RESUMEN
The consumption of different types of diets influences not only body health but the bone remodeling process as well. Nutritional components can directly affect maxillary and mandibular alveolar bone microarchitecture. In this review, we focus on the current knowledge regarding the influence of diets and dietary supplementation on alveolar bone. Accumulating evidence from experimental models suggests that carbohydrate- and fat-rich diets are detrimental for alveolar bone, whereas protective effects are associated with consumption of calcium, ω-3, and bioactive compounds. Little is known about the effects of protein-free and protein-rich diets, boron, vitamin C, vitamin E, zinc, and caffeine on alveolar bone remodeling. Adipokines and direct effects of nutritional components on bone cells are proposed mechanisms linking diet and bone. Results from animal models substantiate the role of nutritional components on alveolar bone. It is a well-built starting point for clinical studies on nutritional monitoring and intervention for patients with alveolar bone disorders, especially those who are treatment refractory.
Asunto(s)
Densidad Ósea , Dieta , Maxilares/ultraestructura , Adipoquinas/sangre , Animales , Calcio de la Dieta/administración & dosificación , Carbohidratos de la Dieta/administración & dosificación , Grasas de la Dieta/administración & dosificación , Proteínas en la Dieta/administración & dosificación , Suplementos Dietéticos , Ácidos Grasos Omega-3/administración & dosificación , Humanos , Micronutrientes/administración & dosificación , Modelos Animales , Evaluación NutricionalRESUMEN
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.