Background: Vitamin D is a fat-soluble compound responsible for promoting intestinal absorption of calcium, and this, in turn, acts as a signal transmitter or activator as protein in secretory processes and release of hormones. Vitamin D receptors are distributed in various tissues of the body and involved in biochemical reactions in the pathogenesis of several diseases, such as obesity. Objective: The aim of this article is to provide updated information on the role of vitamin D in insulin resistance in obese individuals. Methods: It was conducted a search of articles published in PubMED, SciELO, and LILACS database, without limit for the year of publication, using the keywords "vitamin D", "insulin resistance", and "obesity". Results: Excess adipose tissue seems to impair insulin signaling by inhibiting the phosphorylation of its receptor, resulting in insulin resistance. Studies have evidenced role of vitamin D in mechanisms involved in the pathogenesis of insulin resistance in obesity by acting in improving glycemic control both by increasing hepatic and peripheral glucose uptake and by promoting the secretion of this hormone. Conclusions: Vitamin D exerts a protective effect in the treatment and prevention of insulin resistance in patients with obesity and protects the body against oxidative stress and chronic inflammation, contributing to glycemic control. Unfortunately, current data related to the effects of vitamin D supplementation on insulin resistance are still inconclusive.

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Low calcium and zinc intake, glucocorticoid use, and active disease phase are favorable conditions for bone loss in patients with Crohn's disease.

Cushing’s syndrome (CS) is a disease that promotes several metabolic disorders and redox imbalance. Thus, in this paper, we standardized an experimental model of CS in rats and evaluated the effects of supplementation with leucine (LEU). Rats were injected intraperitoneally with dexamethasone (0.4; 0.6; 0.8; and 1.0 mg/kg) 4x/wk. for four weeks. The effects of LEU supplementation (0.5, 1.0, and 1.5% v/v in water to drink) were also evaluated. In vitro and in vivo evaluation of metabolic and redox parameters by biochemical and molecular assays defined the severity of the disease. Dexamethasone 1.0 mg/kg promoted the most severe symptoms of CS: such as weight loss, adiposity increase, glucose intolerance, and insulin resistance, as well as an increase in oxidative status in the liver. Moreover, LEU promoted a pattern of mixed dyslipidemia, adiposity increase, and raised serum levels of aspartate aminotransferase (AST). Likewise, it increased myeloperoxidase (MPO) activities and decreased the CAT mRNA in the liver, while it reduced NADPH oxidase (NOX) mRNA. Supplementation with LEU worsens metabolic status and liver damage in rats with CS without an evident antioxidant potential, suggesting that the administration of LEU represents a risky strategy to patients suffering from CS.