Soda intake influences phenotype, antioxidants and inflammatory status in high protein-fed wistar rats.

An increasing population of people, especially young adults who exercise, consume high protein diets along with carbonated drinks. While there are numerous studies on the effect of high protein diets, there is a need to understand how protein diets in combination with carbonated drinks impact physiology. In order to assess these effects on wistar rats' phenotype, antioxidants and inflammatory profiles, 64 wistar rats were divided into dietary groups of 8 male and 8 female animals each. The animals were fed standard diet as control (chow), chow and carbonated soda, a high protein diet (48.1% energy from protein) and a high protein diet with carbonated soda according to their groups. Body measurements, blood glucose levels, serum insulin levels, lipid peroxidation, antioxidant activity, adipokines and inflammatory markers concentrations were all determined. At the end of the study, body measurements, inflammatory markers and adipokine concentration were increased in animals fed the high protein diet and high protein-soda diet. There was a decrease in antioxidant and lipid peroxidation levels in protein fed male and female animals but those fed protein in combination with soda had increased lipid peroxidation levels. In conclusion, high protein diet in combination with carbonated soda impacts physiology differently from a high protein diet alone, and may stimulate weight gain, oxidative stress and HPD-related inflammation in Wistar rats.

Gestational Nutrition as a Predisposing Factor to Obesity Onset in Offspring: Role for Involvement of Epigenetic Mechanism.

Maternal lifestyle has been implicated as a predisposing factor in the development of metabolic disorders in adulthood. This lifestyle includes the immediate environment, physical activity and nutrition. Maternal nutrition has direct influence on the developmental programming through biochemical alterations and can lead to modifications in the fetal genome through epigenetic mechanisms. Imbalance in basic micro or macro nutrients due to famine or food deficiency during delicate gestational periods can lead to onset of metabolic syndrome including obesity. A major example is the Dutch famine which led to a serious metabolic disorder in adulthood of affected infants. Notably due to gene variants, individualized responses to nutritional deficiencies are unconventional, therefore intensifying the need to study nutritional genomics during fetal programming. Epigenetic mechanisms can cause hereditary changes without changing the DNA sequence; the major mechanisms include small non-coding RNAs, histone modifications and most stable of all is DNA methylation. The significance association between obesity and DNA methylation is through regulation of genes implicated in lipid and glucose metabolism either directly or indirectly by hypomethylation or hypermethylation. Examples include CPT1A, APOA2, ADRB3 and POMC. Any maternal exposure to malnutrition or overnutrition that can affect genes regulating major metabolic pathways in the fetus, will eventually cause underlying changes that can predispose or cause the onset of metabolic disorder in adulthood. In this review, we examined the interaction between nutrition during gestation and epigenetic programming of metabolic syndrome.

Maternal exposure to Bonny Light Crude Oil Altered Reproductive indices in Male and Female offspring of Wistar rats.

In this study, the effects of maternal exposure to Bonny Light Crude Oil (BLCO) on reproductive functions of the offspring was investigated in Wistar rats. Ten pregnant rats were divided into two groups (n=5). Group 1 served as the control, it was administered 0.75ml/Kg bwt/day normal saline and Group 2 was administered 0.75ml/Kg bwt/day BLCO. Serum hormonal profile, sperm indices, estrous cycle length and pubertal timing were assessed as measures of reproductive function. Tissue Malondialdehyde, Catalase and SOD activities were assessed as indices of oxidative stress. Results obtained showed that BLCO significantly (p<0.05) reduced birth weight, anogenital distance (AGD) at birth, sperm count, motility and normal morphology, serum testosterone, testicular and epididymal SOD and catalase activities in the male offsprings. However, days of preputial separation, relative weight of testis and epididymis, testicular and epididymal MDA were significantly (p<0.05) raised by gestational exposure to BLCO. In the female offspring, birth weight, AGD at birth, relative weight of ovaries and uterus, SOD, catalase activities, serum LH were significantly reduced by BLCO exposure during gestation. Moreover, uterine and testicular MDA, serum estradiol and FSH were significantly increased by BLCO treatment during gestation. In conclusion, maternal exposure to BLCO during gestation may alter reproductive indices in the offspring and increased occurrence of oxidative stress in reproductive structures in male and female offspring of Wistar rats.