PPARgamma activation in adipocytes is sufficient for systemic insulin sensitization. - Wikidata - awgldk - TriplyDB

PPARgamma activation in adipocytes is sufficient for systemic insulin sensitization.

PPARgamma activation in adipocytes is sufficient for systemic insulin sensitization.

http://www.wikidata.org/entity/Q37478987

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Adipocyte NCoR knockout decreases PPARγ phosphorylation and enhances PPARγ activity and insulin sensitivity Is the Mouse a Good Model of Human PPARγ-Related Metabolic Diseases?Smooth Muscle-Targeted Overexpression of Peroxisome Proliferator Activated Receptor-γ Disrupts Vascular Wall Structure and Function CMHX008, a novel peroxisome proliferator-activated receptor γ partial agonist, enhances insulin sensitivity in vitro and in vivo Nr4a1 is required for fasting-induced down-regulation of Pparγ2 in white adipose tissue.Mechanisms of inflammatory responses in obese adipose tissue.Selective Tissue Distribution Mediates Tissue-Dependent PPARγ Activation and Insulin Sensitization by INT131, a Selective PPARγ Modulator.Involvement of inducible 6-phosphofructo-2-kinase in the anti-diabetic effect of peroxisome proliferator-activated receptor gamma activation in mice.AMPK-Dependent Metabolic Regulation by PPAR Agonists.Maternal obesity and fetal metabolic programming: a fertile epigenetic soil.Thiazolidinediones and the promise of insulin sensitization in type 2 diabetes.Human CD68 promoter GFP transgenic mice allow analysis of monocyte to macrophage differentiation in vivo.Multi-tissue, selective PPARγ modulation of insulin sensitivity and metabolic pathways in obese rats.α3(V) collagen is critical for glucose homeostasis in mice due to effects in pancreatic islets and peripheral tissues Transcriptional and epigenetic control of brown and beige adipose cell fate and function.Differential lipid partitioning between adipocytes and tissue macrophages modulates macrophage lipotoxicity and M2/M1 polarization in obese mice Suppression of adipogenesis by pathogenic seipin mutant is associated with inflammatory response A role for central nervous system PPAR-γ in the regulation of energy balance Feeder-dependent and feeder-independent iPS cell derivation from human and mouse adipose stem cells.PPARs are a unique set of fatty acid regulated transcription factors controlling both lipid metabolism and inflammation Butter naturally enriched in cis-9, trans-11 CLA prevents hyperinsulinemia and increases both serum HDL cholesterol and triacylglycerol levels in rats.PPARγ: a molecular link between systemic metabolic disease and benign prostate hyperplasia.Disruption of hypoxia-inducible factor 1 in adipocytes improves insulin sensitivity and decreases adiposity in high-fat diet-fed mice Increasing adipocyte lipoprotein lipase improves glucose metabolism in high fat diet-induced obesity Adipocyte SIRT1 knockout promotes PPARγ activity, adipogenesis and insulin sensitivity in chronic-HFD and obesity.Adipose tissue plasticity from WAT to BAT and in between.The ubiquitin ligase Siah2 regulates PPARγ activity in adipocytes.Controlling a master switch of adipocyte development and insulin sensitivity: covalent modifications of PPARγ A PPARγ-FGF1 axis is required for adaptive adipose remodelling and metabolic homeostasis.Naturally improving insulin resistance with amorfrutins.Targeted overexpression of inducible 6-phosphofructo-2-kinase in adipose tissue increases fat deposition but protects against diet-induced insulin resistance and inflammatory responses.Improved insulin sensitivity after treatment with PPARγ and PPARα ligands is mediated by genetically modulated transcripts.Tissue resident regulatory T cells: novel therapeutic targets for human disease.Proteomic Analysis of GLUT4 Storage Vesicles Reveals Tumor Suppressor Candidate 5 (TUSC5) as a Novel Regulator of Insulin Action in Adipocytes Animal models as tools to investigate antidiabetic and anti-inflammatory plants.FABP4-Cre Mediated Expression of Constitutively Active ChREBP Protects Against Obesity, Fatty Liver, and Insulin Resistance Insulin-containing lipogenic stimuli suppress mast cell degranulation potential and up-regulate lipid body biogenesis and eicosanoid secretion in a PPARγ-independent manner.Novel Podophyllotoxin Derivatives as Partial PPARγ Agonists and their Effects on Insulin Resistance and Type 2 Diabetes.Coordinated Regulation of PPARγ Expression and Activity through Control of Chromatin Structure in Adipogenesis and Obesity.Defining the molecular nexus of cancer, type 2 diabetes and cardiovascular disease.

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PPARgamma activation in adipocytes is sufficient for systemic insulin sensitization.

http://www.wikidata.org/entity/Q37478987

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

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bilimsel makale

@tr

scientific article published on 16 December 2009

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

PPARgamma activation in adipocytes is sufficient for systemic insulin sensitization.

@en

PPARgamma activation in adipocytes is sufficient for systemic insulin sensitization.

@nl

type

label

PPARgamma activation in adipocytes is sufficient for systemic insulin sensitization.

@en

PPARgamma activation in adipocytes is sufficient for systemic insulin sensitization.

@nl

prefLabel

PPARgamma activation in adipocytes is sufficient for systemic insulin sensitization.

@en

PPARgamma activation in adipocytes is sufficient for systemic insulin sensitization.

@nl

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PNAS.0912487106

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Proceedings of the National Academy of Sciences of the United States of America

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PPARgamma activation in adipocytes is sufficient for systemic insulin sensitization.

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Annette R Atkins

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Dorothy D Sears

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Gene Hsiao

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Glenda L Castro

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Grant D Barish

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Maziyar Saberi

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Michael C Nelson

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Michael Downes

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Peter Olson

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Ruth T Yu

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P2860

Effect of Rosiglitazone on the Risk of Myocardial Infarction and Death from Cardiovascular Causes

Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance

Obesity is associated with macrophage accumulation in adipose tissue

Lack of macrophage fatty-acid-binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis

Muscle-specific Pparg deletion causes insulin resistance

Macrophage-specific PPARgamma controls alternative activation and improves insulin resistance

Fat and beyond: the diverse biology of PPARgamma

An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-activated receptor gamma (PPAR gamma)

mPPAR gamma 2: tissue-specific regulator of an adipocyte enhancer

Peroxisome-proliferator-activated receptor delta activates fat metabolism to prevent obesity

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22504-22509

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scholarly article

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10.1073/PNAS.0912487106

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52

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106

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David R Greaves

Jerrold M. Olefsky

Ronald M. Evans

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2009-12-16T00:00:00Z

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40696114

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20018750

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2794650

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