3 research outputs found

    Association Between Vitamin D Intake and Obesity During Pre- and Early Adolescence

    Get PDF
    Background: Prevalence of obesity in US children has increased substantially. The influence of vitamin D intake on body mass index (BMI) is yet to be clearly defined. Results are mixed regarding the relationship of vitamin D deficiency with obesity in children. The objective of this study was to examine the association between vitamin D intake and BMI over a 6 month period in pre-to early adolescent children in Pittsburgh, PA. Methods: Secondary analysis was done on 256 healthy 6-14 year old (54% male) Caucasian and African American (70%) children from Pittsburgh, PA. Participants completed a food frequency questionnaire (FFQ) and a Sun Exposure Questionnaire (SEQ) and provided anthropometric measures at 2 time points 6 months apart. Vitamin D intake was compared by BMI status (normal = \u3c85th percentile, overweight = 85th to 95th percentile, obese = \u3e95th percentile) as well as by change in BMI over 6 months. Statistical analysis included descriptive statistics, Kruskal-Wallis analysis of variance, Spearman’s correlation, Chi Square test, and regression analysis (vitamin D intake, gender, race, baseline BMI, total energy intake, sun exposure and sunscreen use). Results: Median reported vitamin D intake was 245.85 IU at baseline and 382.51 IU at 6 month follow up. After subdividing children by BMI, at baseline the obese group reported lowest median intake (188 IU) and at 6 month follow up the normal group reported lowest median intake (374 IU) (P=0.03). Overall relation between vitamin D intake and BMI was significant (P=0.033) but weak (r=-0.015). Regression analysis revealed only baseline BMI status (P=\u3c0.001) as a predictor of 6 month follow up BMI. No relation was observed between change in BMI and vitamin D intake. Conclusion: The results of this study do not support a strong relationship between vitamin D intake and change in BMI status over a 6 month time period

    Mitochondrial injury, oxidative stress, and antioxidant gene expression are induced by hepatitis C virus core protein

    Get PDF
    Background and Aims: The mechanisms of liver injury in chronic hepatitis C virus (HCV) infection are poorly understood. Indirect evidence suggests that oxidative stress and mitochondrial injury play a role. The aim of this study was to determine if the HCV core protein itself alters mitochondrial function and contributes to oxidative stress. Methods: HCV core protein was expressed in 3 different cell lines, and reactive oxygen species (ROS) and lipid peroxidation products were measured. Results: Core expression uniformly increased ROS. In 2 inducible expression systems, core protein also increased lipid peroxidation products and induced antioxidant gene expression as well. A mitochondrial electron transport inhibitor prevented the core-induced increase in ROS. A fraction of the expressed core protein localized to the mitochondria and was associated with redistribution of cytochrome c from mitochondrial to cytosolic fractions. Sensitivity to oxidative stress was also seen in HCV transgenic mice in which increased intrahepatic lipid peroxidation products occurred in response to carbon tetrachloride. Conclusions: Oxidative injury occurs as a direct result of HCV core protein expression both in vitro and in vivo and may involve a direct effect of core protein on mitochondria. These results provide new insight into the pathogenesis of hepatitis C and provide an experimental rationale for investigation of antioxidant therapy
    corecore