Comparison of Sodium Selenite and Selenium-Enriched Spirulina Supplementation Effects After Selenium Deficiency on Growth, Tissue Selenium Concentrations, Antioxidant Activities, and Selenoprotein Expression in Rats.

Selenium contributes to physiological functions through its incorporation into selenoproteins. It is involved in oxidative stress defense. A selenium deficiency results in the onset or aggravation of pathologies. Following a deficiency, the repletion of selenium leads to a selenoprotein expression hierarchy misunderstood. Moreover, spirulina, a microalga, exhibits antioxidant properties and can be enriched in selenium.. Our objective was to determine the effects of a sodium selenite or selenium-enriched spirulina supplementation. Thirty-two female Wistar rats were fed for 12 weeks with a selenium-deficient diet. After 8 weeks, rats were divided into 4 groups and were fed with water, sodium selenite (20 µg Se/kg body weight), spirulina (3 g/kg bw), or selenium-enriched spirulina (20 µg Se/kg bw + 3 g spirulina/kg bw). Another group of 8 rats was fed with normal diet during 12 weeks. Selenium concentration and antioxidant enzyme activities were measured in plasma, urine, liver, brain, kidney, heart, and soleus. Expression of GPx (1, 3), Sel (P, S, T, W), SEPHS2, TrxR1, ApoER2, and megalin were quantified in liver, kidney, brain, and heart. We showed that a selenium deficiency leads to a growth delay, reversed by selenium supplementation despite a minor loss of weight in week 12 for SS rats. All tissues displayed a decrease in selenium concentration following deficiency. The brain seemed protected. We demonstrated a hierarchy in selenium distribution and selenoprotein expression. A supplementation of sodium selenite improved GPx activities and selenoprotein expression while a selenium-enriched spirulina was more effective to restore selenium concentration especially in the liver, kidney, and soleus.

Inadequate dietary intake is not the cause of stunting amongst young children living in an informal settlement in Gauteng and rural Limpopo Province in South Africa: the NutriGro study.

OBJECTIVE: To measure dietary intakes of young children aged 12-24 months and to determine the impact of poor diets on stunting. DESIGN: A quantitative food-frequency questionnaire was adapted, tested and standardised. Trained enumerators conducted in-depth interviews with the mothers/caregivers of the children. Forty stunted children in urban informal settlements and 30 stunted children in rural areas were selected and pair-matched with controls. The data were captured on the Food Finder Program of the Medical Research Council. RESULTS: In both urban and rural areas, the diet of stunted and non-stunted groups did differ significantly and all diets were of poor nutritional quality. CONCLUSION: Diets in both areas resembled the recommended prudent diet, i.e. low in fat and high in carbohydrates. Poor quality diets were not the primary cause of stunting.