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Mas Deficiency in FVB/N Mice Produces Marked Changes in Lipid and Glycemic Metabolism

SANTOS, Sérgio Henrique S ; FERNANDES, Luciana Rodrigues ; GUILHEN MARIO, Erica ; FERREIRA, Adaliene Versiani M ; PORTO, Laura Cristina J ; ISAURA ALVAREZ-LEITE, Jaqueline ; BOTION, Leida Maria ; BADER, Michael ; ALENINA, Natalia ; SANTOS, Robson Augusto S

Diabetes (New York, N.Y.), 2008-02, Vol.57 (2), p.340-347 [Periódico revisado por pares]

Alexandria, VA: American Diabetes Association

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Mas Deficiency in FVB/N Mice Produces Marked Changes in Lipid and Glycemic Metabolism
Autor: SANTOS, Sérgio Henrique S ; FERNANDES, Luciana Rodrigues ; GUILHEN MARIO, Erica ; FERREIRA, Adaliene Versiani M ; PORTO, Laura Cristina J ; ISAURA ALVAREZ-LEITE, Jaqueline ; BOTION, Leida Maria ; BADER, Michael ; ALENINA, Natalia ; SANTOS, Robson Augusto S
Assuntos: Adipocytes - metabolism ; Adipose Tissue - anatomy & histology ; Adipose Tissue - physiology ; Animals ; Biological and medical sciences ; Biological Transport ; Blood Glucose - metabolism ; Body Weight ; Cytokines - blood ; Development and progression ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Energy Intake ; Epididymis - pathology ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Genetic aspects ; Glucose - metabolism ; Glucose Tolerance Test ; Insulin - blood ; Lipid metabolism ; Lipids - blood ; Male ; Medical sciences ; Metabolic Syndrome - genetics ; Metabolic Syndrome - pathology ; Metabolic syndrome X ; Mice ; Mice, Knockout ; Physiological aspects ; Proto-Oncogene Proteins - deficiency ; Proto-Oncogene Proteins - genetics ; Receptors, G-Protein-Coupled - deficiency ; Receptors, G-Protein-Coupled - genetics ; Renin-angiotensin system ; Reverse Transcriptase Polymerase Chain Reaction ; Triglycerides - blood
É parte de: Diabetes (New York, N.Y.), 2008-02, Vol.57 (2), p.340-347
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
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Descrição: Mas Deficiency in FVB/N Mice Produces Marked Changes in Lipid and Glycemic Metabolism Sérgio Henrique S. Santos 1 , Luciana Rodrigues Fernandes 2 , Érica Guilhen Mario 3 , Adaliene Versiani M. Ferreira 3 , Laura Cristina J. Pôrto 2 , Jaqueline Isaura Alvarez-Leite 2 , Leida Maria Botion 3 , Michael Bader 4 , Natalia Alenina 4 and Robson Augusto S. Santos 1 1 Laboratory of Hypertension, Department of Physiology and Biophysics, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil 2 Laboratory of Nutritional Biochemistry, Department of Biochemistry, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil 3 Laboratory of Cellular Metabolism, Department of Physiology and Biophysics, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil 4 Max-Delbrück-Center for Molecular Medicine, Berlin-Buch, Germany Address correspondence and reprint requests to Robson A.S. Santos, Laborátorio de Hipertensão, Departamento de Fisiologia e Biofisica, Universidade Federal de Minas Gerais, Av Antonio Carlos 6627-ICB, 31270-901, Belo Horizonte, Minas Gerais, Brazil. E-mail: robsonsant{at}gmail.com Abstract OBJECTIVE— Metabolic syndrome is characterized by the variable coexistence of obesity, hyperinsulinemia, insulin resistance, dyslipidemia, and hypertension. It is well known that angiotensin (Ang) II is importantly involved in the metabolic syndrome. However, the role of the vasodilator Ang-(1-7)/ Mas axis is not known. The aim of this study was to evaluate the effect of genetic deletion of the G protein–coupled receptor, Mas , in the lipidic and glycemic metabolism in FVB/N mice. RESEARCH DESIGN AND METHODS— Plasma lipid, insulin, and cytokine concentrations were measured in FVB/N Mas- deficient and wild-type mice. A glucose tolerance test was performed by intraperitoneally injecting d -glucose into overnight-fasted mice. An insulin sensitivity test was performed by intraperitoneal injection of insulin. Uptake of 2-deoxy-[ 3 H]glucose by adipocytes was used to determine the rate of glucose transport; adipose tissue GLUT4 was quantified by Western blot. Gene expression of transforming growth factor (TGF)-β, type 1 Ang II receptor, and angiotensinogen (AGT) were measured by real-time PCR. RESULTS— Despite normal body weight, Mas- knockout ( Mas -KO) mice presented dyslipidemia, increased levels of insulin and leptin, and an ∼50% increase in abdominal fat mass. In addition, Mas gene–deleted mice presented glucose intolerance and reduced insulin sensitivity as well as a decrease in insulin-stimulated glucose uptake by adipocytes and decreased GLUT4 in adipose tissue. Mas −/− presented increased muscle triglycerides, while liver triglyceride levels were normal. Expression of TGF-β and AGT genes was higher in Mas -KO animals in comparison with controls. CONCLUSIONS— These results show that Mas deficiency in FVB/N mice leads to dramatic changes in glucose and lipid metabolisms, inducing a metabolic syndrome–like state. 2DOG, 2-deoxy-[3H]glucose AGT, angiotensinogen Ang, angiotensin AT1R, type 1 Ang II receptor RAS, renin-Ang system TGF, transforming growth factor TNF, tumor necrosis factor Footnotes Published ahead of print at http://diabetes.diabetesjournals.org on 19 November 2007. DOI: 10.2337/db07-0953. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Accepted November 13, 2007. Received July 17, 2007. DIABETES
Editor: Alexandria, VA: American Diabetes Association
Idioma: Inglês

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Mas Deficiency in FVB/N Mice Produces Marked Changes in Lipid and Glycemic Metabolism

SANTOS, Sérgio Henrique S ; FERNANDES, Luciana Rodrigues ; GUILHEN MARIO, Erica ; FERREIRA, Adaliene Versiani M ; PORTO, Laura Cristina J ; ISAURA ALVAREZ-LEITE, Jaqueline ; BOTION, Leida Maria ; BADER, Michael ; ALENINA, Natalia ; SANTOS, Robson Augusto S

Alexandria, VA: American Diabetes Association

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