Mas deficiency in FVB/N mice produces marked changes in lipid and glycemic metabolism. - Wikidata - awgldk - TriplyDB

Mas deficiency in FVB/N mice produces marked changes in lipid and glycemic metabolism.

Mas deficiency in FVB/N mice produces marked changes in lipid and glycemic metabolism.

http://www.wikidata.org/entity/Q46891673

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Angiotensin-(1-7): new perspectives in atherosclerosis treatment Vascular stiffness in insulin resistance and obesity Review article: pancreatic renin-angiotensin systems in health and disease Obesity associated hypertension: new insights into mechanism Divergent mechanism regulating fluid intake and metabolism by the brain renin-angiotensin system Modulation of glucose metabolism by the renin-angiotensin-aldosterone system Anti-Inflammatory Effects of Ang-(1-7) in Ameliorating HFD-Induced Renal Injury through LDLr-SREBP2-SCAP Pathway Physiology of kidney renin Long-term systemic angiotensin II type 1 receptor blockade regulates mRNA expression of dorsomedial medulla renin-angiotensin system components The metabolic syndrome The renin angiotensin system and the metabolic syndrome ACE2 and diabetes: ACE of ACEs?The brain Renin-angiotensin system controls divergent efferent mechanisms to regulate fluid and energy balance.Renin-angiotensin system blockers protect pancreatic islets against diet-induced obesity and insulin resistance in mice Chronic treatment with angiotensin-(1-7) improves renal endothelial dysfunction in apolipoproteinE-deficient mice Reduced levels of two modifiers of epigenetic gene silencing, Dnmt3a and Trim28, cause increased phenotypic noise.Atypical signaling and functional desensitization response of MAS receptor to peptide ligands.The combination of high-fat diet-induced obesity and chronic ulcerative colitis reciprocally exacerbates adipose tissue and colon inflammation Angiotensin I-converting enzyme type 2 (ACE2) gene therapy improves glycemic control in diabetic mice.Deficiency of ACE2 in Bone-Marrow-Derived Cells Increases Expression of TNF-α in Adipose Stromal Cells and Augments Glucose Intolerance in Obese C57BL/6 Mice MAS C-Terminal Tail Interacting Proteins Identified by Mass Spectrometry- Based Proteomic Approach.The link between the renin-angiotensin-aldosterone system and renal injury in obesity and the metabolic syndrome.Polymorphism in miR-31 and miR-584 binding site in the angiotensinogen gene differentially influences body fat distribution in both sexes.Angiotensin converting enzyme 2: a new important player in the regulation of glycemia.International Union of Basic and Clinical Pharmacology. XCIX. Angiotensin Receptors: Interpreters of Pathophysiological Angiotensinergic Stimuli [corrected].Physical activity prevents alterations in mitochondrial ultrastructure and glucometabolic parameters in a high-sugar diet model.Effect of Angiotensin(1-7) on Heart Function in an Experimental Rat Model of Obesity Opposing tissue-specific roles of angiotensin in the pathogenesis of obesity, and implications for obesity-related hypertension Loss of ACE2 exaggerates high-calorie diet-induced insulin resistance by reduction of GLUT4 in mice.The renin angiotensin aldosterone system and insulin resistance in humans.Angiotensin-converting enzyme 2/angiotensin-(1-7)/Mas axis activates Akt signaling to ameliorate hepatic steatosis Metabolic rate regulation by the renin-angiotensin system: brain vs. body.Mice lacking angiotensin-converting enzyme have increased energy expenditure, with reduced fat mass and improved glucose clearance Angiotensin 1-7 as means to prevent the metabolic syndrome: lessons from the fructose-fed rat model.Chronic Angiotensin-(1-7) Improves Insulin Sensitivity in High-Fat Fed Mice Independent of Blood Pressure.ACE2 is expressed in mouse adipocytes and regulated by a high-fat diet.Angiotensin (1-7)/Mas receptor axis activation ameliorates the changes in fatty acid composition in diabetic rats with nephropathy.Control of adipogenesis by the autocrine interplays between angiotensin 1-7/Mas receptor and angiotensin II/AT1 receptor signaling pathways Upregulation of the angiotensin-converting enzyme 2/angiotensin-(1-7)/Mas receptor axis in the heart and the kidney of growth hormone receptor knock-out mice.Angiotensin-converting enzyme 2 and the kidney.

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P2860

Mas deficiency in FVB/N mice produces marked changes in lipid and glycemic metabolism.

http://www.wikidata.org/entity/Q46891673

description

2007 nî lūn-bûn

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2007年の論文

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年学术文章

@zh-my

2007年学术文章

@zh-sg

2007年學術文章

@yue

2007年學術文章

@zh-hant

name

Mas deficiency in FVB/N mice produces marked changes in lipid and glycemic metabolism.

@en

Mas deficiency in FVB/N mice produces marked changes in lipid and glycemic metabolism.

@nl

type

label

Mas deficiency in FVB/N mice produces marked changes in lipid and glycemic metabolism.

@en

Mas deficiency in FVB/N mice produces marked changes in lipid and glycemic metabolism.

@nl

prefLabel

Mas deficiency in FVB/N mice produces marked changes in lipid and glycemic metabolism.

@en

Mas deficiency in FVB/N mice produces marked changes in lipid and glycemic metabolism.

@nl

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Mas deficiency in FVB/N mice produces marked changes in lipid and glycemic metabolism.

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Adaliene Versiani M Ferreira

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Erica Guilhen Mario

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Jaqueline Isaura Alvarez-Leite

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Laura Cristina J Pôrto

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Luciana Rodrigues Fernandes

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Natalia Alenina

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Robson Augusto S Santos

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Sérgio Henrique S Santos

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340-347

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scholarly article

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10.2337/DB07-0953

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2

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57

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Leida Maria Botion

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2007-11-19T00:00:00Z

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5822630

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18025412

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