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The aim of this study was to evaluate dietary vitamin D intake and its relationship with an inflammation marker in obese women. A cross-sectional study was designed involving obese women (n=44) and women with normal weight (n=44). Anthropometric assessment using weight and height measurements and classification of nutritional status according to body mass index and waist circumference measurement was performed. The intake of vitamin D was assessed using food diaries kept for three days and the Dietpro 5.i program. Determination of C-reactive protein in serum was carried out by turbidimetry measurement. About the results, the mean values ​​of vitamin D intake by obese women were lower than those of the control group and the reference values ​​(p=0.001). The mean C-reactive protein concentrations for obese women and the control group were 2.45±1.72 mg/L and 1.79±0.48 mg/L, respectively. The results of the analysis of correlation between the intake of vitamin D and the inflammatory marker evaluated in this study revealed no significant association. About the conclusion, the obese women evaluated in this study ingested vitamin D at an amount lower than the recommended value. The study does not show any relationship between vitamin D intake and serum C-reactive protein concentrations in obese women evaluated. However, considering the important anti-inflammatory function of vitamin D, it is necessary to deepen knowledge about the impact of this vitamin on obesity.

Introduction: The accumulation of visceral fat affects the metabolism of hormones and some nutrients, but these mechanisms remain unclear. Objective: To assess the influence of cortisol on the metabolism of zinc in morbidly obese women. Method: Cross-sectional, case-control study involving 80 women aged between 20 and 59 years. The participants were divided into two groups: experimental (morbidly obese, n = 40) and control (normal weight, n = 40). Zinc concentrations were determined by atomic absorption spectroscopy and serum and urinary cortisol by chemiluminescence method. Results: Zinc intake was significantly different between groups. Mean plasma zinc was lower in obese compared to control group. Mean values for erythrocyte zinc were 44.52 ± 7.84 μg/gHb and 40.17 ± 6.71 μg/gHb for obese and control groups, respectively. Urinary excretion of this mineral was higher in obese compared to control subjects (p < 0.05). Mean values for plasma cortisol were 9.58 ± 4.86 μg/dL for obese and 9.89 ± 5.61 μg/dL for control groups. Mean values for urinary cortisol were 163.00 ± 100.35 μg/dL and 109.71 ± 34.88 μg/dL for obese and control groups, respectively (p > 0.05). The correlation analysis between cortisol and zinc was not significant (p > 0.05). Conclusions: Obese patients have hypozincemia and high erythrocyte zinc levels. The correlation between zinc parameters and cortisol concentration showed no influence of this hormone on zinc metabolism.

Oxidative stress is a metabolic dysfunction that favors the oxidation of biomolecules, contributing to the oxidative damage of cells and tissues. This consequently contributes to the development of several chronic diseases. In particular, zinc is one of the most relevant minerals to human health, because of its antioxidant properties. This review aims to provide updated information about the mechanisms involved in the protective role of zinc against oxidative stress. Zinc acts as a co-factor for important enzymes involved in the proper functioning of the antioxidant defense system. In addition, zinc protects cells against oxidative damage, acts in the stabilization of membranes and inhibits the enzyme nicotinamide adenine dinucleotide phosphate oxidase (NADPH-Oxidase). Zinc also induces the synthesis of metallothioneins, which are proteins effective in reducing hydroxyl radicals and sequestering reactive oxygen species (ROS) produced in stressful situations, such as in type 2 diabetes, obesity and cancer. Literature provides strong evidence for the role of zinc in the protection against oxidative stress in several diseases.

Chronic hyperglycemia statue noticed in diabetes mellitus favors the manifestation of oxidative stress by increasing the production of reactive oxygen species and/or by reducing the antioxidant defense system activity. Zinc plays an important role in antioxidant defense in type 2 diabetic patients by notably acting as a cofactor of the superoxide dismutase enzyme, by modulating the glutathione metabolism and metallothionein expression, by competing with iron and copper in the cell membrane and by inhibiting nicotinamide adenine dinucleotide phosphate-oxidase enzyme. Zinc also improves the oxidative stress in these patients by reducing chronic hyperglycemia. It indeed promotes phosphorylation of insulin receptors by enhancing transport of glucose into cells. However, several studies reveal changes in zinc metabolism in individuals with type 2 diabetes mellitus and controversies remain regarding the effect of zinc supplementation in the improvement of oxidative stress in these patients. Faced with the serious challenge of the metabolic disorders related to oxidative stress in diabetes along with the importance of antioxidant nutrients in the control of this disease, new studies may contribute to improve our understanding of the role played by zinc against oxidative stress and its connection with type 2 diabetes mellitus prognosis. This could serve as a prelude to the development of prevention strategies and treatment of disorders associated with this chronic disease.