Dietary Excess Research Articles

Differential effects of dietary copper deficiency and excess on lipid metabolism in yellow catfish Pelteobagrus fulvidraco.

The present study was conducted to investigate the effects and mechanism of dietary Cu deficiency and excess on lipid metabolism in the liver, muscle and VAT of juvenile Pelteobagrus fulvidraco. To this end, yellow catfish were fed 0.76 (Cu deficiency), 4.18 (adequate Cu) and 92.45 (Cu excess) mg Cu kg(-1) diet, respectively, for 8 weeks. WG and SGR in the adequate Cu group were significantly higher than those in Cu deficiency and excess groups. In liver, Cu deficiency showed no significant effect on Cu and lipid contents, the activities of 6PGD, G6PD and FAS, and the mRNA levels of many tested genes, including 6PGD, G6PD, FAS, ACCα, PPARγ, LXR, HSL, PPARα and ATGL. Cu excess induced Cu accumulation, reduced the lipid content, FAS activity as well as the mRNA levels of 6PGD, G6PD, FAS, ACCα, PPARγ, HSL and ATGL. In muscle, dietary Cu levels showed no significant effects on lipid content, the activities of lipogenic enzymes and the mRNA levels of the most tested genes, including of 6PGD, G6PD, FAS, SREBP-1, PPARγ, HSL and LPL. In VAT, Cu and lipid contents, FAS activity, and the mRNA levels of 6PGD, G6PD, FAS, SREBP-1, LXR, PPARα and LPL were not significantly influenced by dietary Cu levels. Thus, the change of lipid contents among tissues could be related to the enzymatic activities and gene expression related to lipid metabolism. Different response patterns of enzymatic activities and gene expression in various tissues following dietary Cu levels indicated the tissue-specific regulatory effect by Cu.

Hypothalamic inflammation in the control of metabolic function.

Diet-induced obesity leads to devastating and common chronic diseases, fueling ongoing interest in determining new mechanisms underlying both obesity and its consequences. It is now well known that chronic overnutrition produces a unique form of inflammation in peripheral insulin target tissues, and efforts to limit this inflammation have met with some success in preserving insulin sensitivity in obese individuals. Recently, the activation of inflammatory pathways by dietary excess has also been observed among cells located in the mediobasal hypothalamus, a brain area that exerts central control over peripheral glucose, fat, and energy metabolism. Here we review progress in the field of diet-induced hypothalamic inflammation, drawing key distinctions between metabolic inflammation in the hypothalamus and that occurring in peripheral tissues. We focus on specific stimuli of the inflammatory response, the roles of individual hypothalamic cell types, and the links between hypothalamic inflammation and metabolic function under normal and pathophysiological circumstances. Finally, we explore the concept of controlling hypothalamic inflammation to mitigate metabolic disease.

Preventing aggressive prostate cancer with proven cardiovascular disease preventive methods.

Cardiovascular disease (CVD) has been the number one cause of death in the U.S. for 114 of the last 115 years. Risk factors for prostate cancer have primarily mirrored risk proven risk factors for CVD, especially aggressive disease. Obesity, dyslipidemia, glucose intolerance, metabolic syndrome, unhealthy dietary habits or caloric excess, lack of physical activity, and inflammation are just some of these shared risk factors. The evidence also suggests proven CVD preventive measures are identical to prostate cancer preventive measures, especially in regard to aggressive disease. Thus, apart from lifestyle measures that can encourage optimal heart and prostate health there are potentially several dietary supplements that need to be avoided in healthy men because they may also increase the risk of prostate cancer. However, there are also several low-cost, generic, safe in the appropriate individuals, and naturally derived agents that could reduce prostate cancer risk, and these can be discussed and remembered utilizing the acronym S.A.M. (statins, aspirin, and/or metformin).

Body mass index and eating habits of secondary schoolchildren in Indjija

Mistakes in diet of adolescents go in the direction of dietary excesses and deficits. The aim of the study was to determine the dietary habits of adolescents and the impact of schoolwork on the quality of nutrition among adolescent population, and calculating body mass index (BMI) in the examined adolescents in order to assess obesity. The research was designed as a cross sectional study conducted in 2013/14 school year among secondary school adolescents in Inđija during the performance of preventive examinations. The study involved 189 adolescents, 114 girls (60.3%) and 75 boys (39.7%). The average age of adolescents was 16.1. The largest number of female respondents and male respondents had the BMI within the normal. The number of boys with BMI > 2SD was significantly higher than in girls, χ²=5.328, p<0.05. Half of male adolescents and only a third of adolescent girls used to have three main meals and two snacks. A regular breakfast had 60% of respondents, while 3.70% did not have breakfast. The percentage of male respondents who had lunch at 'fast food' places five or more days a weak rose from 12%, when attending morning classes, to 18%, when attending afternoon classes, while in the female respondents it was 4.38% in the morning up to 14.03% in the afternoon. Most adolescents in Inđija have a normal body mass index. The number of pre-obese and overweight is small, but significantly more common in boys. The afternoon attendance affects the regularity of meals, i.e. schoolchildren do not have lunch or they eat food of low nutritional value. Fruit, vegetables, fish, whole grains is poorly presented in the diet of adolescents. Regular eating patterns are acquired from the early childhood and heavily influenced by family, peers, school and the environment in which children and adolescents grow up.

Snacking for a cause: nutritional insufficiencies and excesses of U.S. children, a critical review of food consumption patterns and macronutrient and micronutrient intake of U.S. children.

The objective of this review was to identify dietary insufficiencies and excesses in children aged two to 11 in the United States (U.S.) and eating habits that merit concern in terms of nutrient and energy density to improve overall diet quality. Data from the What We Eat in America (WWEIA) tables from the National Health and Nutrition Examination Survey (NHANES) were examined as well as survey data from the School Nutrition Dietary Assessment Study (SNDA). Analysis of survey data revealed that children consume insufficient Vitamin D, calcium, and potassium and excess energy, carbohydrates, and sodium. Dietary modifications are necessary to prevent serious deficiencies and the development of chronic illness. Snacking has steadily increased in this population since the 1970s, and snacks provide necessary nutrients. However, carbohydrates and added sugars tend to be over-consumed at snacking occasions. Replacement of current snack choices with nutrient-dense foods could lower the risks of nutrient deficiencies and help lower excess nutrient consumption. Increased consumption of low sugar dairy foods, especially yogurt, at snack times could increase intake of important micronutrients without contributing to dietary excesses.

Decrease in ATP biosynthesis and dysfunction of biological membranes. Two possible key mechanisms of phenoptosis.

Metabolic syndrome is extremely prevalent in the world and can be considered as one of main factors leading to accelerated aging and premature death. This syndrome may be closely linked with age-related disruptions in hypothalamic-pituitary system function, which perhaps represent a trigger mechanism of development of endocrine and cardiovascular pathologies. Age-related elevation of the sensitivity threshold of the hypothalamus to regulatory signals in association with low mobility and excessive diet trigger a cascade of biochemical reactions that might be used for activation of programmed death of the organism - phenoptosis. Accumulation of fatty acids in a cell and resulting lipotoxicity include resistance to insulin and leptin, endoplasmic reticulum stress, uncoupling of oxidation and phosphorylation, and dysfunction of biological membranes. Decrease in ATP synthesis is correlated with accumulation of calcium ions in cells, dysfunction of mitochondria, and increasing apoptotic activity. Age-related activation of mTOR (which is greatly influenced by excess energy substrates) has deleterious impact on one of the main mechanisms of cell defense by which defective mitochondria are replaced: mitophagy and biogenesis of mitochondria will be suppressed, and this will increase in greater degree mitochondrial dysfunction and oxidative stress. Fatty acid-induced inflammation will increase activity of nuclear factor NF-κB, the well-known stimulator of age-related pathologies. The final stage of phenoptosis can be represented by endothelium dysfunction related with oxidative stress, insulin resistance, and the most prevalent cardiovascular pathologies.

Different effects of dietary Zn deficiency and excess on lipid metabolism in yellow catfish Pelteobagrus fulvidraco

The present study was conducted to determine the potential mechanisms of dietary Zn influencing lipid deposition in yellow catfish Pelteobagrus fulvidraco. For that purpose, yellow catfish were fed three diets containing different Zn levels including 19.82 (adequate Zn), 11.45 (Zn deficiency), 155.97 (Zn excess) mg Zn kg− 1 for 8 weeks, respectively. Lipid and Zn contents, CPT I and LPL activities, and mRNA expression of 12 genes involved in lipid metabolism in the liver and muscle, were determined. As compared to adequate Zn group, excessive dietary Zn apparently reduced lipid content in the liver and muscle, and LPL activity in the muscle, and increased activities of CPT I and LPL in the liver. Dietary Zn deficiency tended to enhance lipid accumulation and CPT I activity in both tissues. Dietary Zn excess increased Zn accumulation in the liver, muscle and whole fish, but dietary Zn deficiency reduced Zn content in the liver and whole fish. In the liver, dietary Zn deficiency significantly down-regulated the transcriptional levels of CPT 1A, PPARα, LepR, G6PD, 6PGD and ACCb, but up-regulated FAS mRNA levels. Dietary Zn excess up-regulated mRNA levels of CPT 1A, PPARα, Lep, LepR, SREBP-1, G6PD, 6PGD, ACCb and LPL, but down-regulated mRNA levels of FAS, ACCa and PPARγ. In the muscle, dietary Zn deficiency down-regulated mRNA levels of PPARα, Lep, SREBP-1, FAS and ACCa, and increased 6PGD and LPL gene expression. Dietary excess Zn down-regulated mRNA levels of PPARγ, SREBP-1, G6PD, ACCa, and LPL, and up-regulated mRNA levels of CPT 1A and Lep. For the first time, our study clearly indicated the different effects of dietary Zn deficiency and excess on lipid deposition and metabolism, which provided new insights into Zn nutrition and toxicology in fish.

Dietary acid load, kidney function, osteoporosis, and risk of fractures in elderly men and women.

Because kidney dysfunction reduces the ability to excrete dietary acid excess, we hypothesized that underlying kidney function may have confounded the mixed studies linking dietary acid load with the risk of osteoporosis and fractures in the community. In a relatively large survey of elderly men and women, we report that dietary acid load did neither associate with DEXA-estimated bone mineral density nor with fracture risk. Underlying kidney function did not modify these null findings. Our results do not support the dietary acid-base hypothesis of bone loss. Impaired renal function reduces the ability to excrete dietary acid excess. We here investigate the association between dietary acid load and bone mineral density (BMD), osteoporosis, and fracture risk by renal function status. An observational study was conducted in 861 community-dwelling 70-year-old men and women (49% men) with complete dietary data from the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS). The exposure was dietary acid load as estimated from 7-day food records by the net endogenous acid production (NEAP) and potential renal acid load (PRAL) algorithms. Renal function assessed by cystatin C estimated glomerular filtration rate was reduced in 21% of the individuals. Study outcomes were BMD and osteoporosis state (assessed by DEXA) and time to fracture (median follow-up of 9.2 years). In cross-section, dietary acid load had no significant associations with BMD or with the diagnosis of osteoporosis. During follow-up, 131 fractures were validated. Neither NEAP (adjusted hazard ratios (HR) (95% confidence interval (CI)), 1.01 (0.85-1.21), per 1 SD increment) nor PRAL (adjusted HR (95% CI), 1.07 (0.88-1.30), per 1 SD increment) associated with fracture risk. Further multivariate adjustment for kidney function or stratification by the presence of kidney disease did not modify these null associations. The hypothesis that dietary acid load associates with reduced BMD or increased fracture risk was not supported by this study in community-dwelling elderly individuals. Renal function did not influence on this null finding.

The ω6-fatty acid, arachidonic acid, regulates the conversion of white to brite adipocyte through a prostaglandin/calcium mediated pathway.

ObjectiveBrite adipocytes are inducible energy-dissipating cells expressing UCP1 which appear within white adipose tissue of healthy adult individuals. Recruitment of these cells represents a potential strategy to fight obesity and associated diseases.Methods/ResultsUsing human Multipotent Adipose-Derived Stem cells, able to convert into brite adipocytes, we show that arachidonic acid strongly inhibits brite adipocyte formation via a cyclooxygenase pathway leading to secretion of PGE2 and PGF2α. Both prostaglandins induce an oscillatory Ca++ signaling coupled to ERK pathway and trigger a decrease in UCP1 expression and in oxygen consumption without altering mitochondriogenesis. In mice fed a standard diet supplemented with ω6 arachidonic acid, PGF2α and PGE2 amounts are increased in subcutaneous white adipose tissue and associated with a decrease in the recruitment of brite adipocytes.ConclusionOur results suggest that dietary excess of ω6 polyunsaturated fatty acids present in Western diets, may also favor obesity by preventing the “browning” process to take place.

Outcome measures of behavioral weight loss programs in perimenopause.

Obesity and being overweight are associated with many comorbid conditions and are major contributing factors to cardiovascular disease. The increased proportion of overweight and obese people in Western societies has been attributed largely to behaviors that include sedentary lifestyle and dietary excess. Women are at particular risk during perimenopause, when hormones change and metabolism slows. The purpose of this review was to examine published studies of weight loss programs for perimenopausal women using behavioral change strategies of diet alone, regular physical activity alone, or both in combination to determine the range of potential outcomes and reduction of cardiovascular risks. Based on the findings from this review, practice applications and recommendations for future research are proposed.

Gut microbiota. Tackling the effects of diet and exercise on the gut microbiota.

A new study published in Gut highlights that high levels of exercise and an accompanying high-protein diet are associated with changes to the gut microbiota, with elite athletes having a more diverse range of microorganisms in their gut than control individuals. “In addition to microbial diversity, we also found specific compositional changes in the [gut] microbiota of the athletes, including a significant increase in the abundance of Akkermansia muciniphila,” notes author Fergus Shanahan. The vast majority of studies investigating the gut microbiota have focused on the effects of obesity, disease or dietary excess (high-fat diets). As awareness increases about the influence of the gut microbiota on health, attention has turned to how the modern lifestyle (such as poor diet and low levels of exercise) might have a role in maintaining a healthy gut microbiota. Shanahan and colleagues examined the gut microbiota of professional rugby players at a preseason training camp (n = 40) as well as two different control groups of healthy individuals matched for age and gender, but split by BMI (low BMI ≤25, n = 23; high BMI >28, n = 23) to account for the large physical size of the rugby players. Nutritional (including detailed information on diet) and clinical data were collected for all participants, as well as metagenomic compositional analysis of the faecal microbiota. As expected, athletes had higher plasma levels of creatine kinase (a marker of extreme exercise) than controls; lower levels of inflammatory markers and improvements in metabolic markers were also observed. Moreover, compared with controls, athletes had a more diverse range of microbes in their gut—22 distinct phyla versus only 11 and nine phyla in the low-BMI and high-BMI controls, respectively. Importantly, this change in diversity positively correlated with protein intake and creatine kinase levels. “An important caveat to the study is that the athletes’ diet differed from that of the controls,” warns Shanahan. “They eat more of everything than the controls, but particularly protein supplements.” As such, further prospective studies are now planned to separate out the effects of exercise from the dietary changes that often accompany a healthy lifestyle in general. Crucially, more work is needed to prove that exercise has a direct effect on the gut microbiota and a causative role in changing the diversity of these microbes.

Effects on liver hydrogen peroxide metabolism induced by dietary selenium deficiency or excess in chickens.

To determine the relationship between dietary selenium (Se) deficiency or excess and liver hydrogen peroxide (H2O2) metabolism in chickens, 1-day-old chickens received insufficient Se (0.028mg Se per kg of diet) or excess Se (3.0 or 5.0mg Se per kg of diet) in their diets for 8weeks. Body and liver weight changes, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, H2O2 content, and activities and mRNA levels of enzymes associated with H2O2 metabolism (catalase (CAT) and superoxide dismutase (SOD) 1-3) were determined in the liver. This study showed that Se deficiency or excess Se intake elicited relative severe changes. Se deficiency decreased growth, while Se excess promoted growth in chickens. Both diets vastly altered the liver function, but no obvious histopathological changes were observed in the liver. Se deficiency significantly lowered SOD and CAT activities, and the H2O2 content in the liver and serum increased. Se excess (3.0mg/kg) decreased SOD and CAT activities with changes in their mRNA levels, and the H2O2 content increased. The larger Se excess (5.0mg/kg) showed more serious effects but was not fatal. These results indicated that the H2O2 metabolism played a destructive role in the changes in bird liver function induced by Se deficiency or excess.

Characterization of the alterations in the differentiation potential of porcine mesenchymal stem cell caused by neonatal dietary calcium nutrition (819.2)

Neonatal Ca nutrition affects bone development and mesenchymal stem cell (MSC) activity; however, its effect on MSC differentiation potential has not been well characterized. We assessed the differentiation potential of both the heterogenous MSC population as well as the individual clones isolated from neonatal pigs (n=5) fed either a Ca deficient, adequate, or excessive diet. The most and least osteogenic (O+/O‐) and the most and least adipogenic (A+/A‐) clones were selected from each pig by functional staining. The MSC from Ca deficient pigs had reduced osteogenic potential and enhanced adipogenic potential based on functional staining and the gene expression of osteocalcin (OC), PPARG, and AP2 compared with MSC from Ca adequate pigs. Interestingly, MSC from pigs receiving excess Ca also had increased adipogenic potential. Evaluation of clonal isolates indicated that the O+ clones from Ca deficient pigs had reduced OC expression (P &lt; 0.05), and O‐ clones from the Ca excess pigs had increased gene expression of both PPARG and AP2. Among the A+ clones of both Ca deficient and excess pigs, Runx2 expression was decreased (P &lt; 0.05). These data suggest that the alterations in the differentiation potential of MSC based on neonatal Ca status of the pig may be caused by changes in both the lineage priming and the lineage allocation of MSC.

Poster #S184 META-ANALYSIS OF “LEARNING POTENTIAL” ON THE DYNAMIC WISCONSIN CARD SORTING TEST (D-WCST): DISTINCT COGNITIVE SUBGROUPS WITH DIVERGENT FUNCTIONAL OUTCOMES

“Natural” phenomena allow conclusions that maternal dietary deficiencies or excesses can affect development of the human embryo and fetus adversely. The most important finding in recent years has been the relationship between maternal folic acid status and neural tube defects. J Am Diet Assoc. 1997;97(suppl 2):S184–S185.

Telmisartan improves survival and ventricular function in SHR rats with extensive cardiovascular damage induced by dietary salt excess

Excessive dietary salt intake induces extensive cardiovascular and renal damage in spontaneously hypertensive rats (SHR) that may be prevented by antihypertensive agents. This study examines whether salt-induced cardiac damage may be reversed by angiotensin II (type 1) receptor blockade (telmisartan). Eight-week-old male SHRs were divided into four groups; Group 1 (NS) was fed regular rat chow, and Group 2 (HS) received high-salt diet (HS; 8% NaCl). After 8 weeks on their respective diets, systemic hemodynamics and indices of left ventricular (LV) function were determined. Group 3 (HSnoT) was given HS for 8 weeks and then switched to a regular chow (0.6% NaCl) diet with no other treatment, and Group 4 (HSArb) received HS for 8 weeks and was then given regular diet plus telmisartan. Rats from these latter two groups were monitored for the ensuing 30 days. Compared with the NS group, rats in the HS group exhibited increased mean arterial pressure (161 ± 7 vs 184 ± 8 mm Hg) and LV diastolic dysfunction, as evidenced by a decreased rate of LV pressure decline (−8754 ± 747 vs −4234 ± 754 mmHg/sec) at the end of the 8 weeks of their respective treatment. After switching to regular chow, only one of 11 rats in the HSnoT group survived for the 30 days, whereas 10 died within 18 days; in the HSArb group only one of nine rats died; eight survived 30 days (P < .01). Telmisartan significantly improved LV function and survival in those SHR rats having extensive cardiovascular damage induced by dietary salt excess.

Supporting effective lifestyle behaviour change interventions

Improving the health of the population, and morbidity and mortality associated with non-communicable diseases, is a national priority. Health education and promotion should focus on avoiding harmful behaviours such as excessive alcohol intake, smoking and poor diet. It is argued that each patient contact should involve health promotion and that healthcare professionals should be encouraged to discuss and support effective lifestyle behaviour change interventions.

Feeding health: problems, opportunities, goals.

Food security is when all people at all times have access to sufficient, safe, nutritious food to maintain a healthy and active life. On the one hand, the European Union Commission proposes new laws to achieve the highest possible levels of protection for human health and consumer interests in relation to food, plants and biodiversity. On the other hand, International Agencies (WHO, FAO, EU) pay attention to malnutrition and its consequences for health; poor people are usually the ones that suffer the consequences of underfeeding or dietary excess. In Italy, the mission of Food and Nutrition Services (Public Health National Service) is to promote food safety and good nutrition for the population; furthermore, they must pay attention to social equity. Suppressing or reducing their activity would be detrimental for public health and the national economy.

Fortified Foods Are Major Contributors to Nutrient Intakes in Diets of US Children and Adolescents

BackgroundEven in an era of obesity and dietary excess, numerous shortfall micronutrients have been identified in the diets of US children and adolescents. To help tailor strategies for meeting recommendations, it is important to know what foods contribute greatly to micronutrient intakes. Data are lacking on specific contributions made by added nutrients. ObjectiveOur aims were to examine the impact of fortification on nutrient adequacy and excess among US children and adolescents and to rank food sources of added nutrient intake and compare rankings with those based on total nutrient intake from foods. Design and statistical analysesData were from 7,250 respondents 2 to 18 years old in the National Health and Nutrition Examination Survey 2003-2006. Datasets were developed that distinguished nutrient sources: intrinsic nutrients in foods; added nutrients in foods; foods (intrinsic plus added nutrients); and total diet (foods plus supplements). The National Cancer Institute method was used to determine usual intakes of micronutrients by source. The impact of fortification on the percentages of children having intakes less than the Estimated Average Requirement and more than the Upper Tolerable Intake Level was assessed by comparing intakes from intrinsic nutrients to intakes from intrinsic plus added nutrients. Specific food sources of micronutrients were determined as sample-weighted mean intakes of total and added nutrients contributed from 56 food groupings. The percentage of intake from each grouping was determined separately for total and added nutrients. ResultsWithout added nutrients, a high percentage of all children/adolescents had inadequate intakes of numerous micronutrients, with the greatest inadequacy among older girls. Fortification reduced the percentage less than the Estimated Average Requirement for many, although not all, micronutrients without resulting in excessive intakes. Data demonstrated the powerful influence of fortification on food-source rankings. ConclusionsKnowledge about nutrient intakes and sources can help put dietary advice into a practical context. Continued monitoring of top food sources of nutrients and nutrient contributions from fortification will be important.

Ovarian and uterine characteristics and onset of puberty in adolescent offspring: Effects of maternal diet and selenium supplementation in sheep

The aim of this study was to determine the effects of maternal diet with adequate (A) or high (H) selenium (Se) supplementation on ovarian and uterine characteristics, and onset of puberty in adolescent offspring. Sheep were fed a maintenance (M) diet with ASe or HSe levels from breeding to parturition. From Day 50 to parturition, a portion of the ewes from ASe and HSe groups was fed restricted (R, 60% of M) or excess (E, 140% of M) diet. Immediately after birth, lambs were separated from their dams and given artificial colostrum for 20 hours, followed by milk replacer. From Day 57.3 ± 0.6, ewe lambs were fed a pelleted grower diet until Day 116.3 ± 0.6 when they were transitioned to a finisher diet. From Day 99 to 180, serum samples were collected weekly from jugular vein for progesterone analysis to determine onset of puberty. Reproductive tissues were collected on Day 180.1 ± 0.4 of age. Maternal diet or Se supplementation did not affect uterine or ovarian weight and onset of puberty. However, area under the curve for progesterone was greater (P = 0.05) in ASe compared with HSe groups, and was greater in ASeM than HSeM group. In CLs, labeling index (LI; a proportion of proliferating cells) was less (P < 0.04) in HSeM than ASeM group, and in stroma was less (P < 0.05) in R and E groups than M group. Maternal diet did not affect the LI of any follicle types. For all groups combined, LI was the greatest (P < 0.001) in antral, less in early antral and secondary, and the least in atretic follicles. Our results demonstrate that maternal diet influenced ovarian but not uterine characteristics or onset of puberty. These results indicate that maternal plane of nutrition and/or Se supplementation may have specific effects on reproductive function in offspring.

Effects of dietary excess of vitamin e and selenium on some production traits, lipid peroxide state and amount/activity of the glutathione redox system in African catfish Clarias gariepinus (siluriformes, clariidae) fingerlings

Purpose of present study was to investigate the effect of excess dietary amount of vitamin E and selenium also short-term starvation on some production traits and parameters of the lipid peroxide state and glutathione redox system in African catfish fingerlings. Three purified diets were formulated: diet 1 (control) contained 114 mg.kg -1 tocopherol and 0.43 mg.kg -1 selenium, diet 2 contained high level of tocopherol (245mg kg -1 ) and control level of selenium (0.5 mg kg -1 ), while diet 3 contained high level of selenium (2.5 mg kg -1 ) and control level of tocopherol (170 mg kg -1 ). Fingerlings of C. gariepinus (3.16-3.93 g) were investigated in four groups, three consumed the above mentioned diets and the fourth served as unfed control. The experiment lasted 30 days except in the case of the unfed group which was terminated on the 15 th day because of high mortality. The vitamin E / selenium treated groups showed significantly (P£0.001) lower final body weight and specific growth rate as compared to the control. Vitamin E and selenium content of the fish body in diet 2 group increased significantly (P£0.001) as compared to the control. Vitamin E content did not changed in the unfed group, but selenium content decreased significantly (P£0.001) during the 15-days starvation period. Reduced glutathione (GSH) content increased significantly (P£0.05) only in the high selenium group. Glutathione-disulphide (GSSG) content, and glutathione peroxidase activity did not changed neither during the period of investigation and nor as effect of treatments, but the value of GSH/GSSG ratio was significantly higher (P£0.05) in the high selenium as compared to the high vitamin E group. Lipid peroxide state of the body, as was measured by the malondialdehyde content, changed as effect of age and/or maturation but not as effect of the treatments.