Zinc supplementation improves glucose homeostasis in patients with ß-thalassemia major complicated with diabetes mellitus: A randomized controlled trial.

OBJECTIVES: The development of abnormal glucose tolerance in ß-thalassemia major (ß-TM) is associated with alterations in the oxidant-antioxidant status. Zinc is an antioxidant and an essential element for insulin synthesis, storage, and secretion. This randomized controlled trial assessed the effect of oral zinc supplementation on glucose homeostasis in pediatric ß-TM patients complicated with diabetes mellitus (DM). METHODS: Eighty patients were randomly assigned into two groups: an intervention group that received oral zinc in a dose of 40 mg/d for 12 wk and a placebo group. Hemolysis markers, serum ferritin, fasting blood glucose (FBG), fructosamine, fasting C-peptide, urinary albumin excretion (UAE), and serum zinc levels were assessed. Homeostasis model assessment insulin resistance index (HOMA-IR) was calculated. RESULTS: Baseline clinical and laboratory parameters were consistent among both groups. Baseline zinc levels were decreased in both groups compared with control values. After 12 wk, supplementation with zinc for the intervention group resulted in a significant decrease in lactate dehydrogenase, serum ferritin, FBG, fructosamine, HOMA-IR, and UAE, whereas fasting C-peptide was higher compared with baseline levels and with the placebo group (P < 0.05). Baseline serum zinc was negatively correlated to FBG (r = -0.534, P < 0.001) and fructosamine (r = -0.555, P < 0.001) but positively correlated to fasting C-peptide (r = 0.777, P = 0.002). CONCLUSIONS: Zinc supplementation as an adjuvant therapy in ß-TM patients with DM reduced iron burden, decreased hyperglycemia, increased insulin secretion, and improved glycemic control without any adverse effects.

Resveratrol inhibits inflammatory signaling implicated in ionizing radiation-induced premature ovarian failure through antagonistic crosstalk between silencing information regulator 1 (SIRT1) and poly(ADP-ribose) polymerase 1 (PARP-1).

This study hypothesized that resveratrol, a silencing information regulator 1 (SIRT1) activator, would counteract the inflammatory signaling associated with radiotherapy-induced premature ovarian failure (POF). Immature female Sprague-Dawley rats were subjected to a single dose of γ-radiation to induce POF and treated with resveratrol (25mg/kg) once daily for two weeks before and three days post irradiation. Resveratrol preserves the entire ovarian follicle pool manifested by increasing serum anti-Müllerian hormone (AMH) levels. Radiation triggered inflammatory process in the ovary through enhanced NF-κB and poly(ADP-ribose) polymerase (PARP)-1 expression which convinced the expression of inflammatory markers including IL-6, IL-8, and visfatin mRNA levels, as well as inducible nitric oxide synthase and cyclooxygenase-2 protein expression with a concomitant reduction in IL-10 mRNA levels. Resveratrol significantly counteracted the effect of radiation and upregulated the gene expression of peroxisome proliferator-activated receptor γ (PPAR-γ) and SIRT1. Resveratrol-activated SIRT1 expression was associated with inhibition of PARP-1 and NF-κB expression-mediated inflammatory cytokines. Our findings suggest that resveratrol restored ovarian function through increasing AMH levels, and diminishing ovarian inflammation, predominantly via upregulation of PPAR-γ and SIRT1 expression leading to inhibition of NF-κB provoked inflammatory cytokines.

Sodium selenite treatment restores long-lasting ovarian damage induced by irradiation in rats: impact on oxidative stress and apoptosis.

The deleterious damage of reproductive function following radiotherapy is of increasing importance. In the present study, we investigated the impact of long-term sodium selenite (SS) treatment on radiotherapy-induced ovarian injury in a rat model. Two-week after radiation exposure vaginal cyclicity was arrested, and serum FSH level was elevated in irradiated female rats. SS significantly ameliorated ovarian and uterine oxidative stress induced by irradiation through decreasing the lipid peroxide level and increasing the glutathione level, and glutathione peroxidase activity. In the presence of SS, ovarian cytochrome c and caspase 3 expressions triggered by radiotherapy were decreased. SS significantly counteracted radiation-induced a widespread loss of ovarian follicles and caused further stimulation of follicular proliferation through enhancing PCNA expression. Despite such alteration in ovarian function, serum estradiol level did not change after irradiation, whereas SS significantly increased it. In conclusion, long-term SS treatment improved reproductive development, which was impaired by radiotherapy.

Cord blood iron profile and breast milk micronutrients in maternal iron deficiency anemia.

BACKGROUND: Micronutrient deficiencies among pregnant women are widespread in low-income countries, including Egypt. Iron deficiency anemia (IDA) is the most frequent nutritional deficiency during pregnancy, with an impact on maternal and fetal morbidity and mortality. We aimed to evaluate the effect of maternal IDA and nutritional status on birth anthropometry, cord blood iron profile and breast milk micronutrients in 50 anemic (hemoglobin <11 g/dl) and 30 healthy pregnant women. PROCEDURE: Maternal and neonatal anthropometric measures were recorded. Hemoglobin, red blood cell (RBC) indices, and indices of iron nutriture were measured in maternal and cord blood. Breast milk minerals; iron, copper, zinc, calcium, and magnesium were assessed. RESULTS: Hemoglobin, RBC indices, and iron profile showed significant differences in the neonates born to anemic mothers compared to controls, particularly in moderate to severe anemia and linear correlations with maternal hemoglobin, iron, and ferritin levels were found (P < 0.01). Anthropometric measurements of anemic mothers and their neonates were positively correlated (P < 0.05). Breast milk micronutrients were significantly reduced in all anemic mothers showing significant relations with maternal serum iron (P < 0.01). CONCLUSIONS: Maternal IDA wields a significant influence on maternal and fetal nutritional status. IDA during pregnancy adversely affects both cord blood iron and breast milk mineral status, particularly in moderate to severe anemia and concurrent micronutrient deficiencies occur in maternal IDA. Further investigations including larger population of pregnant women with severe anemia are needed to verify the nutritional interrelation between maternal anemia and breast milk mineral status.