Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes. - Wikidata - awgldk - TriplyDB

Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes.

Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes.

http://www.wikidata.org/entity/Q38324231

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Incretin-Based Therapies for Diabetic Complications: Basic Mechanisms and Clinical Evidence Hypoglycemic agents and potential anti-inflammatory activity Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control Inflammation Meets Metabolic Disease: Gut Feeling Mediated by GLP-1 Concise Review: Macrophages: Versatile Gatekeepers During Pancreatic β-Cell Development, Injury, and Regeneration.Liraglutide reduces body weight by upregulation of adenylate cyclase 3.Expression of CTRP3, a novel adipokine, in rats at different pathogenic stages of type 2 diabetes mellitus and the impacts of GLP-1 receptor agonist on it Effects of glucagon-like peptide-1 receptor agonists on non-alcoholic fatty liver disease and inflammation Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation Sarcoid-like lung granulomas in a hemodialysis patient treated with a dipeptidyl peptidase-4 inhibitor Crosstalk between intestinal microbiota, adipose tissue and skeletal muscle as an early event in systemic low-grade inflammation and the development of obesity and diabetes.Liraglutide, a glucagon-like peptide-1 analog, increased insulin sensitivity assessed by hyperinsulinemic-euglycemic clamp examination in patients with uncontrolled type 2 diabetes mellitus.Obesity, immunomodulation and chronic kidney disease.DPP-4 Inhibitor Reduces Central Blood Pressure in a Diabetic and Hypertensive Patient: A Case Report.Hepatic adenylate cyclase 3 is upregulated by Liraglutide and subsequently plays a protective role in insulin resistance and obesity.Extrapancreatic effects of incretin hormones: evidence for weight-independent changes in morphological aspects and oxidative status in insulin-sensitive organs of the obese nondiabetic Zucker rat (ZFR).Nonalcoholic Fatty liver: a possible new target for type 2 diabetes prevention and treatment.Does Glucagon-like Peptide-1 Ameliorate Oxidative Stress in Diabetes? Evidence Based on Experimental and Clinical Studies.Glucagon-like peptide 1 improves insulin resistance in vitro through anti-inflammation of macrophages.Effects of Exendin-4 on human adipose tissue inflammation and ECM remodelling.Exenatide improves hepatic steatosis by enhancing lipid use in adipose tissue in nondiabetic rats.GLP-1-mediated gene therapy approaches for diabetes treatment.GLP-1 receptor agonists: effects on the progression of non-alcoholic fatty liver disease.GLP-1: a mediator of the beneficial metabolic effects of bariatric surgery?An updated review on cancer risk associated with incretin mimetics and enhancers.Diabetes therapies in hemodialysis patients: Dipeptidase-4 inhibitors.Sitagliptin and liraglutide reversed nigrostriatal degeneration of rodent brain in rotenone-induced Parkinson's disease.DPP-IV inhibitor anagliptin exerts anti-inflammatory effects on macrophages, adipocytes, and mouse livers by suppressing NF-κB activation.Effect of Sipjeondaebo-tang on cancer-induced anorexia and cachexia in CT-26 tumor-bearing mice.JTT-130, a novel intestine-specific inhibitor of microsomal triglyceride transfer protein, improves hyperglycemia and dyslipidemia independent of suppression of food intake in diabetic rats Chronic exposure to air pollution particles increases the risk of obesity and metabolic syndrome: findings from a natural experiment in Beijing.Exendin-4 attenuates adverse cardiac remodelling in streptozocin-induced diabetes via specific actions on infiltrating macrophages.GLP-1 receptor agonist increases the expression of CTRP3, a novel adipokine, in 3T3-L1 adipocytes through PKA signal pathway.Inflammation and incretins.Modulation of GLP-1 Levels by a Genetic Variant That Regulates the Cardiovascular Effects of Intensive Glycemic Control in ACCORD.Role of Incretin Axis in Inflammatory Bowel Disease.Efficacy of exenatide on weight loss, metabolic parameters and pregnancy in overweight/obese polycystic ovary syndrome.Duodenal-jejunal bypass improves glucose metabolism and adipokine expression independently of weight loss in a diabetic rat model.Anti-obesogenic effects of calcium prevent changes in the GLP-1 profile in adult rats primed by early weaning.Glucagon-like peptide-1 receptor activation reverses cardiac remodeling via normalizing cardiac steatosis and oxidative stress in type 2 diabetes.

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Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes.

http://www.wikidata.org/entity/Q38324231

description

2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年學術文章

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2012年學術文章

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2012年學術文章

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name

Glucagon-like peptide-1 inhibi ...... obese mouse model of diabetes.

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Glucagon-like peptide-1 inhibi ...... obese mouse model of diabetes.

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J-S Choung

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P2860

The LIM-only protein Lmo2 is a bridging molecule assembling an erythroid, DNA-binding complex which includes the TAL1, E47, GATA-1 and Ldb1/NLI proteins

NF-kappaB activation by tumour necrosis factor requires the Akt serine-threonine kinase

Glucagon-like peptide-1 gene therapy in obese diabetic mice results in long-term cure of diabetes by improving insulin sensitivity and reducing hepatic gluconeogenesis

Prevention of fat-induced insulin resistance by salicylate

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

IKK-beta links inflammation to obesity-induced insulin resistance

Local and systemic insulin resistance resulting from hepatic activation of IKK-beta and NF-kappaB

CCR2 modulates inflammatory and metabolic effects of high-fat feeding

Gene expression profiling and network analysis reveals lipid and steroid metabolism to be the most favored by TNFalpha in HepG2 cells.

Adipocyte-mononuclear cell interaction, Toll-like receptor 4 activation, and high glucose synergistically up-regulate osteopontin expression via an interleukin 6-mediated mechanism.

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