SOCS2 modulates adipose tissue inflammation and expansion in mice.

Introduction: Obesity is usually triggered by a nutrient overload that favors adipocyte hypertrophy and increases the number of pro-inflammatory cells and mediators into adipose tissue. These mediators may be regulated by suppressors of cytokine signaling (SOCS), such as SOCS2, which is involved in the regulation of the inflammatory response of many diseases, but its role in obesity is not yet known. We aimed to investigate the role of SOCS2 in metabolic and inflammatory dysfunction induced by a high-refined carbohydrate-containing diet (HC).

Diet versus jaw bones: Lessons from experimental models and potential clinical implications.

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.

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

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.