Nutrient stress activates inflammation and reduces glucose metabolism by suppressing AMP-activated protein kinase in the heart. - Wikidata - awgldk - TriplyDB

Nutrient stress activates inflammation and reduces glucose metabolism by suppressing AMP-activated protein kinase in the heart.

Nutrient stress activates inflammation and reduces glucose metabolism by suppressing AMP-activated protein kinase in the heart.

http://www.wikidata.org/entity/Q42593363

about

Regulation and function of AMPK in physiology and diseases The mitochondria in diabetic heart failure: from pathogenesis to therapeutic promise Redox regulation of mitochondrial biogenesis Diabetic cardiomyopathy: bench to bedside AMP-activated protein kinase mediates myogenin expression and myogenesis via histone deacetylase 5 Administration of granulocyte-colony stimulating factor accompanied with a balanced diet improves cardiac function alterations induced by high fat diet in mice.Characterization of Bglu3, a mouse fasting glucose locus, and identification of Apcs as an underlying candidate gene.Metformin protects against infection-induced myocardial dysfunction.Hyperinsulinemia Down-Regulates TLR4 Expression in the Mammalian Heart.Inflammation and insulin resistance: an old story with new ideas.Dietary epicatechin promotes survival of obese diabetic mice and Drosophila melanogaster.Adipose tissue remodeling in a novel domestic porcine model of diet-induced obesity.AMPK inhibition in health and disease.Resveratrol retards progression of diabetic nephropathy through modulations of oxidative stress, proinflammatory cytokines, and AMP-activated protein kinase.New insights into insulin resistance in the diabetic heart.A newly designed curcumin analog Y20 mitigates cardiac injury via anti-inflammatory and anti-oxidant actions in obese rats.Loss of Toll-Like Receptor 4 Function Partially Protects against Peripheral and Cardiac Glucose Metabolic Derangements During a Long-Term High-Fat Diet Transition from obesity to metabolic syndrome is associated with altered myocardial autophagy and apoptosis.Antidiabetic drug metformin suppresses endotoxin-induced uveitis in rats Myocardial ischemia reperfusion injury: from basic science to clinical bedside.Macrophages modulate cardiac function in lipotoxic cardiomyopathy.Free fatty acid oxidation in insulin resistance and obesity.A high-fat diet decreases AMPK activity in multiple tissues in the absence of hyperglycemia or systemic inflammation in rats.Insulin resistance: metabolic mechanisms and consequences in the heart.Short-term weight loss attenuates local tissue inflammation and improves insulin sensitivity without affecting adipose inflammation in obese mice CARD9 knockout ameliorates myocardial dysfunction associated with high fat diet-induced obesity.Maladaptive immune and inflammatory pathways lead to cardiovascular insulin resistance.Altered Interleukin-10 Signaling in Skeletal Muscle Regulates Obesity-Mediated Inflammation and Insulin Resistance.AMPKα Is Suppressed in Bladder Cancer through Macrophage-Mediated Mechanisms.Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases Perivascular fat, AMP-activated protein kinase and vascular diseases.Activation of toll-like receptors and inflammasome complexes in the diabetic cardiomyopathy-associated inflammation.AMP-activated protein kinase inhibits NF-κB signaling and inflammation: impact on healthspan and lifespan.AMP-activated protein kinase: a potential player in Alzheimer's disease.Autophagy as a therapeutic target in diabetic nephropathy.Transcriptional control of mitochondrial biogenesis and its interface with inflammatory processes.Autophagy, myocardial protection, and the metabolic syndrome.Cellular cross-talk between epicardial adipose tissue and myocardium in relation to the pathogenesis of cardiovascular disease.AMP-activated protein kinase regulation and biological actions in the heart.Sphingolipids, lipotoxic cardiomyopathy, and cardiac failure.

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P2860

Nutrient stress activates inflammation and reduces glucose metabolism by suppressing AMP-activated protein kinase in the heart.

http://www.wikidata.org/entity/Q42593363

description

2009 nî lūn-bûn

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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2009年论文

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2009年论文

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name

Nutrient stress activates infl ...... d protein kinase in the heart.

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type

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Nutrient stress activates infl ...... d protein kinase in the heart.

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Nutrient stress activates infl ...... d protein kinase in the heart.

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Dae Young Jung

http://www.w3.org/2001/XMLSchema#string

Hwi Jin Ko

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Jason K Kim

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John Y Jun

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Kelly E Jones

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Sook Y Chan

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Zhexi Ma

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Zhiyou Zhang

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P2860

Inflammation, stress, and diabetes

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

Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance

SOCS-1 and SOCS-3 block insulin signaling by ubiquitin-mediated degradation of IRS1 and IRS2

Cloning and functional expression of mCCR2, a murine receptor for the C-C chemokines JE and FIC

MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity

The hormone resistin links obesity to diabetes

TLR4 links innate immunity and fatty acid-induced insulin resistance

Adiponectin and adiponectin receptors

CCR2 modulates inflammatory and metabolic effects of high-fat feeding

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10.2337/DB08-1361

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11

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58

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19690060

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2768176

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