Are Phosphatidylcholine and Lysophosphatidylcholine Body Levels Potentially Reliable Biomarkers in Obesity? A Review of Human Studies.

Phosphatidylcholines (PCs) are the major components of biological membranes in animals and are a class of phospholipids that incorporate choline as a headgroup. Lysophosphatidylcholines (LPCs) are a class of lipid biomolecules derived from the cleavage of PCs, and are the main components of oxidized low-density lipoproteins (oxLDLs) that are involved in the pathogenesis of atherosclerosis. Since obesity is associated with a state of chronic low-grade inflammation, one can anticipate that the lipidomic profile changes in this context and both PCs and LPCs are gaining attention as hypothetically reliable biomarkers of obesity. Thus, a literature search is performed on PubMed, Latin American and Caribbean Health Science Literature (LILACS), and Excerpta Medica DataBASE (Embase) to obtain the findings of population studies to clarify this hypothesis. The search strategy resulted in a total of 2403 reports and 21 studies were included according to the eligibility criteria. Controversial data on the associations of PCs and LPCs with body mass index (BMI) and body fat parameters have been identified. There is an inverse relationship between BMI and most species of PCs, and a majority of studies exhibited negative associations between BMI and LPCs. Other findings regarding the differences between PCs and LPCs in obesity are presented, and the associated uncertainties are discussed in detail.

Effects of selenium supplementation on glycaemic control markers in healthy rodents: a systematic review and meta-analysis.

Overexposure to Se is detrimental to glucose metabolism, mainly because of its pro-oxidant effects and the overexpression of selenoproteins. This systematic review evaluated the effects of Se supplementation on glycaemic control in healthy rodents. The methodology followed the PRISMA. We searched the databases for articles published up to May 2022. The risk of bias and the methodological quality were assessed using the SYRCLE and CAMARADES. The results are presented as meta-analytic estimates of the overall standardised mean difference (SMD) and 95 % CI. Of the 2359 records retrieved, thirteen studies were included, of which eleven used sodium selenite and two used zero-valent Se nanoparticles as supplement. Nine studies were included in the meta-analysis. Generally, the risk of bias was high, and 23·1 % of the studies were of high quality. Supplementation with sodium selenite significantly increased fasting blood glucose (SMD = 2·57 (95 % CI (1·07, 4·07)), I2 = 93·5 % (P = 0·001). Subgroup analyses showed effect size was larger for interventions lasting between 21 and 28 d (SMD = 25·74 (95 % CI (2·29, 9·18)), I2 = 96·1 % (P = 0·001)) and for a dose of 864·7 µg/kg/d of sodium selenite (SMD = 10·26 (95 % CI (2·42, 18·11), I2 = 97·1 % (P = 0·010)). However, it did not affect glutathione peroxidase activity (SMD = 0·60 (95 % CI (-0·71, 1·91)), I2 = 83·2 % (P = 0·37)). The current analysis demonstrated the adverse effects of sodium selenite supplementation on glycaemic control in healthy rodents.

The impact of essential and toxic elements on cardiometabolic risk factors in adults and older people.

BACKGROUND AND AIM: Evidence suggests an association between essential and toxic elements and the worsening of cardiometabolic risk factors. This study aimed to investigate the concentrations of zinc, copper, selenium, arsenic, cadmium, and mercury and their relationship with cardiometabolic risk factors in adults and older people. METHODS: This cross-sectional study was carried out with 112 adults with a mean age of 59 (sd 14) years old and a BMI of 29.30 (sd 5.11) Kg/m2. The subject's weight and height were measured for body mass index (BMI) calculation, classified according to the cut-off points recommended by the World Health Organization (WHO). We evaluated sociodemographic, clinical, lifestyle, waist circumference - WC, visceral adiposity index - VAI, glycemic lipid profile, blood pressure, and high-sensitive C-reactive protein (hs-CRP). Cardiovascular risk was defined by The Global Risk Score (GRS) score. Plasma zinc, selenium, copper levels, urinary arsenic, cadmium, and mercury levels were measured using the inductively coupled plasma mass spectrometry technique (ICP-MS). RESULTS: There was a negative association between urinary arsenic and VAI (ß - 0.03, p < 0.01), triglycerides (ß - 1.10, p < 0.01), and VLDL cholesterol (ß - 0.14, p = 0.02). Plasma copper and copper/zinc ratio were positively associated with fasting glucose and hs-CRP (ß 0.38, p < 0.01; ß 36.02, p = 0.01, ß 0.004, p < 0.01, ß 0.68, p < 0.001, respectively). Urinary arsenic (ß - 0.14, p = 0.04) and cadmium (ß - 36.42, p = 0.04) were negatively associated with systolic blood pressure. Also, urinary cadmium was negatively associated with diastolic blood pressure (ß - 21.55, p = 0.03), and urinary mercury showed an opposite behavior (ß 1.45, p = 0.03). CONCLUSION: Essential and toxic elements in urine and plasma could be potential biomarkers for cardiovascular risk factors. A healthy lifestyle should be adopted; in addition, government policies should be developed to guarantee sustainable production and a safe environment.

Effects of selenium supplementation on glycemic control markers in healthy rodents: A systematic review protocol.

BACKGROUND: In vivo and in vitro studies have shown that Se has an insulin-mimetic action associated with its antioxidant activity. Other studies, in turn, suggest that high Se doses and high selenoprotein expression interfere with insulin signaling. This study aims to evaluate the effects of Se supplementation on glycemic control markers in healthy rodents. METHODS: The protocol was developed according to the Preferred Reporting Items for Systematic Review and Metaanalysis Protocol (PRISMA-P) and was published in the International Prospective Register of Systematic Reviews database (PROSPERO; CRD4202121201142019119181). Experimental, randomized, or non-randomized studies of healthy rodents models will be included. All forms of supplemented Se will be considered, including organic, inorganic, and synthetic compounds, selenium-enriched yeasts, zerovalent Se nanoparticles, and selenized polysaccharides. Fasting blood glucose will be considered the primary outcome. Homeostatic model assessment, plasma and erythrocyte Se concentration, GPX activity, SELENOP concentration, and other Se biomarkers will be considered secondary outcomes. EMBASE, Scopus, Pubmed/Medline, Web of Science, and CINAHL will be searched for articles published with no language restrictions. Two reviewers will independently conduct the search and selection of articles, data extraction, and quality analysis. The risk of bias and methodological quality analyses of the included studies will be performed using the Systematic Review Center for Laboratory Animal Experimentation (SYRCLE) and Collaborative Approach to Meta-Analysis and Review (CAMARADES) tools, respectively. The results will be presented as a narrative synthesis according to the Synthesis Without Meta-analysis (SWiM) Reporting Guideline. Meta-analyses will be conducted where appropriate using random-effects models. DISCUSSION: The review may clarify the interaction between different forms of supplemented Se and glycemic control in rodents models. The results will provide evidence that will help select doses and forms of Se to administer in clinical trials while according to impact on the glycemic control while elucidating mechanisms of Se metabolism.

Selenium in Human Health and Gut Microflora: Bioavailability of Selenocompounds and Relationship With Diseases.

This review covers current knowledge of selenium in the dietary intake, its bioavailability, metabolism, functions, biomarkers, supplementation and toxicity, as well as its relationship with diseases and gut microbiota specifically on the symbiotic relationship between gut microflora and selenium status. Selenium is essential for the maintenance of the immune system, conversion of thyroid hormones, protection against the harmful action of heavy metals and xenobiotics as well as for the reduction of the risk of chronic diseases. Selenium is able to balance the microbial flora avoiding health damage associated with dysbiosis. Experimental studies have shown that inorganic and organic selenocompounds are metabolized to selenomethionine and incorporated by bacteria from the gut microflora, therefore highlighting their role in improving the bioavailability of selenocompounds. Dietary selenium can affect the gut microbial colonization, which in turn influences the host's selenium status and expression of selenoproteoma. Selenium deficiency may result in a phenotype of gut microbiota that is more susceptible to cancer, thyroid dysfunctions, inflammatory bowel disease, and cardiovascular disorders. Although the host and gut microbiota benefit each other from their symbiotic relationship, they may become competitors if the supply of micronutrients is limited. Intestinal bacteria can remove selenium from the host resulting in two to three times lower levels of host's selenoproteins under selenium-limiting conditions. There are still gaps in whether these consequences are unfavorable to humans and animals or whether the daily intake of selenium is also adapted to meet the needs of the bacteria.

Effects of vitamin D supplementation on fasting glucose, dyslipidemia, blood pressure, and abdominal obesity among patients with metabolic syndrome: a protocol for systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: Vitamin D deficiency can play a role in extraskeletal functions that are involved with a set of risk factors associated with metabolic syndrome (MetS). The purpose of this review is to investigate the impact of vitamin D supplementation on fasting glucose, dyslipidemia, blood pressure, and abdominal obesity among patients with MetS. METHODS: EMBASE, Medline, Web of Science, Lilacs, the Cochrane Central Register of Controlled Trials, clinicaltrials.gov databases, and grey literature will be systematically searched for randomized controlled trials (RCTs) of vitamin D supplementation compared with placebo, through December 2020. We will include in the study patients with MetS diagnosed by the criteria set forth by the National Cholesterol Education Program Adult Treatment Panel III or the International Diabetes Federation. The effect of oral vitamin D supplementation on lipid profile improvement (triglycerides, high-density lipoprotein cholesterol-HDL-C) is this review's primary outcome. The systematic review will be performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The study screening, data extraction, and quality assessment will be fulfilled by two independent reviewers according to the Cochrane Risk of Bias tool (RoB 2.0). The results of the systematic review will be provided according to the type of intervention, characteristics of the target population, the methods of measurement of vitamin D, the calculated vitamin D concentrations, types of biological samples, and types of outcomes. Meta-analyses will be conducted where appropriate. The Cochran's Q test and the I2-heterogeneity test will be used to assess the presence of heterogeneity and whether the fixed or the random-effects model would be appropriate for combining study results using the inverse variance method or the DerSimonian-Lair method, respectively. Publication bias will be evaluated using funnel plots and Egger's and Begg's tests. The strength of the evidence will be assessed according to the Grading of Recommendations Assessment, Development, and Evaluation (GRADE). DISCUSSION: This systematic review will assess the effects of vitamin D supplementation on fasting glucose and triglyceride levels, waist circumference and mean blood pressure, and HDL-C among individuals with MetS. These findings may assist with decision-making within a clinical setting. SYSTEMATIC REVIEW REGISTRATION: PROSPERO registration number CRD42019123212.

Processed and ultra-processed foods are associated with high prevalence of inadequate selenium intake and low prevalence of vitamin B1 and zinc inadequacy in adolescents from public schools in an urban area of northeastern Brazil.

Changes in eating behavior of adolescents are associated with high consumption of processed and ultra-processed foods. This study evaluated the association between these foods and the prevalence of inadequate micronutrient intake in adolescents. A cross-sectional study was conducted with 444 adolescents from public schools in the city of Natal, northeastern Brazil. The adolescents' habitual food consumption was evaluated using two 24-hour dietary recalls. Foods were categorized according to the degree of processing (processed and ultra-processed) and distributed into energy quartiles, using the NOVA classification system. Inadequacies in micronutrient intake were assessed using the estimated average requirement (EAR) as the cutoff point. Multivariate logistic regression models were used to estimate the relationship between energy percentage from processed and ultra-processed foods and prevalence of inadequate micronutrient intake. The mean (Standard Deviation (SD)) consumption of total energy from processed foods ranged from 5.8% (1.7%) in Q1 to 20.6% (2.9%) in Q4, while the mean consumption of total energy from ultra-processed foods ranged from 21.4% (4.9%) in Q1 to 61.5% (11.7%) in Q4. The rates of inadequate intake of vitamin D, vitamin E, folate, calcium, and selenium were above 80% for both sexes across all age groups. Energy consumption from processed foods was associated with higher prevalence of inadequate selenium intake (p < 0.01) and lower prevalence of inadequate vitamin B1 intake (p = 0.04). Energy consumption from ultra-processed foods was associated with lower prevalence of inadequate zinc and vitamin B1 intake (p < 0.01 and p = 0.03, respectively). An increase in the proportion of energy obtained from processed and ultra-processed foods may reflect higher prevalence of inadequate selenium intake and lower prevalence of vitamin B1 and zinc inadequacy.

The hypolipidemic and pleiotropic effects of rosuvastatin are not enhanced by its association with zinc and selenium supplementation in coronary artery disease patients: a double blind randomized controlled study.

OBJECTIVE: Statins treatment may modify the levels of zinc and selenium, minerals that can improve vascular function and reduce oxidative damage and inflammation in atherosclerotic patients. This study aimed to evaluate the effects of rosuvastatin, alone or associated with zinc and selenium supplementation, on lipid profile, antioxidant enzymes and mineral status in coronary artery disease patients. MATERIAL AND METHODS: A double-blind randomized clinical trial was performed in which patients (n = 76) were treated with 10 mg rosuvastatin over 4 months associated or not with zinc (30 mg/d) and selenium (150 µg/d) supplementation. The following parameters were analyzed before and after the intervention: anthropometric measurements, lipid profile, high sensitivity C-reactive protein (hs-CRP), electronegative low density lipoprotein (LDL(-)) concentrations, activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), zinc and selenium concentrations in blood plasma and erythocytes. Significance was determined using an α of 5% (two-tailed). RESULTS: We found that rosuvastatin therapy was efficient in reducing total cholesterol, LDL-cholesterol, non-HDL cholesterol, triglycerides, and hs-CRP independently of mineral supplementation. Neither treatment was associated with significant changes in LDL(-). Similarly, the antioxidant enzymes GPx and SOD activity were unchanged by treatments. Neither treatment was associated with significant differences in concentrations of zinc or selenium in blood plasma and erythocytes of studied groups. CONCLUSION: Rosuvastatin treatment did not affect zinc and selenium levels in coronary artery disease patients. The zinc and selenium supplementation at doses used in this study did not change lipid profile or SOD and GPx activity in patients receiving rosuvastatin. Further studies should be focused on testing alternative doses and supplements in different populations to contribute for a consensus on the ideal choice of antioxidants to be used as possible complementary therapies in atherosclerotic patients. TRIAL REGISTRATION: ClinicalTrials.gov NCT01547377.

The beneficial effects of rosuvastatin are independent of zinc supplementation in patients with atherosclerosis.

BACKGROUND: Statins have multiple antiatherosclerotic effects, but can reduce blood plasma concentrations of minerals, including zinc. As zinc possesses antiinflammatory and antioxidant effects, low zinc status can promote injuries or inadequate tissue repair in endothelial cells. Metallothionein (MT) expression might modulate responses induced by statins in patients with atherosclerosis. However, research regarding mineral status and the use of statins is scarce. This study evaluated the effects of zinc supplementation on zinc status and expression of the zinc-dependent MT1F and MT2A genes in patients with atherosclerosis treated with rosuvastatin. METHODS: A double-blind, randomized clinical trial was performed with 54 participants treated with 10mg rosuvastatin for 4 months with or without zinc supplementation (30mg/day). Diet, lipid profile, high-sensitivity reactive protein C (hs-CRP), plasma and erythrocyte zinc concentrations, erythrocyte superoxide dismutase (SOD) activity, and MT1F and MT2A genes expression were analyzed before and after intervention. RESULTS: Rosuvastatin therapy was effective in reducing low- and non-high-density lipoprotein, total cholesterol, triglycerides, and hs-CRP levels, independent of zinc supplementation. Additionally, zinc treatment had no effect on SOD enzyme activity (P=0.201), plasma (P>0.671) and erythrocyte (P>0.123) zinc concentrations, or the pattern of MT1F and MT2A genes expression (P=0.088 and P=0.229, respectively). CONCLUSIONS: The effectiveness of rosuvastatin treatment is independent of the effects of zinc supplementation. Moreover, rosuvastatin treatment did not have a significant impact on zinc status or MT1F and MT2A genes expression in patients with atherosclerosis.