Selenium and Its Supplementation in Cardiovascular  Disease—What do We Know?

Benstoem, Carina; Goetzenich, Andreas; Kraemer, Sandra; Borosch, Sebastian; Manzanares, William; Hardy, Gil; Stoppe, Christian

doi:10.3390/nu7053094

Cited by 287 publications

(209 citation statements)

References 126 publications

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“…The present study demonstrated that treatment with EPO reduced FBG, ameliorated glucose tolerance and insulin sensitivity, and lowered glyconeogenesis in experimental diabetic rats, which was in agreement with the previous studies. A previous randomized placebo controlled trial (18) demonstrated that insulin sensitivity is not improved following treatment with EPO in healthy humans. This may be due to exogenous EPO normalizing the low EPO levels in these patients.…”

Section: Discussionmentioning

confidence: 97%

“…Numerous clinical assays have demonstrated significantly lower plasma and serum concentrations of selenium in patients with cardiovascular diseases, compared with those measured in healthy individuals (18). Selenium is a trace element, which exerts certain insulin-like actions on the glucose homeostasis of diabetic rats.…”

Section: Epo Increases Blood Selenium In Diabetic Ratsmentioning

confidence: 99%

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Erythropoietin improves glucose metabolism and pancreatic β-cell damage in experimental diabetic rats

et al. 2015

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Abstract. Previous studies have implicated erythropoietin (EPO) signaling in the regulation of glucose metabolism. Whether EPO can be used treat diabetes and the underlying mechanism remain to be elucidated. The present study aimed to investigate whether EPO affects glucose metabolism, and the underlying mechanisms, in experimental diabetic rats. The effects of EPO (300 U/kg three times a week for 4 weeks) on glucose metabolism, hematopoietic function, blood selenium content and the ultrastructure of pancreatic β-cells were investigated in low dose (25 mg/kg body weight) streptozotocin-induced experimental diabetic rats provided with a high-fat diet. The results demonstrated that EPO significantly decreased the fasting blood glucose, the area under the curve of the oral glucose tolerance and insulin tolerance tests and L-alanine gluconeogenesis. Ultrastructural examination of the pancreatic islets revealed that EPO prevented the dysfunction of pancreatic β-cells in experimental diabetic rats, ameliorated cytoplasmic vacuolation and fragmentation of mitochondria, and increased the number of secretory granules. EPO administration increased the activities of superoxide dismutase and glutathione peroxidase, and decreased the level of malondialdehyde. Additionally, EPO increased blood selenium in the diabetic rats and produced a hematopoietic effect. These results indicated that EPO modulated glucose metabolism and improved pancreatic β-cells damage by increasing anti-oxidation. The detailed mechanisms underlying these effects require further investigation.

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Section: Discussionmentioning

confidence: 97%

Section: Epo Increases Blood Selenium In Diabetic Ratsmentioning

confidence: 99%

Erythropoietin improves glucose metabolism and pancreatic β-cell damage in experimental diabetic rats

et al. 2015

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“…Selenium plays a role in many important physiological functions in human and animal health because it's a component of selenoproteins such as glutathione peroxidase, thioredoxin reductase, and thyroid hormone deiodinase families [2]. These Se dependent enzymes play a wide range of biological functions involving thyroid hormone metabolism, the body's antioxidant defense systems, the adaptive and acquired immune system and prevention of certain cancers [3]. In addition, selenoproteins such as glutathione peroxidase and thioredoxin reductase play an important role in maintaining bone homeostasis and protecting against bone loss [4].…”

Section: Introductionmentioning

confidence: 99%

Selenium in Soil-Crop-Animal System: A Holistic Perspective to Manage Animal and Human Health

Saha¹

2017

IJAAS

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Selenium (Se) dependent enzymes play important roles in physiological functions such as thyroid hormone metabolism, strengthens anti-oxidant defense system and immune system. However, about 800 million people worldwide are believed to be deficient in Se which is attributed to low Se levels in the soil. This is because Se in plant and animal products in human diet depends upon the available Se in the soil. Deficiency of Se can be prevented or treated by adequate dietary intake or through direct supplementation. There have been reports that patients with dilated cardiomyopathy, HIV viral loads and cancer have responded to Se supplementation. However, food fortification has been found to be more efficient than supplementation. Both agronomic biofortification and genetic biofortification have been used to increase Se content of food crops and animal products. Genetic engineering makes use of key genes of Se hyperaccumulators to increase Se accumulating potential of food crops. Agronomic biofortification increases Se content of food crops by adding Se rich fertilizers to the soil or foliar application of Se. Selenium can also be added to animal diets or feedstuff to increase Se content of meat, eggs, and milk. Although inorganic forms of Se are approved as feed additives, they are less efficient than organic sources such as selenomethionine (SeMet) which is the dominant form in plants and animals. Animal products have been found to have higher Se content than plant products with fish having the highest Se content. Fruits and vegetables have a low content of Se probably because of their low protein content. Recommendations for dietary intake of Se vary with country, age and sex. There are concerns that the present recommended Se daily allowance may not be adequate due to discovery of other selenoenzymes with higher Se requirements than gluthathione peroxidase. There may be a need to review the current recommended daily allowance for Se in order to improve human health.

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“…3 Cardiovascular comorbidities are prevalent in individuals with obstructive sleep apnea (OSA). The most accepted hypothesis is that intermittent hypoxia leads to oxidative stress contributing to proatherogenic effects: lipid peroxidation, endothelial dysfunction, and systemic inflammation.…”

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confidence: 99%