Effect of Zinc Deficiency on Blood Glucose, Lipid Profile, and Antioxidant Status in Streptozotocin Diabetic Rats and the Potential Role of Sesame Oil.

Zinc is recognized to have a crucial function in insulin production. As a result, its absence may have a deleterious impact on the progression of diabetes and associated consequences. So, this study was undertaken to evaluate the effect of sesame oil on biochemical parameters, zinc status, and oxidative stress biomarkers in streptozotocin (STZ)-induced diabetic rats fed zinc-deficient diet. Rats were divided into four groups. The first group consisted of non-diabetic rats that were fed in a sufficient zinc diet, whereas the second was a diabetic group which received also sufficient zinc diet, while the third and fourth groups were diabetic rats fed in a deficient zinc diet, one was non-treated and the other was treated with sesame oil 6% diet for 27 days. Zinc deficiency has affected the weight of the diabetic animals. It was also noticed that inadequate dietary zinc intake increased concentrations of glucose, cholesterol, triglycerides, malondialdehyde, and transaminases activities. Furthermore, zinc deficiency feed provoked a decrease in zinc level in tissues (femur, liver, and pancreas); glutathione concentration; and lactic dehydrogenase, amylase, catalase, superoxide dismutase, and glutathione-S-transferase activities. However, sesame oil treatment ameliorated all the previous parameters approximately to their normal values. It was found out that sesame oil supplementation is a potent factor in mitigating the oxidative severity of zinc deficiency in diabetes through its effective antioxidant potential.

Effect of curcuma on zinc, lipid profile and antioxidants levels in blood and tissue of streptozotocin-induced diabetic rats fed zinc deficiency diet.

Due to the importance of zinc as an antioxidant and its crucial role in insulin synthesis, its deficiency may affect adversely diabetic state. So, this study aimed to modulate these effects using Curcuma longa as natural antioxidant. Rats were divided into four groups: two groups fed a zinc sufficient diet one non-diabetic and the other diabetic, while the others two groups diabetic rats fed a zinc-deficient diet, one non-treated group and the other treated with curcuma 1% diet. After four weeks of dietary manipulation, fasting animals were scarified. Zinc deficiency decreased body weight, insulin, zinc tissues, alkaline phosphatase, reduced glutathione, glutathione peroxidase, superoxide dismutase and catalase. Conversely glucose, lipids profile, transaminases and malondialdehyde were increased. However, the above-mentioned parameters were significantly improved following curcuma supplementation. So it seems that curcuma is a potent factor for reducing the oxidative severity of zinc deficiency in experimental diabetes through its antioxidants actions.

Effect of Ruta chalepensis on Zinc, Lipid Profile and Antioxidant Levels in the Blood and Tissue of Streptozotocin-Induced Diabetes in Rats Fed Zinc-Deficient Diets.

OBJECTIVES: In diabetes, oxidative stress and lipid abnormalities are common and pronounced and represent important factors that are involved in the development of complications of diabetes. Zinc deficiency generally induces oxidative stress, but it is well known that the antioxidant Ruta chalepensis has an effective modulator role in oxidative stress in metabolic diseases. The aim of this study was to investigate the effect of R. chalepensis extract on blood biochemical parameters, tissue zinc status and antioxidant systems in rats with diabetes that were fed zinc-deficient diets. METHODS: We divided 28 male albino Wistar rats into 4 groups: 2 groups (1 group with diabetes, 1 group without diabetes) were fed zinc-sufficient diets, while the other 2 groups of rats with diabetes were fed zinc-deficient diets. One group was not treated, and the other was treated with the extract of R. chalepensis. After 3 weeks of dietary manipulation, the fasting animals were killed. RESULTS: The body-weight gains of the zinc-deficient animals with diabetes were lower than those of the zinc-adequate animals with diabetes. It was noticed also that inadequate dietary zinc intake increased the glucose, cholesterol, triglyceride, urea, uric acid, creatinine and lipid peroxidation levels. In addition, the zinc-deficient diet led to a decrease in zinc tissues (femur, liver, kidney), glutathione concentration and both glutathione peroxidase and glutathione-S-transferase activities. However, R. chalepensis treatment ameliorated all the previous parameters approximately to their normal levels. CONCLUSIONS: It seems that R. chalepensis supplementation is a potent factor in reducing the oxidative severity of zinc deficiency in experimental diabetes through its hypoglycemic and antioxidant actions.

Evaluation of Some Biochemical Parameters and Brain Oxidative Stress in Experimental Rats Exposed Chronically to Silver Nitrate and the Protective Role of Vitamin E and Selenium.

Due to undesirable hazardous interactions with biological systems, this investigation was undertaken to evaluate the effect of chronic exposure to silver on certain biochemical and some oxidative stress parameters with histopathological examination of brain, as well as the possible protective role of selenium and/or vitamin E as nutritional supplements. Thirty six male rats were divided into six groups of six each: the first group used as a control group. Group II given both vitamin E (400 mg/kg) of diet and selenium (Se) (1 mg/L) in their drinking water. Group III given silver as silver nitrate (AgNO3) (20 mg/L). Group IV given vitamin E and AgNO3. Group V given both AgNO3 and selenium. Group VI given AgNO3, vitamin E and Se. The animals were in the same exposure conditions for 3 months. According to the results which have been obtained; there was an increase in serum lactate dehydrogenase (LDH), lipase activities and cholesterol level, a decrease in serum total protein, calcium and alkaline phosphatase (ALP) activity in Ag-intoxicated rats. Moreover, the findings showed that Ag+ ions affected antioxidant defense system by decreasing superoxide dismutase (SOD) activity and increasing vitamin E concentration with a high level of malondialdehyde (MDA) in brain tissue. The histological examination also exhibited some nervous tissue alterations including hemorrhage and cytoplasm vacuolization. However, the co-administration of selenium and/or vitamin E ameliorated the biochemical parameters and restored the histological alterations. In conclusion, this study indicated that silver could cause harmful effects in animal body and these effects can be more toxic in high concentrations or prolonged time exposure to this metal. However, selenium and vitamin E act as powerful antioxidants which may exercise adverse effect against the toxicity of this metal.

Zinc Supplementation Overcomes Effects of Copper on Zinc Status, Carbohydrate Metabolism and Some Enzyme Activities in Diabetic and Nondiabetic Rats.

OBJECTIVE: The aim of this study was to investigate the effect of zinc supplementation on zinc status, carbohydrate metabolism and some enzyme activities in rats with alloxan-induced diabetes that were fed high-copper feed. METHODS: Male albino Wistar rats were randomly divided into 6 groups (n=10). The first and fourth groups were nondiabetic and diabetic controls. The second, third, fifth and sixth groups were copper, copper + zinc, diabetes + copper and diabetes + copper + zinc groups, respectively. Diabetes in the fourth, fifth and sixth groups was induced by alloxan. Copper (30 mg/kg feed) as CuSO4 5H2O and zinc (231 mg/kg feed) as ZnSO4 7H2O were added to the feed of the animals in the copper and zinc groups for 21 days. RESULTS: Copper supplementation caused a significant decrease in body weight gain, serum zinc, tissue zinc, serum protein concentrations, alkaline phosphatase, lactic dehydrogenase and amylase activities. In contrast, it led to an augmentation in creatinine, uric acid and transaminases activities in rats with and without diabetes. Zinc supplementation in the feed for animals given copper ensured a partial correction of the previous parameters. CONCLUSIONS: The study demonstrated the beneficial effects of zinc treatment in copper-induced metabolic disturbance in diabetic and nondiabetic rats.

Selenium supplementation modulates zinc levels and antioxidant values in blood and tissues of diabetic rats fed zinc-deficient diet.

Diabetes mellitus is associated to a reduction of antioxidant defenses that leads to oxidative stress and complications in diabetic individuals. The present study was undertaken to investigate the effect of selenium on blood biochemical parameters, antioxidant enzyme activities, and tissue zinc levels in alloxan-induced diabetic rats fed a zinc-deficient diet. The rats were divided into two groups; the first group was fed a zinc-sufficient diet, while the second group was fed a zinc-deficient diet. Half of each group was treated orally with 0.5 mg/kg sodium selenite. Tissue and blood samples were taken from all animals after 28 days of treatment. At the end of the experiment, the body weight gain and food intake of the zinc-deficient diabetic animals were lower than that of zinc-adequate diabetic animals. Inadequate dietary zinc intake increased glucose, lipids, triglycerides, urea, and liver lipid peroxidation levels. In contrast, serum protein, reduced glutathione, plasma zinc and tissue levels were decreased. A zinc-deficient diet led also to an increase in serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, and liver glutathione-S-transferase and to a decrease in serum alkaline phosphatase activity and glutathione peroxidase. Selenium treatment ameliorated all the values approximately to their normal levels. In conclusion, selenium supplementation presumably acting as an antioxidant led to an improvement of insulin activity, significantly reducing the severity of zinc deficiency in diabetes.

Vitamin D supplementation modulates blood and tissue zinc, liver glutathione and blood biochemical parameters in diabetic rats on a zinc-deficient diet.

Previous studies suggest a protective effect of vitamin D3 on zinc deficiency-induced insulin secretion and on pancreas ß-cell function. The aim of this study was to investigate the effect of vitamin D on blood biochemical parameters, tissue zinc and liver glutathione in diabetic rats fed a zinc-deficient diet. For that purpose, Alloxan-induced diabetic rats were divided into four groups. The first group was fed a zinc-sufficient diet while the second group was fed a zinc-deficient diet. The third and fourth groups received zinc-sufficient or zinc-deficient diets plus oral vitamin D3 for 27 days. At the end of the experiment, blood, femur, pancreas, kidney and liver samples were taken from all rats. The serum, femur, pancreas, kidney and liver zinc concentrations, liver glutathione, serum alkaline phosphatase activity, daily body weight gain and food intake were lower in the zinc-deficient rats in comparison with those receiving adequate amounts of zinc. These values were increased in the zinc-deficient group that was supplemented with vitamin D3. The serum total cholesterol, triglycerides, total protein, urea, glutamate oxaloacetate transaminase, glutamate pyruvate transaminase and blood glucose values were higher in rats fed a zinc adequate diet, but their concentrations were decreased by vitamin D3 supplementation. The serum total protein levels were not changed by zinc deficiency and vitamin D3 supplementation. These results suggest that vitamin D3 modulates tissue zinc, liver glutathione and blood biochemical values in diabetic rats fed a zinc-deficient diet.