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Teace Elements in Parenteral Nutrition*
Published in Fima Lifshitz, Childhood Nutrition, 2020
Adib A. Moukarzel, Marvin E. Ament
Selenium was recognized to prevent dietary liver necrosis in the rat in the early 1950s.113 Subsequent to this, additional selenium-responsive conditions were recognized in a variety of animal diseases. All of these conditions occurred with low soil selenium content and were prevented by supplementing animal rations with selenium. In the late 1960s, pure selenium deficiency, defined as a pathological clinical condition when vitamin E was adequate, was produced in animals in the laboratory. Pure selenium deficiency in chicks caused pancreatic degeneration.114 Growth retardation, partial alopecia, aspermatogenesis, and cataracts were manifestations of selenium deficiency in rats.115–117 The selenium concentration of food depends on the soil in which it is produced and its content of protein. Selenium is typically found in protein fractions of foods; therefore, plants such as fruits and vegetables are poor sources of selenium, and meats are reliable sources of this element. In the United States, the daily dietary selenium intake is 60 to 216 meg.118,119 In the areas of China where Keshan disease occurs, selenium intake is less than 30 mcg/day.109 In the late 1970s, some therapeutic and formula diets were found to contain less than 5 mcg of selenium in the daily intake.120,121 In some parts of the world, selenium intake is quite high, and intakes have been reported up to 500 mcg/day without any toxicity.122
The minerals
Published in Geoffrey P. Webb, Nutrition, 2019
Selenium is present in food largely as the selenium-containing amino acids selenomethionine and selenocysteine where selenium replaces the sulphur present in the parent amino acids cysteine and methionine. The selenium content of the soil in any particular region will have a major effect upon the selenium content of food grown in that area and thus upon the dietary intakes of the people who live there. Affluent populations tend not to be so reliant on food grown locally and may eat selenium-rich seafood and so are to some extent protected from these localised problems. Areas of China have low intakes of selenium in the soil and this is where a progressive cardiomyopathy (Keshan disease) attributed to selenium deficiency has been reported. Other factors like a viral infection are thought to be involved in triggering the condition in those who are selenium deficient.
Section 1
Published in Padmanabhan Ramnarayan, MCQs in Paediatrics for the MRCPCH, Part 1, 2017
Selenium is a trace element, which is now commonly added to TPN, although it was common to find deficiency states in the past. Deficiency causes a form of cardiomyopathy called Keshan disease. Abnormal liver functions and cholestasis are common problems with long-term administration of TPN. Although the exact mechanisms are unknown, intralipid and high concentrations of amino acids are implicated. Osteopenia results from inadequate phosphate, unless supplemented. Hyperglycaemia is more a short-term problem.
Sex-specific relationship between blood selenium levels and platelet count in a large cohort representative of the United States population
Published in Platelets, 2022
Selenium, a metalloid that shares several properties with sulfur, is an essential trace element for human health [1,2]. Selenium deficiency is associated with immune impairment, endocrine and reproductive disorders, and juvenile cardiomyopathy (Keshan disease) [1]. Selenium deficiency often results from low selenium content in the diet – food from plants grown or animals raised on soil with low selenium concentration has low selenium content. Several parts of the world have low selenium soil concentration and by some estimates, up to 10% of the world population may have subclinical selenium deficiency [3]. Dietary selenium, through incorporation into selenoproteins, participates in several important functions including redox homeostasis, modulation of intracellular signaling cascades and transcription factors, and thyroid hormone metabolism [4].
Insights into cancer and neurodegenerative diseases through selenoproteins and the connection with gut microbiota – current analytical methodologies
Published in Expert Review of Proteomics, 2019
Ana Arias-Borrego, Belén Callejón-Leblic, Marta Calatayud, José Luis Gómez-Ariza, Maria Carmen Collado, Tamara García-Barrera
In general, among the wide range of physiological functions of selenium, selenium is well known for its pivotal roles in health, for example in inhibiting angiogenesis [15], controlling proliferation of malignant cells [16], enhancing the immune response [17], inhibiting the activation of certain transcription factors [18], controlling of human Kaschin-Beck disease, Keshan disease, maintaining thyroid function, preventing cardiovascular disease, improving fertility, preventing cancer, preventing neurodegenerative diseases [1,19], as well as antagonizing the toxicity action of several elements being mercury the most known [20]. Table 1 shows the selenoproteins determined in biofluids and tissues from cancer and neurodegenerative disease patients and model organisms or cells.
Association Between Dietary Selenium Intake and the Prevalence of Nonalcoholic Fatty Liver Disease: A Cross-Sectional Study
Published in Journal of the American College of Nutrition, 2020
Jing Wu, Chao Zeng, Zidan Yang, Xiaoxiao Li, Guanghua Lei, Dongxing Xie, Yilun Wang, Jie Wei, Tubao Yang
The level of dietary selenium intake varies greatly among countries and regions (56). In the present study, the mean dietary selenium intake was 42.3 μg/d, which is similar to the level of daily selenium intake in some other countries, for example, Germany (35 μg/d), France (29–43 μg/d), and India (27–48 μg/d) (35,56). In China, the suggested minimum dietary selenium intake to prevent Keshan disease is about 19 μg/d for men and 14 μg/d for women, while the tolerable upper selenium intake level is 400 μg/d (54). The present study shows that dietary selenium intake, even far below the tolerable upper selenium intake level (400 μg/d), is positively associated with the prevalence of NAFLD. Consistent with these findings, another cross-sectional study of 8550 subjects conducted by Yang and colleagues showed that plasma selenium was positively associated with the prevalence of NAFLD in an Asian community-based population (21). In contrast, two in vivo animal studies showed that zinc and selenium co-supplementation containing 1.1 mg Se/kg, which is higher than the recommended intake of selenium for rats (around 0.2 mg/kg) (57–59), could improve the serum lipid profile and reduce hepatic lipid accumulation, which could ameliorate NAFLD (60,61). However, it remains unclear whether such effect is contributed solely by the supplement of selenium. Previous in vivo animal studies have also shown that a higher level of selenium intake is associated with increased hepatic lipid accumulation (17–20). For example, Mueller et al. (20) reported that rats with a selenium-enriched diet (75 or 150 μg/kg) had higher liver triglyceride concentrations than those with a selenium-deficient diet (< 30 μg/kg). Another in vivo animal study also observed that dietary selenate supplementation increased hepatic lipid accumulation significantly in diabetic db/db mice (19). In addition, Chadio et al. (17) suggested that a diet containing enriched selenium and energy (0.576 mg Se/kg) could increase the content of liver unsaturated fatty acid in chickens compared to a diet with adequate selenium and energy (0.289 mg Se/kg). Furthermore, a recent study showed that selenium diet with 3.0 mg/kg increased hepatic lipid concentration in pigs compared with a selenium control diet (0.3 mg/kg) (18). All of these findings suggest that a higher level of selenium intake may have a detrimental effect on the pathogenesis of NAFLD. The present study is the first to test and confirm that such a positive association may still exist in humans.