1.
Selenium Homeostasis and Clustering of Cardiovascular Risk Factors: A Systematic Review.
Gharipour, M, Sadeghi, M, Behmanesh, M, Salehi, M, Nezafati, P, Gharpour, A
Acta bio-medica : Atenei Parmensis. 2017;(3):263-270
Abstract
Selenium is a trace element required for a range of cellular functions. It is widely used for the biosynthesis of the unique amino acid selenocysteine [Sec], which is a structural element of selenoproteins. This systematic review focused on the possible relation between selenium and metabolic risk factors. The literature was searched via PubMed, Scopus, ISI Web of Science, and Google Scholar. Searches were not restricted by time or language. Relevant studies were selected in three phases. After an initial quality assessment, two reviewers extracted all the relevant data, whereas the third reviewer checked their extracted data. All evidence came from experimental and laboratory studies. Selenoprotein P is the best indicator for selenium nutritional levels. In addition, high levels of selenium may increase the risk of metabolic syndrome while the lack of sufficient selenium may also promote metabolic syndrome. selenium supplementation in subjects with sufficient serum selenium levels has a contrary effect on blood pressure, LDL, and total cholesterol. According to the bioavailability of different types of selenium supplementation such as selenomethionine, selenite and selenium-yeast, it seems that the best nutritional type of selenium is selenium-yeast. Regarding obtained results of longitudinal studies and randomized controlled trials, selenium supplementation should not be recommended for primary or secondary cardio-metabolic risk prevention in populations with adequate selenium status.
2.
The Effects of Selenium Supplementation on Glucose Metabolism and Lipid Profiles Among Patients with Metabolic Diseases: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.
Tabrizi, R, Akbari, M, Moosazadeh, M, Lankarani, KB, Heydari, ST, Kolahdooz, F, Mohammadi, AA, Shabani, A, Badehnoosh, B, Jamilian, M, et al
Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2017;(11):826-830
Abstract
This systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted to summarize the effect of selenium administration on glucose metabolism and lipid profiles among patients with diseases related to metabolic syndrome (MetS). We searched the following databases up to May 2017: MEDLINE, EMBASE, Web of Science, and Cochrane Central Register of Controlled Trials. The relevant data were extracted and assessed for quality of the studies according to the Cochrane risk of bias tool. Data were pooled using the inverse variance method and expressed as standardized mean difference (MDs) with 95% confidence intervals (95% CI). Five studies were included in the meta-analyses. The results showed that selenium supplementation significantly reduced insulin levels (SMD -0.42; 95% CI, -0.83 to -0.01) and increased quantitative insulin sensitivity check index (QUICKI) (SMD 0.83; 95% CI, 0.58 to 1.09). Selenium supplementation had no beneficial effects on other glucose homeostasis parameters, such as fasting plasma glucose (FPG) (SMD -0.29; 95% CI, -0.73 to 0.15), homeostasis model assessment of insulin resistance (HOMA-IR) (SMD -0.80; 95% CI, -1.58 to -0.03), and lipid profiles, such as triglycerides (SMD -0.42; 95% CI, -0.83 to -0.01), VLDL- (SMD -0.42; 95% CI, -0.83 to -0.01), total- (SMD -0.42; 95% CI, -0.83 to -0.01), LDL- (SMD 0.02; 95% CI, -0.20 to 0.24), and HDL-cholesterol (SMD 0.16; 95% CI, -0.06 to -0.38). Overall, this meta-analysis showed that selenium administration may lead to an improvement in insulin and QUICKI, but did not affect FPG, HOMA-IR, and lipid profiles.
3.
Systematic review and meta-analysis shows a specific micronutrient profile in people with Down Syndrome: Lower blood calcium, selenium and zinc, higher red blood cell copper and zinc, and higher salivary calcium and sodium.
Saghazadeh, A, Mahmoudi, M, Dehghani Ashkezari, A, Oliaie Rezaie, N, Rezaei, N
PloS one. 2017;(4):e0175437
Abstract
Different metabolic profiles as well as comorbidities are common in people with Down Syndrome (DS). Therefore it is relevant to know whether micronutrient levels in people with DS are also different. This systematic review was designed to review the literature on micronutrient levels in people with DS compared to age and sex-matched controls without DS. We identified sixty nine studies from January 1967 to April 2016 through main electronic medical databases PubMed, Scopus, and Web of knowledge. We carried out meta-analysis of the data on four essential trace elements (Cu, Fe, Se, and Zn), six minerals (Ca, Cl, K, Mg, Na, and P), and five vitamins (vitamin A, B9, B12, D, and E). People with DS showed lower blood levels of Ca (standard mean difference (SMD) = -0.63; 95% confidence interval (CI): -1.16 to -0.09), Se (SMD = -0.99; 95% CI: -1.55 to -0.43), and Zn (SMD = -1.30; 95% CI: -1.75 to -0.84), while red cell levels of Zn (SMD = 1.88; 95% CI: 0.48 to 3.28) and Cu (SMD = 2.77; 95% CI: 1.96 to 3.57) were higher. They had also higher salivary levels of Ca (SMD = 0.85; 95% CI: 0.38 to 1.33) and Na (SMD = 1.04; 95% CI: 0.39 to 1.69). Our findings that micronutrient levels are different in people with DS raise the question whether these differences are related to the different metabolic profiles, the common comorbidities or merely reflect DS.
4.
Disorders of selenium metabolism and selenoprotein function.
Schweizer, U, Dehina, N, Schomburg, L
Current opinion in pediatrics. 2011;(4):429-35
Abstract
PURPOSE OF REVIEW Inborn errors of metabolism are increasingly recognized as underlying causes in pediatric diseases. Selenium and selenoproteins have only recently been identified as causes of inherited defects. Respective case reports have broadened our understanding of selenoprotein function and their developmental importance. This review presents the characterized defects and tries to attract attention to the spectrum of potential phenotypes. RECENT FINDINGS The characterization of patients with inherited mutations in selenoprotein N has corroborated the physiological importance of selenium for muscle function. Individuals with inherited defects in selenocysteine insertion sequence (SECIS)-binding protein 2 display a syndrome of selenoprotein-related defects including abnormal thyroid hormone metabolism, delayed bone maturation, and other more individual phenotypes. The recent identification of mutations in selenocysteine synthase causing progressive cerebello-cerebral atrophy underlines the central role of selenoproteins in brain development and protection from neurodegeneration. SUMMARY The spectrum of diseases related to inborn defects of selenium utilization, transport, and metabolism is expanding. However, only few examples are already known, resulting from defects in one selenoprotein gene and two genes involved in selenoprotein biosynthesis, respectively. Complex syndromes with impaired muscle function, stunted growth, neurosensory and/or immune defects may point to the involvement of impaired selenium metabolism and selenoprotein function, necessitating specific diagnostic procedures.