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  • 1
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    Increased insulin sensitivity and obesity resistance in mice lacking the protein tyrosine phosphatase-1B gene (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-05
    Description: Protein tyrosine phosphatase-1B (PTP-1B) has been implicated in the negative regulation of insulin signaling. Disruption of the mouse homolog of the gene encoding PTP-1B yielded healthy mice that, in the fed state, had blood glucose concentrations that were slightly lower and concentrations of circulating insulin that were one-half those of their PTP-1B+/+ littermates. The enhanced insulin sensitivity of the PTP-1B-/- mice was also evident in glucose and insulin tolerance tests. The PTP-1B-/- mice showed increased phosphorylation of the insulin receptor in liver and muscle tissue after insulin injection in comparison to PTP-1B+/+ mice. On a high-fat diet, the PTP-1B-/- and PTP-1B+/- mice were resistant to weight gain and remained insulin sensitive, whereas the PTP-1B+/+ mice rapidly gained weight and became insulin resistant. These results demonstrate that PTP-1B has a major role in modulating both insulin sensitivity and fuel metabolism, thereby establishing it as a potential therapeutic target in the treatment of type 2 diabetes and obesity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elchebly, M -- Payette, P -- Michaliszyn, E -- Cromlish, W -- Collins, S -- Loy, A L -- Normandin, D -- Cheng, A -- Himms-Hagen, J -- Chan, C C -- Ramachandran, C -- Gresser, M J -- Tremblay, M L -- Kennedy, B P -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1544-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, McGill University, 3655 Drummond Street, Montreal, Quebec, Canada, H3G 1Y6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10066179" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Diabetes Mellitus, Type 2/therapy ; Dietary Fats/administration & dosage ; Gene Targeting ; Glucose Tolerance Test ; Insulin/blood/*metabolism/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance ; Liver/metabolism ; Male ; Mice ; Mice, Knockout ; Muscle, Skeletal/metabolism ; Obesity/*metabolism/therapy ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Tyrosine Phosphatases/*genetics/*metabolism ; Receptor, Insulin/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Dietary intervention impact on gut microbial gene richness (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-08-30
    Description: Complex gene-environment interactions are considered important in the development of obesity. The composition of the gut microbiota can determine the efficacy of energy harvest from food and changes in dietary composition have been associated with changes in the composition of gut microbial populations. The capacity to explore microbiota composition was markedly improved by the development of metagenomic approaches, which have already allowed production of the first human gut microbial gene catalogue and stratifying individuals by their gut genomic profile into different enterotypes, but the analyses were carried out mainly in non-intervention settings. To investigate the temporal relationships between food intake, gut microbiota and metabolic and inflammatory phenotypes, we conducted diet-induced weight-loss and weight-stabilization interventions in a study sample of 38 obese and 11 overweight individuals. Here we report that individuals with reduced microbial gene richness (40%) present more pronounced dys-metabolism and low-grade inflammation, as observed concomitantly in the accompanying paper. Dietary intervention improves low gene richness and clinical phenotypes, but seems to be less efficient for inflammation variables in individuals with lower gene richness. Low gene richness may therefore have predictive potential for the efficacy of intervention.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cotillard, Aurelie -- Kennedy, Sean P -- Kong, Ling Chun -- Prifti, Edi -- Pons, Nicolas -- Le Chatelier, Emmanuelle -- Almeida, Mathieu -- Quinquis, Benoit -- Levenez, Florence -- Galleron, Nathalie -- Gougis, Sophie -- Rizkalla, Salwa -- Batto, Jean-Michel -- Renault, Pierre -- ANR MicroObes consortium -- Dore, Joel -- Zucker, Jean-Daniel -- Clement, Karine -- Ehrlich, Stanislav Dusko -- England -- Nature. 2013 Aug 29;500(7464):585-8. doi: 10.1038/nature12480.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut National de la Sante et de la Recherche Medicale, U872, Nutriomique, Equipe 7, Centre de Recherches des Cordeliers, Paris 75006, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23985875" target="_blank"〉PubMed〈/a〉
    Keywords: Basal Metabolism ; Body Weight/drug effects ; *Diet ; Diet, Carbohydrate-Restricted ; Dietary Fiber/pharmacology/therapeutic use ; Dietary Proteins/pharmacology ; Eating ; Energy Intake ; Female ; Fruit ; Gastrointestinal Tract/drug effects/*microbiology ; Gene-Environment Interaction ; Genes, Bacterial/genetics ; Humans ; Inflammation/microbiology ; Male ; Metagenome/drug effects/*genetics ; Obesity/diet therapy/microbiology ; Overweight/diet therapy/microbiology ; Vegetables ; Weight Loss/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    beta-catenin mediates stress resilience through Dicer1/microRNA regulation (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-11-11
    Description: beta-catenin is a multi-functional protein that has an important role in the mature central nervous system; its dysfunction has been implicated in several neuropsychiatric disorders, including depression. Here we show that in mice beta-catenin mediates pro-resilient and anxiolytic effects in the nucleus accumbens, a key brain reward region, an effect mediated by D2-type medium spiny neurons. Using genome-wide beta-catenin enrichment mapping, we identify Dicer1-important in small RNA (for example, microRNA) biogenesis--as a beta-catenin target gene that mediates resilience. Small RNA profiling after excising beta-catenin from nucleus accumbens in the context of chronic stress reveals beta-catenin-dependent microRNA regulation associated with resilience. Together, these findings establish beta-catenin as a critical regulator in the development of behavioural resilience, activating a network that includes Dicer1 and downstream microRNAs. We thus present a foundation for the development of novel therapeutic targets to promote stress resilience.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4257892/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4257892/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dias, Caroline -- Feng, Jian -- Sun, Haosheng -- Shao, Ning Yi -- Mazei-Robison, Michelle S -- Damez-Werno, Diane -- Scobie, Kimberly -- Bagot, Rosemary -- LaBonte, Benoit -- Ribeiro, Efrain -- Liu, XiaoChuan -- Kennedy, Pamela -- Vialou, Vincent -- Ferguson, Deveroux -- Pena, Catherine -- Calipari, Erin S -- Koo, Ja Wook -- Mouzon, Ezekiell -- Ghose, Subroto -- Tamminga, Carol -- Neve, Rachael -- Shen, Li -- Nestler, Eric J -- P50 MH096890/MH/NIMH NIH HHS/ -- R00 MH094405/MH/NIMH NIH HHS/ -- England -- Nature. 2014 Dec 4;516(7529):51-5. doi: 10.1038/nature13976. Epub 2014 Nov 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA. ; Department of Psychiatry, University of Texas Southwestern, Dallas, Texas 75390, USA. ; Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25383518" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/genetics ; Animals ; DEAD-box RNA Helicases/*genetics/metabolism ; Depression/physiopathology ; Gene Expression Profiling ; *Gene Expression Regulation ; Genome-Wide Association Study ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; MicroRNAs/*genetics/metabolism ; Neurons/metabolism ; *Resilience, Psychological ; Ribonuclease III/*genetics/metabolism ; Signal Transduction ; Stress, Physiological/*genetics ; beta Catenin/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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