Iron supplementation does not aggravate impaired glucose tolerance and sugar overload-induced genotoxicity in rats.

High sugar intake is a major risk factor for metabolic disorders. Genotoxicity is an important factor in diabetes onset, and iron (Fe) may be an aggravating element. However, this relationship is still poorly established. Thus, this study evaluated whether Fe supplementation could aggravate obesity, impaired glucose tolerance, and sugar overload-induced genotoxicity in rats. A total of 24 rats were treated with different diets: standard diet (SD, n = 8), invert sugar overload (320 g/L, HSD, n = 8), or Fe plus invert sugar overload (2.56 mg/L of Fe2+, Fe-HSD, n = 8) for four months. After treatment, the Fe-HSD group showed no excessive weight gain or impaired glucose tolerance. DNA damage in blood, as assessed by comet assay, gradually increased in HSD during treatment (p < 0.001), whereas Fe-HSD showed a nonlinear increase in DNA damage. Moreover, Fe-HSD presented 0.6-fold more DNA damage compared with SD (p = 0.0055) in the 1st month of treatment. At months 2 and 3, results show a ≥ 1.4-fold increase in HSD and Fe-HSD DNA damage, respectively, compared with SD (p < 0.01). At the end of the experiment, only HSD DNA damage differed from SD (1.5-fold more, p = 0.0196). Fe supplementation did not aggravate the invert sugar-induced DNA damage (p > 0.05). In the pancreas, results showed no differences in DNA damage. Mutagenicity, evaluated by micronucleus testing, was not observed regardless of treatment (p = 0.428). Fe supplementation, in the evaluated concentration, did not aggravate weight gain, impaired glucose tolerance, and sugar overload-induced genotoxicity in rats.

Cardiorespiratory fitness, screen time and cardiometabolic risk in South Brazilian school children.

BACKGROUND: Cardiorespiratory fitness (CRF) is considered a beneficial effect of physical activity (PA). PA and excessive screen time have implications for cardiometabolic risk. OBJECTIVE: To verify the association between screen time and CRF grouped by cardiometabolic risk factors. SUBJECTS AND METHODS: Cross-sectional study evaluated 1,253 schoolchildren (54.2% girls) aged seven to 17 years from southern Brazil. The outcomes were body mass index (BMI), waist circumference (WC), systolic blood pressure (SBP), and diastolic (DBP), glucose, and lipid profile. Exposure was a combined variable of self-reported screen time (television, video game, computer) and CRF. RESULTS: The main result is that CRF had a more consistent association with anthropometric factors than with metabolic variables. Low CRF students, regardless of screen time, showed a 15% increase in the risk of elevated WC (p < 0.001) and a 24% (<2 h screen time) and 19% (≥2 h) higher risk of overweight (p < 0.001). Second, the increase in SBP was associated with a combination of the two risk factors, ≥2 h screen time/low CRF was associated with a 7% increase in elevated SBP (p = 0.025). CONCLUSION: Low CRF was a risk factor for elevated BMI and WC, regardless of screen time. High screen time and low CRF were associated with higher SBP values.

High urate concentration is associated with elevated blood pressure in schoolchildren.

Background Studies in adults have shown a relationship between high blood pressure and hyperuricemia, but few studies have investigated this association in children and adolescents. The aim of the present study was to associate urate concentration with systolic blood pressure (SBP) and diastolic blood pressure (DBP) in schoolchildren. Methods This cross-sectional study used a sample of 2335 schoolchildren in basic education between 7 and 17 years old. Blood pressure was classified by percentile according to Brazilian parameters for sex and age, reclassified into two categories: normal and borderline/hypertension. Blood collection to obtain serum for urate concentration analysis was performed after a 12-h fast. Values above 5.5 mg/dL were considered hyperuricemia. Descriptive data were presented in frequency and percentage. Linear regression and Poisson regression (prevalence ratio [PR]) was used to test the association between urate concentration and blood pressure. Results Urate concentration was weakly associated with SBP (ß: 0.05; 95% CI: 0.02-0.08) and DBP (ß: 0.03; 95% CI: 0.01-0.05) z-scores. Schoolchildren with hyperuricemia had a higher prevalence of high SBP (PR: 1.12; p<0.001) and DBP (PR: 1.08; p<0.001). Conclusions Elevated urate concentration is associated with altered blood pressure in schoolchildren.

A possible link between iron deficiency and gastrointestinal carcinogenesis.

There is definitive evidence that iron overload induces oxidative stress and DNA damage, which can enhance carcinogenic risk. However, other evidence suggests that iron deficiency and anemia also increase oxidative stress and DNA damage, which might increase carcinogenesis risk, especially in the gastrointestinal (GI) tract. The aim of this review is to provide essential background information for the accurate interpretation of future research on iron deficiency and increased GI cancer risk. Based on clinical, epidemiological, and experimental evidence, we discuss how iron deficiency might contribute to increased cancer risk through the impairment of several iron-dependent metabolic functions that are related to genome protection and maintenance (e.g., immune responses against cancer-initiated cells, metabolism of toxic compounds, and redox regulation of DNA biosynthesis and repair). Some epidemiological studies have indicated increased risk of GI tumors among individuals with low iron intake or low somatic iron stores, and in vivo data from rodent cancer models indicates the early progression of GI tumors during iron deficiency. Given the preliminary but consistent evidence relating iron deficiency to cancer risk and the fact that iron deficiency affects about one third of the world's population, further studies are needed to define the extent to which iron deficiency might increase GI cancer risk.