Effect of Maternal Marginal Zinc Deficiency on Development, Redox Status, and Gene Expression Related to Oxidation and Apoptosis in an Avian Embryo Model.

Maternal severe zinc (Zn) deficiency resulted in growth retardation and high mortality during embryonic development in human. Therefore, this study is aimed at evaluating the effect of maternal marginal Zn deficiency on the development and redox status to avoid severe Zn deficiency using an avian model. A total of 324 laying duck breeders at 214 days old were randomly allotted into 3 dietary Zn levels with 6 replicates of 18 ducks per replicate. The birds were fed experimental diets including 3 dietary supplemental Zn levels of 0 mg/kg (maternal Zn-deficient group, 29.2 mg Zn/kg diet), 60 mg/kg (maternal Zn-adequate group), and 120 mg/kg (maternal Zn-high group) for 6 weeks. Dietary Zn levels had on effect on egg production and fertility (P > 0.05), whereas dietary Zn deficiency decreased breeder plasma Zn concentration and erythrocytic alkaline phosphatase activity at week 6 and inhibited erythrocytic 5'-nucleotidase (5'-NT) activity at weeks 2, 4, and 6 (P < 0.05), indicating that marginal Zn-deficient status occurred after Zn depletion. Maternal marginal Zn deficiency increased embryonic mortality and contents of superoxide anion radical, MDA, and PPC and reduced MT content and CuZnSOD activity in duck embryonic livers on E29. The MDA content was positively correlated with embryonic mortality. Maternal marginal Zn deficiency increased BCL2-associated X protein and Caspase-9 mRNA expressions as well as decreased B-cell lymphoma-2 and MT1 mRNA and signal AKT1 and ERK1 protein expressions (P < 0.05). Breeder plasma Zn concentration and erythrocytic 5'-NT activities at week 6 were positively correlated with GSH-Px activity and GPx, MT1, and BCL2 mRNA expressions in embryonic livers on E29. In conclusion, erythrocytic 5'-NT activity could be more rapid and reliable to monitor marginal Zn-deficient status. Marginal Zn deficiency impaired hatchability and antioxidant defense system and then induced oxidative damage and apoptosis in the embryonic liver, contributing to the greater loss of duck embryonic death.

Dietary Selenium Deficiency Partially Mimics the Metabolic Effects of Arsenic.

Chronic arsenic exposure via drinking water is associated with diabetes in human pop-ulations throughout the world. Arsenic is believed to exert its diabetogenic effects via multiple mechanisms, including alterations to insulin secretion and insulin sensitivity. In the past, acute arsenicosis has been thought to be partially treatable with selenium supplementation, though a potential interaction between selenium and arsenic had not been evaluated under longer-term exposure models. The purpose of the present study was to explore whether selenium status may augment arsenic's effects during chronic arsenic exposure. To test this possibility, mice were exposed to arsenic in their drinking water and provided ad libitum access to either a diet replete with selenium (Control) or deficient in selenium (SelD). Arsenic significantly improved glucose tolerance and decreased insulin secretion and ß-cell function in vivo. Dietary selenium deficiency resulted in similar effects on glucose tolerance and insulin secretion, with significant interactions between arsenic and dietary conditions in select insulin-related parameters. The findings of this study highlight the complexity of arsenic's metabolic effects and suggest that selenium deficiency may interact with arsenic exposure on ß-cell-related physiological parameters.

Selenium status and oxidative stress in obese: Influence of adiposity.

BACKGROUND: Selenium deficiency appears to limit antioxidant defense in obese individuals. This study evaluated the association between adiposity indices, selenium status, and oxidative stress in obese women. METHODS: This was a cross-sectional study involving 139 women who were divided into the following two groups: the case group (obese women, n = 63) and the control group (normal-weight women, n = 76). Plasma, erythrocyte, and urinary selenium levels were determined using inductively coupled plasma optical emission spectrometry. Body weight, height, waist circumference, hip circumference and neck circumference were measured. Body mass index, waist/height ratio, conicity index, body fat index, body adiposity index, body circularity index, and visceral adiposity index were calculated. Plasma levels of thiobarbituric acid reactive substances were determined. The erythrocyte glutathione peroxidase activity was determined using an automatic biochemical analyzer and Ransel kit. RESULTS: Obese women had selenium deficiency characterized by reduction in plasma and erythrocyte concentrations (P < .001). The urinary selenium excretion was higher in the case group compared to the control group (P < .001). Adiposity indices values and plasma concentrations of thiobarbituric acid reactive substances were significantly elevated in obese women (P < .001). There was a significant association between adiposity indices and selenium status (P < .001), and between erythrocyte selenium and erythrocyte glutathione peroxidase activity (P < .001). CONCLUSION: Obese women evaluated in the study have reduced plasma and erythrocyte concentrations of selenium and an increased urinary excretion of selenium. The correlation analysis reveals an association between intra-abdominal fat accumulation and selenium metabolism and oxidative stress.

Benefits and Adverse Effects of Histidine Supplementation.

Histidine is a nutritionally essential amino acid with many recognized benefits to human health, while circulating concentrations of histidine decline in pathologic conditions [e.g., chronic obstructive pulmonary disease (COPD) and chronic kidney disease (CKD)]. The purpose of this review is to examine the existing literature regarding the benefits of histidine intake, the adverse effects of excess histidine, and the upper tolerance level for histidine. Supplementation with doses of 4.0-4.5 g histidine/d and increased dietary histidine intake are associated with decreased BMI, adiposity, markers of glucose homeostasis (e.g., HOMA-IR, fasting blood glucose, 2-h postprandial blood glucose), proinflammatory cytokines, and oxidative stress. It is unclear from the limited number of studies in humans whether the improvements in glucoregulatory markers, inflammation, and oxidative stress are due to reduced BMI and adiposity, increased carnosine (a metabolic product of histidine with antioxidant effects), or both. Histidine intake also improves cognitive function (e.g., reduces appetite, anxiety, and stress responses and improves sleep) potentially through the metabolism of histidine to histamine; however, this relation is ambiguous in humans. At high intakes of histidine (>24 g/d), studies report adverse effects of histidine such as decreased serum zinc and cognitive impairment. There is limited research on the effects of histidine intake at doses between 4.5 and 24 g/d, and thus, a tolerable upper level has not been established. Determining tolerance to histidine supplementation has been limited by small sample sizes and, more important, a lack of a clear biomarker for histidine supplementation. The U-shaped curve of circulating zinc concentrations with histidine supplementation could be exploited as a relevant biomarker for supplemental histidine tolerance. Histidine is an important amino acid and may be necessary as a supplement in some populations; however, gaps in knowledge, which this review highlights, need to be addressed scientifically.

Maternal Selenium Deficiency in Mice Alters Offspring Glucose Metabolism and Thyroid Status in a Sexually Dimorphic Manner.

Selenium is an essential micronutrient commonly deficient in human populations. Selenium deficiency increases the risks of pregnancy complications; however, the long-term impact of selenium deficiency on offspring disease remains unclear. This study investigates the effects of selenium deficiency during pregnancy on offspring metabolic function. Female C57BL/6 mice were allocated to control (>190 µg selenium/kg, n = 8) or low selenium (<50 µg selenium/kg, n = 8) diets prior to mating and throughout gestation. At postnatal day (PN) 170, mice underwent an intraperitoneal glucose tolerance test and were culled at PN180 for biochemical analysis. Mice exposed to selenium deficiency in utero had reduced fasting blood glucose but increased postprandial blood glucose concentrations. Male offspring from selenium-deficient litters had increased plasma insulin levels in conjunction with reduced plasma thyroxine (tetraiodothyronine or T4) concentrations. Conversely, females exposed to selenium deficiency in utero exhibited increased plasma thyroxine levels with no change in plasma insulin. This study demonstrates the importance of adequate selenium intake around pregnancy for offspring metabolic health. Given the increasing prevalence of metabolic disease, this study highlights the need for appropriate micronutrient intake during pregnancy to ensure a healthy start to life.

Brain Susceptibility to Methyl Donor Deficiency: From Fetal Programming to Aging Outcome in Rats.

Deficiencies in methyl donors, folate, and vitamin B12 are known to lead to brain function defects. Fetal development is the most studied but data are also available for such an impact in elderly rats. To compare the functional consequences of nutritional deficiency in young versus adult rats, we monitored behavioral outcomes of cerebellum and hippocampus circuits in the offspring of deficient mother rats and in adult rats fed a deficient diet from 2 to 8 months-of-age. We present data showing that the main deleterious consequences are found in young ages compared to adult ones, in terms of movement coordination and learning abilities. Moreover, we obtained sex and age differences in the deleterious effects on these functions and on neuronal layer integrity in growing young rats, while deficient adults presented only slight functional alterations without tissue damage. Actually, the cerebellum and the hippocampus develop and maturate according to different time lap windows and we demonstrate that a switch to a normal diet can only rescue circuits that present a long permissive window of time, such as the cerebellum, whereas the hippocampus does not. Thus, we argue, as others have, for supplements or fortifications given over a longer time than the developmental period.

Nutrient Deficiency-Related Dermatoses after Bariatric Surgery.

GENERAL PURPOSE: To provide information on obesity, bariatric surgery, and the nutrient deficiency-related dermatoses that may result from these surgeries. TARGET AUDIENCE: This continuing education activity is intended for physicians, physician assistants, NPs, and nurses with an interest in skin and wound care. LEARNING OBJECTIVES/OUTCOMES: After participating in this educational activity, the participant should be better able to:1. Examine issues related to obesity and bariatric surgery.2. Identify the sources and role of specific nutrients.3. Recognize the clinical signs and symptoms of nutrient deficiency following bariatric surgery. ABSTRACT: Obesity is a global epidemic that increases the risk of weight-related comorbidities in modern society. It is complex, multifactorial, and largely preventable. Noninvasive treatments for obesity include diet, exercise, and medication. However, bariatric surgeries are becoming popular procedures for those who do not achieve success with noninvasive weight management treatment. Bariatric surgeries often result in dietary restriction and/or malabsorption, which lead to drastic weight loss. Individuals who had bariatric surgeries need lifelong follow-up and monitoring to ensure adequate intake of nutrients. Nutrient deficiencies can ensue when long-term vitamin and mineral supplementation is not followed. Severe nutrient deficiencies may lead to dermatoses that can be corrected by nutrient repletion and careful monitoring. A case report of nutrient deficiency-related dermatoses is followed by a review of obesity and its treatments with a focus on bariatric surgeries.

Comparison of iodine status pre- and post-mandatory iodine fortification of bread in South Australia: a population study using newborn thyroid-stimulating hormone concentration as a marker.

OBJECTIVE: The present study aimed to evaluate the effect of mandatory iodine fortification of bread on the iodine status of South Australian populations using newborn thyroid-stimulating hormone (TSH) concentration as a marker. DESIGN: The study used an interrupted time-series design. SETTING: TSH data collected between 2005 and 2016 (n 211 033) were extracted from the routine newborn screening programme in South Australia for analysis. Iodine deficiency is indicated when more than 3 % of newborns have TSH > 5 mIU/l. PARTICIPANTS: Newborns were classified into three groups: the pre-fortification group (those born before October 2009); the transition group (born between October 2009 and June 2010); and the post-fortification group (born after June 2010). RESULTS: The percentage of newborns with TSH > 5 mIU/l was 5·1, 6·2 and 4·6 % in the pre-fortification, transition and post-fortification groups, respectively. Based on a segmented regression model, newborns in the post-fortification period had a 10 % lower risk of having TSH > 5 mIU/l than newborns in the pre-fortification group (incidence rate ratio (IRR) = 0·90; 95 % CI 0·87, 0·94), while newborns in the transitional period had a 22 % higher risk of having TSH > 5 mIU/l compared with newborns in the pre-fortification period (IRR = 1·22; 95 % CI 1·13, 1·31). CONCLUSIONS: Using TSH as a marker, South Australia would be classified as mild iodine deficiency post-fortification in contrast to iodine sufficiency using median urinary iodine concentration as a population marker. Re-evaluation of the current TSH criteria to define iodine status in populations is warranted in this context.

Zinc and atopic dermatitis: a systematic review and meta-analysis.

Zinc plays a central role in skin integrity via barrier and immune mechanisms and may also be relevant in the pathogenesis of atopic dermatitis (AD). However, little is known about the relationship between zinc and AD. We performed a systematic review to determine (i) the association between zinc levels or zinc deficiency and AD and (ii) the efficacy of oral zinc supplementation in the treatment of AD. We searched PubMed, Scopus, Web of Science and article references for observational studies on zinc levels or zinc deficiency in participants with AD vs. controls and for randomized control trials (RCTs) on zinc supplementation in AD. For observational studies, we calculated pooled standardized mean differences (SMDs) or odds ratios (ORs) along with 95% confidence intervals (CIs) using a random effects model. We included 14 observational studies and two RCTs. The pooled SMD demonstrated significantly lower serum (SMD 0.66, 95% CI 0.21-1.10, P = 0.004), hair (SMD 0.95, 95% CI 0.38-1.52, P = 0.001) and erythrocyte (SMD 0.95, 95% CI 0.38-1.52, P = 0.001) zinc levels in participants with AD compared to controls. Pooled unadjusted data from three studies showed a non-significant increased odds of AD in those with zinc deficiency compared with those without zinc deficiency (OR = 1.50, 95% CI 0.71-3.16, P = 0.28). One RCT of oral zinc supplementation among AD patients with zinc deficiency showed improvement in extent and severity of AD, while another RCT among all AD patients showed no significant improvement. All the studies were of low or moderate quality. We conclude that low serum, hair and erythrocyte zinc levels are associated with AD. However, the poor quality of included studies makes interpretation of these results problematic. High-quality observational studies are needed to confirm the association between low zinc levels and AD, and RCTs are required to evaluate the merit of zinc supplementation for the treatment or prevention of AD.

Methionine Partially Replaced by Methionyl-Methionine Dipeptide Improves Reproductive Performance over Methionine Alone in Methionine-Deficient Mice.

Decreased protein breakdown in pregnant women results in lower concentration of methionine (Met) in plasma, causing pregnancy-related metabolic disturbance. Its dipeptide methionyl-methionine (Met-Met) may exert positive influence in fetal development. This study mainly investigated whether Met-Met can be used as part of free Met to promote reproductive outcomes in mice and the underlying mechanisms. Met-deficient pregnant mice were treated with Met alone or with Met-Met during pregnancy. Daily intraperitoneal injection of 35% dietary Met in pregnant mice was the best dose among the 15⁻45% doses. Embryo development and newborn birth weight were enhanced when 25% of the Met in the 35% Met group was replaced with Met-Met. Met-Met replacement had higher plasma insulin, glucose, and free amino acids (AA) concentrations. Besides, in the placenta, the AA transporter mRNA abundances and peptide transporters (PhT1 and PepT1) protein levels were higher in Met-Met treatment group. Moreover, Met-Met increased 4E-BP1, S6K1 and AKT/mTOR phosphorylation. These results suggest that Met-Met could be used as a partial source of Met to promote reproductive outcomes in Met-restricted pregnant mice, which might be mediated by promoting nutrient availability and activating AKT/mTOR-mediated signaling pathway.

Anticipated burden and mitigation of carbon-dioxide-induced nutritional deficiencies and related diseases: A simulation modeling study.

BACKGROUND: Rising atmospheric carbon dioxide concentrations are anticipated to decrease the zinc and iron concentrations of crops. The associated disease burden and optimal mitigation strategies remain unknown. We sought to understand where and to what extent increasing carbon dioxide concentrations may increase the global burden of nutritional deficiencies through changes in crop nutrient concentrations, and the effects of potential mitigation strategies. METHODS AND FINDINGS: For each of 137 countries, we incorporated estimates of climate change, crop nutrient concentrations, dietary patterns, and disease risk into a microsimulation model of zinc and iron deficiency. These estimates were obtained from the Intergovernmental Panel on Climate Change, US Department of Agriculture, Statistics Division of the Food and Agriculture Organization of the United Nations, and Global Burden of Disease Project, respectively. In the absence of increasing carbon dioxide concentrations, we estimated that zinc and iron deficiencies would induce 1,072.9 million disability-adjusted life years (DALYs) globally over the period 2015 to 2050 (95% credible interval [CrI]: 971.1-1,167.7). In the presence of increasing carbon dioxide concentrations, we estimated that decreasing zinc and iron concentrations of crops would induce an additional 125.8 million DALYs globally over the same period (95% CrI: 113.6-138.9). This carbon-dioxide-induced disease burden is projected to disproportionately affect nations in the World Health Organization's South-East Asia and African Regions (44.0 and 28.5 million DALYs, respectively), which already have high existing disease burdens from zinc and iron deficiencies (364.3 and 299.5 million DALYs, respectively), increasing global nutritional inequalities. A climate mitigation strategy such as the Paris Agreement (an international agreement to keep global temperatures within 2°C of pre-industrial levels) would be expected to avert 48.2% of this burden (95% CrI: 47.8%-48.5%), while traditional public health interventions including nutrient supplementation and disease control programs would be expected to avert 26.6% of the burden (95% CrI: 23.8%-29.6%). Of the traditional public health interventions, zinc supplementation would be expected to avert 5.5%, iron supplementation 15.7%, malaria mitigation 3.2%, pneumonia mitigation 1.6%, and diarrhea mitigation 0.5%. The primary limitations of the analysis include uncertainty regarding how food consumption patterns may change with climate, how disease mortality rates will change over time, and how crop zinc and iron concentrations will decline from those at present to those in 2050. CONCLUSIONS: Effects of increased carbon dioxide on crop nutrient concentrations are anticipated to exacerbate inequalities in zinc and iron deficiencies by 2050. Proposed Paris Agreement strategies are expected to be more effective than traditional public health measures to avert the increased inequality.

Stakeholders' Perceptions of Agronomic Iodine Biofortification: A SWOT-AHP Analysis in Northern Uganda.

Agronomic biofortification (i.e., the application of fertilizer to elevate micronutrient concentrations in staple crops) is a recent strategy recommended for controlling Iodine Deficiency Disorders (IDDs). However, its success inevitably depends on stakeholders' appreciation and acceptance of it. By taking Northern Uganda as a case, this study aimed to capture and compare the perceptions of seven key stakeholder groups with respect to agronomic iodine biofortification. Therefore, we employed a SWOT (Strength, Weaknesses, Opportunities & Threats) analysis in combination with an Analytical Hierarchy Process (AHP). Findings show that stakeholders (n = 56) are generally positive about agronomic iodine biofortification in Uganda, as its strengths and opportunities outweighed weaknesses and threats. Cultural acceptance and effectiveness are considered the most important strengths while the high IDD prevalence rate and the availability of iodine deficient soils are key opportunities for further developing agronomic iodine biofortification. Environmental concerns about synthetic fertilizers as well as the time needed to supply iodine were considered crucial weaknesses. The limited use of fertilizer in Uganda was the main threat. While this study provides insight into important issues and priorities for iodine biofortification technology in Uganda, including differences in stakeholder views, the application of the SWOT-AHP method will guide future researchers and health planners conducting stakeholder analysis in similar domains.

Progressive Increases in Dietary Iron Are Associated with the Emergence of Pathologic Disturbances of Copper Homeostasis in Growing Rats.

Background: Consumption of a high-iron diet causes copper deficiency in weanling rodents; however, the minimum amount of dietary iron that disrupts copper homeostasis has not been established. Objective: We tested the hypothesis that dietary iron at only several-fold above physiologic requirements would cause copper depletion. Methods: Weanling male Sprague-Dawley rats (n = 6/group) were fed AIN-93G-based diets with adequate (88 µg Fe/g = 1×), or excessive (4×, 9.5×, 18.5×, 38×, or 110×) iron content for 7 wk (110× group, due to notable morbidity) or 8 wk (all other groups). Copper-related physiologic parameters were then assessed. Results: A hierarchy of copper-related, pathologic symptoms was noted as dietary iron concentrations increased. All statistical comparisons reported here refer to differences from the 1× (i.e., control) group. The highest iron concentration (110×) impaired growth (final body weights decreased ∼40%; P < 0.0001), and caused anemia (blood hemoglobin and hematocrit decreased ∼65%; P < 0.0001) and hepatic copper depletion (>85% reduction; P < 0.01). Cardiac hypertrophy occurred in the 110× (∼130% increase in mass; P < 0.0001) and 38× (∼25% increase; P < 0.05) groups, whereas cardiac copper content was lower in the 110× (P < 0.01), 38× (P < 0.01), and 18.5× (P < 0.05) groups (∼70% reductions). Splenic copper was also depleted in the 110× (>90% reduction; P < 0.0001), and in the 38× (P < 0.001) and 18.5× (P < 0.01) groups (∼70% reductions). Moreover, serum ceruloplasmin activity was decreased in the 110× and 38× (>90% reductions; P < 0.0001), and 18.5× (P < 0.001) and 9.5× (P < 0.05) (∼50% reductions) groups, typifying moderate to severe copper deficiency. Conclusions: Increasing dietary iron intakes to ∼9.5-fold above dietary recommendations caused copper deficiency. Importantly, human iron supplementation is common, and recommended intakes for at-risk individuals may be ≤10-fold above the RDA. Whether these iron intakes perturb copper metabolism is worth considering, especially since copper defi-ciency can impair iron utilization (e.g., by decreasing the ferroxidase activity of ceruloplasmin).

Erythrocyte fatty acid composition of Nepal breast-fed infants.

PURPOSE: Essential fatty acids play a critical role in the growth and development of infants, but little is known about the fatty acid status of populations in low-income countries. The objective was to describe the fatty acid composition of red blood cells (RBC) in breastfeed Nepali infants and a subsample of their mothers and to identify the main sources of fatty acids in the mother's diet, as well as the fatty acid composition of breast milk. METHODS: RBC fatty acid composition was analyzed in a random sample of 303 infants and 72 mother, along with 68 breastmilk samples. Fatty acid profiles of the most important dietary fat sources were analyzed. Information on mother's diet and intake of fat was collected by three 24-h dietary recalls. RESULTS: In infant RBC's, docosahexaenoic acid (DHA) was the main n-3 fatty acid, and arachidonic acid (AA) was the major n-6 fatty acid. Total n-6 PUFA was three times higher than total n-3 PUFA. Height-for-age (HAZ) was positively associated with DHA status and AA status in multivariable models. The concentration of all fatty acids was higher in children, compared to mothers, except Total n-6 PUFA and Linoleic acid (LA) where no differences were found. The mother's energy intake from fat was 13% and cooking oil (sesame, mustard, soybean or sunflower oil) contributed 52% of the fat intake. CONCLUSIONS: RBC-DHA levels in both infants and mother was unexpected high taking into account few dietary DHA sources and the low DHA concentrations in breastmilk.

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.

Development, Prevention, and Treatment of Alcohol-Induced Organ Injury: The Role of Nutrition.

Alcohol and nutrition have the potential to interact at multiple levels. For example, heavy alcohol consumption can interfere with normal nutrition, resulting in overall malnutrition or in deficiencies of important micronutrients, such as zinc, by reducing their absorption or increasing their loss. Interactions between alcohol consumption and nutrition also can affect epigenetic regulation of gene expression by influencing multiple regulatory mechanisms, including methylation and acetylation of histone proteins and DNA. These effects may contribute to alcohol-related organ or tissue injury. The impact of alcohol-nutrition interactions has been assessed for several organs and tissues, including the intestine, where heavy alcohol use can increase intestinal permeability, and the liver, where the degree of malnutrition can be associated with the severity of liver injury and liver disease. Alcohol-nutrition interactions also play a role in alcohol-related lung injury, brain injury, and immune dysfunction. Therefore, treatment involving nutrient supplementation (e.g., with zinc or S-adenosylmethionine) may help prevent or attenuate some types of alcohol-induced organ damage.

Analyses of Selenotranscriptomes and Selenium Concentrations in Response to Dietary Selenium Deficiency and Age Reveal Common and Distinct Patterns by Tissue and Sex in Telomere-Dysfunctional Mice.

Background: The hierarchies of tissue selenium distribution and selenotranscriptomes are thought to critically affect healthspan and longevity.Objective: We determined selenium status and selenotranscriptomes in response to long-term dietary selenium deficiency and age in tissues of male and female mice.Methods: Weanling telomerase RNA component knockout C57BL/6 mice were fed a selenium-deficient (0.03 mg Se/kg) Torula yeast-based AIN-93G diet or a diet supplemented with sodium selenate (0.15 mg Se/kg) until age 18 or 24 mo. Plasma, hearts, kidneys, livers, and testes were collected to assay for selenotranscriptomes, selected selenoproteins, and tissue selenium concentrations. Data were analyzed with the use of 2-factor ANOVA (diet × age) in both sexes.Results: Dietary selenium deficiency decreased (P ≤ 0.05) selenium concentrations (65-72%) and glutathione peroxidase (GPX) 3 (82-94%) and selenoprotein P (SELENOP) (17-41%) levels in the plasma of both sexes of mice and mRNA levels (9-68%) of 4, 4, and 12 selenoproteins in the heart, kidney, and liver of males, respectively, and 5, 16, and 14 selenoproteins, respectively, in females. Age increased selenium concentrations and SELENOP levels (27% and 30%, respectively; P ≤ 0.05) in the plasma of males only but decreased (12-46%; P < 0.05) mRNA levels of 1, 5, and 13 selenoproteins in the heart, kidney, and liver of males, respectively, and 6, 5, and 0 selenoproteins, respectively, in females. Among these mRNAs, selenoprotein H (Selenoh), selenoprotein M (Selenom), selenoprotein W (Selenow), methionine-R-sulfoxide reductase 1 (MsrB1), Gpx1, Gpx3, thioredoxin reductase 1 (Txnrd1), Txnrd2, selenoprotein S (Selenos), selenoprotein F (Selenof), and selenoprotein O (Selenoo) responded in parallel to dietary selenium deficiency and age in ≥1 tissue or sex, or both. Dietary selenium deficiency upregulated (40-160%; P ≤ 0.05) iodothyronine deiodinase 2 (Dio2) and selenoprotein N (Selenon) in the kidneys of males. Age upregulated (11-44%; P < 0.05) Selenon in the kidneys of males, selenoprotein K (Selenok) and selenoprotein I (Selenoi) in the kidneys of females, and Selenof and Selenok in the testes.Conclusions: These results illustrate tissue-specific sexual dimorphisms of selenium status and selenotranscriptomes because of dietary selenium deficiency and age.

Dietary Selenium Deficiency or Excess Reduces Sperm Quality and Testicular mRNA Abundance of Nuclear Glutathione Peroxidase 4 in Rats.

Background: Glutathione peroxidase (GPX) 4 and selenoprotein P (SELENOP) are abundant, and several variants are expressed in the testis.Objective: We determined the effects of dietary selenium deficiency or excess on sperm quality and expressions of GPX4 and SELENOP variants in rat testis and liver.Methods: After weaning, male Sprague-Dawley rats were fed a Se-deficient basal diet (BD) for 5 wk until they were 9 wk old [mean ± SEM body weight (BW) = 256 ± 5 g]. They were then fed the BD diet alone (deficient) or with 0.25 (adequate), 3 (excess), or 5 (excess) mg Se/kg for 4 wk. Testis, liver, blood, and semen were collected to assay for selenoprotein mRNA and protein abundances, selenium concentration, GPX activity, 8-hydroxy-deoxyguanosine concentration, and sperm quality.Results: Dietary selenium supplementations elevated (P < 0.05) tissue selenium concentrations and GPX activities. Compared with those fed BD + 0.25 mg Se/kg, rats fed BD showed lower (P < 0.05) BW gain (86%) and sperm density (57%) but higher (P < 0.05) plasma 8-hydroxy-deoxyguanosine concentrations (189%), and nonprogressive sperm motility (4.4-fold). Likewise, rats fed BD + 5 mg Se/kg had (P = 0.06) lower BW gain and higher (1.9-fold) sperm deformity rates than those in the selenium-adequate group. Compared with the selenium-adequate group, dietary selenium deficiency (BD) or excess (BD + 3 or 5 mg Se/kg) resulted in 45-77% lower (P < 0.05) nuclear Gpx4 (nGpx4) mRNA abundance in the testis. Rats fed BD had lower (P < 0.05) mRNA levels of 2 Selenop variants in both testis and liver than those in the other groups. Testicular SELENOP was 155-170% higher (P < 0.05) in rats fed BD + 5 mg Se/kg and hepatic c/mGPX4 was 13-15% lower (P < 0.05) in rats fed BD than in the other groups.Conclusions: The mRNA abundance of rat testicular nGPX4 responded to dietary selenium concentrations in similar ways to sperm parameters and may be used as a sensitive marker to assess appropriate Se status for male function.

Daily Consumption of Lipid-Based Nutrient Supplements Containing 250 µg Iodine Does Not Increase Urinary Iodine Concentrations in Pregnant and Postpartum Women in Bangladesh.

Background: Maternal iodine deficiency during pregnancy and lactation is common in Bangladesh.Objective: We evaluated the effect of lipid-based nutrient supplements for pregnant and lactating women (LNS-PL) on urinary iodine concentration (UIC).Methods: We conducted a cluster-randomized controlled effectiveness trial in which we enrolled 4011 pregnant women at ≤20 gestational weeks. Women in 48 clusters received iron and folic acid (IFA; 60 mg Fe/d + 400 µg folic acid/d) and women in 16 clusters received LNS-PL (20 g/d, 118 kcal) containing 22 vitamins and minerals (including 250 µg I). We randomly selected a subsample of 1159 women for repeated urine sample collection, i.e., at enrollment, at 36 wk of gestation, and at 6 mo postpartum, for UIC analysis, a secondary outcome of the trial.Results: The geometric mean UIC at 36 wk of gestation and at 6 mo postpartum did not differ significantly between the IFA and LNS-PL groups. The median (quartile 1, quartile 3) UIC at 36 wk was 27.4 µg/L (16.9, 52.7 µg/L) in the IFA group and 30.2 µg/L (17.7, 56.6 µg/L) in the LNS-PL group; at 6 mo, these were 23.0 µg/L (10.0, 45.9 µg/L) in the IFA group and 22.2 µg/L (9.1, 50.4 µg/L) in the LNS-PL group.Conclusion: Daily consumption of LNS-PL containing 250 µg I did not increase the UICs of pregnant and lactating women in Bangladesh. Iodine from lipid-based nutrient supplements may have been stored in the thyroid gland or secreted in breast milk instead of being excreted in urine. Additional research that uses other biomarkers of iodine status is needed to determine how to meet the iodine requirements of pregnant and lactating women in Bangladesh and similar settings. This trial was registered at clinicaltrials.gov as NCT01715038.