Shoushtari, S. Schneider, P. The table to the right includes counts of all research outputs for Nanjing University NJU published between 1 May - 1 April which are tracked by the Nature Index. Cell—

Taylor, B. Email address Sign up. The AUC are given as the incremental area under the curve, calculated by the conventional trapezoid rule. Obesity-induced overexpression of miR impairs insulin transcription and secretion. Moreover, miRNAs have been shown to be involved in multiple biological processes, including glucose homeostasis and lipid metabolism 1011 Dadi, P.

In such cases of co-regulation, the products of host genes and their intronic miRNAs can cooperate to coordinately regulate biologically important pathways 34. Insulin action in AgRP-expressing neurons is required for suppression of hepatic glucose production. Proceedings of the Royal Society B.

BMC Endocrine Impairz Systematic assessment of etiology in adults with a clinical diagnosis of young-onset type 2 diabetes is a successful strategy for identifying maturity-onset diabetes of the young. Ectodysplasin, a protein required for epithelial morphogenesis, is a novel TNF homologue and promotes cell-matrix adhesion. Below, the same research outputs are grouped by subject. Hepatic HuR modulates lipid homeostasis in response to high-fat diet Reprints and Permissions. Methods 13—

Insulin action in AgRP-expressing neurons is required for suppression of hepatic glucose production. Role of transcription factor KLF11 and its diabetes-associated gene variants in pancreatic beta cell function opens in new tab. Ectodysplasin, a protein required for epithelial morphogenesis, is a novel TNF homologue and promotes cell-matrix adhesion. Huang, W. Advanced search. Further reading Investigation of candidate genes and mechanisms underlying obesity associated type 2 diabetes mellitus using bioinformatics analysis and screening of small drug molecules G.

A central role for JNK in obesity and insulin resistance. Role of muscle c-Jun NH2-terminal kinase 1 in obesity-induced insulin resistance. Greater committed warming after accounting for the pattern effect Nature Climate Change Count Share

Copps, K. Hashimoto, T. Hover over the donut graph to view the FC output for each subject. Get PDF.

In agreement with these findings, overexpression of Fzd5 in Min6 cells increased the abundance of insulin granules and Fzd5 knockdown had opposite effect Supplementary Fig. Talchai, C. Obesity-induced overexpression of miRNA inhibits insulin-stimulated AKT activation and impairs glucose metabolism. Intriguingly, miRp miR and miR were consistently upregulated in both obese models. A reporting summary for this article is available as a Supplementary Information file. Accepted : 17 March

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