Key result
Genetic deletion of the Mas receptor in FVB/N mice induced a metabolic syndrome-like state, including dyslipidemia, glucose intolerance, and an approximately 50% increase in abdominal fat mass.
Why the study?
Does genetic deletion of the Mas receptor alter lipid and glycemic metabolism in FVB/N mice?
Does genetic deletion of the Mas receptor alter lipid and glycemic metabolism in FVB/N mice?
Mas deficiency in FVB/N mice induces a metabolic syndrome-like state characterized by dyslipidemia, insulin resistance, and increased abdominal fat.
Mas receptor deletion induces metabolic features in mice; leaves open its role in human cardiometabolic disease and requires translational studies.
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)-beta, 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 approximately 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-beta 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.
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Santos et al. (2007) studied Metabolic syndrome. Genetic deletion of Mas receptor vs. Wild-type mice was evaluated on Lipid and glycemic metabolism. Genetic deletion of the Mas receptor in FVB/N mice induced a metabolic syndrome-like state, including dyslipidemia, glucose intolerance, and an approximately 50% increase in abdominal fat mass.
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