{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T12:25:57Z","timestamp":1784723157361,"version":"3.55.0"},"reference-count":45,"publisher":"American Diabetes Association","issue":"2","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2008,2,1]]},"abstract":"<jats:p>OBJECTIVE\u2014 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\u2013coupled receptor, Mas, in the lipidic and glycemic metabolism in FVB\/N mice.<\/jats:p>\n               <jats:p>RESEARCH DESIGN AND METHODS\u2014 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-[3H]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)-\u03b2, type 1 Ang II receptor, and angiotensinogen (AGT) were measured by real-time PCR.<\/jats:p>\n               <jats:p>RESULTS\u2014 Despite normal body weight, Mas-knockout (Mas-KO) mice presented dyslipidemia, increased levels of insulin and leptin, and an \u223c50% increase in abdominal fat mass. In addition, Mas gene\u2013deleted 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\u2212\/\u2212 presented increased muscle triglycerides, while liver triglyceride levels were normal. Expression of TGF-\u03b2 and AGT genes was higher in Mas-KO animals in comparison with controls.<\/jats:p>\n               <jats:p>CONCLUSIONS\u2014 These results show that Mas deficiency in FVB\/N mice leads to dramatic changes in glucose and lipid metabolisms, inducing a metabolic syndrome\u2013like state.<\/jats:p>","DOI":"10.2337\/db07-0953","type":"journal-article","created":{"date-parts":[[2007,11,20]],"date-time":"2007-11-20T02:15:06Z","timestamp":1195524906000},"page":"340-347","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":220,"title":["<i>Mas<\/i> Deficiency in FVB\/N Mice Produces Marked Changes in Lipid and Glycemic Metabolism"],"prefix":"10.2337","volume":"57","author":[{"given":"Se\u0301rgio Henrique S.","family":"Santos","sequence":"first","affiliation":[{"name":"Laboratory of Hypertension, Department of Physiology and Biophysics, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luciana Rodrigues","family":"Fernandes","sequence":"additional","affiliation":[{"name":"Laboratory of Nutritional Biochemistry, Department of Biochemistry, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E\u0301rica Guilhen","family":"Mario","sequence":"additional","affiliation":[{"name":"Laboratory of Cellular Metabolism, Department of Physiology and Biophysics, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adaliene Versiani M.","family":"Ferreira","sequence":"additional","affiliation":[{"name":"Laboratory of Cellular Metabolism, Department of Physiology and Biophysics, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura Cristina J.","family":"Po\u0302rto","sequence":"additional","affiliation":[{"name":"Laboratory of Nutritional Biochemistry, Department of Biochemistry, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaqueline Isaura","family":"Alvarez-Leite","sequence":"additional","affiliation":[{"name":"Laboratory of Nutritional Biochemistry, Department of Biochemistry, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leida Maria","family":"Botion","sequence":"additional","affiliation":[{"name":"Laboratory of Cellular Metabolism, Department of Physiology and Biophysics, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Bader","sequence":"additional","affiliation":[{"name":"Max-Delbru\u0308ck-Center for Molecular Medicine, Berlin-Buch, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natalia","family":"Alenina","sequence":"additional","affiliation":[{"name":"Max-Delbru\u0308ck-Center for Molecular Medicine, Berlin-Buch, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robson Augusto S.","family":"Santos","sequence":"additional","affiliation":[{"name":"Laboratory of Hypertension, Department of Physiology and Biophysics, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","reference":[{"key":"2022031207580746100_R1","doi-asserted-by":"crossref","unstructured":"Grundy SM, Brewer HB Jr, Cleeman JI, Smith SC Jr, Lenfant C, the National Heart, Lung, and Blood Institute: American Heart Association definition of metabolic syndrome: report of the National Heart, Lung, and Blood Institute\/American Heart Association Conference on scientific issues related to definition. 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