Marginal Deficiency Research Articles

Comparison of Thymulin Activity with Other Measures of Marginal Zinc Deficiency.

Activity of the immunoregulatory peptide thymulin reflects differences in zinc status. This study compared thymulin activity with four other zinc status measures in rats fed zinc at either 5 or 25ppm. Rats fed the lower zinc showed the following results compared with rats with adequate zinc intake: serum thymulin activity 61% lower, serum zinc 31% lower, serum extracellular superoxide dismutase 18% lower, serum 5'-nucleotidase activity 26% lower, and liver metallothionein 28% lower. Thus, thymulin activities showed more sensitivity to restricted zinc intake than did four other parameters.

Japan's Practical Guidelines for Zinc Deficiency with a Particular Focus on Taste Disorders, Inflammatory Bowel Disease, and Liver Cirrhosis.

Zinc deficiency is common in Japan, yet awareness on this disorder is lacking. The Japanese Society of Clinical Nutrition recently issued the Japan’s Practical Guideline for Zinc Deficiency 2018 setting forth criteria for diagnosing zinc deficiency, i.e., (a) one or more symptoms of zinc deficiency or low serum alkaline phosphatase, (b) ruling out other diseases, (c) low serum zinc, and (d) alleviation of symptoms upon zinc administration. Serum zinc <60 μg/dL and 60–80 μg/dL indicate zinc deficiency and marginal deficiency, respectively. Zinc deficiency symptoms vary and include dermatitis and taste disorders among others. Zinc administration improves taste in 50–82% of patients suffering from taste disorders (a common symptom of zinc deficiency). Effects of zinc administration do not appear immediately, and therapy should be continued for at least three months. Zinc deficiency often accompanies various diseases and conditions. Here, we focus on inflammatory bowel diseases and liver cirrhosis. As zinc deficiency enhances intestinal inflammation via macrophage activation, we discuss the pathological mechanism for inflammation and zinc deficiency in the context of IBD. Zinc deficiency can also lead to a nitrogen metabolic disorder in patients with liver cirrhosis. Zinc supplementation can improve not only the ammonia metabolism, but also the protein metabolism. We also discuss directions for future studies of zinc deficiency.

Iron Deficiency and Iron Deficiency Anemia: Implications and Impact in Pregnancy, Fetal Development, and Early Childhood Parameters.

A normal pregnancy consumes 500–800 mg of iron from the mother. Premenopausal women have a high incidence of marginal iron stores or iron deficiency (ID), with or without anemia, particularly in the less developed world. Although pregnancy is associated with a “physiologic” anemia largely related to maternal volume expansion; it is paradoxically associated with an increase in erythrocyte production and erythrocyte mass/kg. ID is a limiting factor for this erythrocyte mass expansion and can contribute to adverse pregnancy outcomes. This review summarizes erythrocyte and iron balance observed in pregnancy; its implications and impact on mother and child; and provides an overview of approaches to the recognition of ID in pregnancy and its management, including clinically relevant questions for further investigation.

A Review of Micronutrients and the Immune System-Working in Harmony to Reduce the Risk of Infection.

Immune support by micronutrients is historically based on vitamin C deficiency and supplementation in scurvy in early times. It has since been established that the complex, integrated immune system needs multiple specific micronutrients, including vitamins A, D, C, E, B6, and B12, folate, zinc, iron, copper, and selenium, which play vital, often synergistic roles at every stage of the immune response. Adequate amounts are essential to ensure the proper function of physical barriers and immune cells; however, daily micronutrient intakes necessary to support immune function may be higher than current recommended dietary allowances. Certain populations have inadequate dietary micronutrient intakes, and situations with increased requirements (e.g., infection, stress, and pollution) further decrease stores within the body. Several micronutrients may be deficient, and even marginal deficiency may impair immunity. Although contradictory data exist, available evidence indicates that supplementation with multiple micronutrients with immune-supporting roles may modulate immune function and reduce the risk of infection. Micronutrients with the strongest evidence for immune support are vitamins C and D and zinc. Better design of human clinical studies addressing dosage and combinations of micronutrients in different populations are required to substantiate the benefits of micronutrient supplementation against infection.

Zinc deficiency in patients with chronic liver disease in Japan.

AimThis study aimed to determine the distributions of serum zinc levels and the prevalence of zinc deficiency in patients with chronic liver disease (CLD) in actual clinical practice, and to analyze the association between serum zinc levels and clinical characteristics.MethodsThis study analyzed 1973 patients with CLD, including 749 with liver cirrhosis, who were admitted to Sapporo Kosei General Hospital in 2017.ResultsZinc deficiency, defined as a serum zinc level of <60 μg/dL, was observed in 555 patients overall (28.1%), including 182 (14.9%) patients without liver cirrhosis and 373 (49.8%) with liver cirrhosis. When marginal zinc deficiency was included, zinc deficiency (serum zinc level <80 μg/dL) was observed in 1594 (80.8%) patients overall, including 924 (75.5%) patients without liver cirrhosis and 670 (89.5%) with liver cirrhosis. Serum zinc levels were most strongly correlated with serum albumin levels. Of the 257 CLD patients with an albumin level of <3.5 g/dL, 234 (91.1%) had a serum zinc level of <60 μg/dL.ConclusionsZinc deficiency is common in patients with CLD. Serum zinc levels should be regularly measured, particularly in patients with liver cirrhosis.

Lessons Learned from Experimental Human Model of Zinc Deficiency.

Zinc is an essential element for humans, and its deficiency was documented in 1963. Nutritional zinc deficiency is now known to affect over two billion subjects in the developing world. Conditioned deficiency of zinc in many diseases has also been observed. In zinc-deficient dwarfs from the Middle East, we reported growth retardation, delayed sexual development, susceptibility to infections, poor appetite, and mental lethargy. We never found a zinc-deficient dwarf who survived beyond the age of 25 y. In an experimental model of human mild zinc deficiency, we reported decreased thymulin (a thymopoietic hormone) activity in Th1 cells, decreased mRNAs of IL-2 and IFN-gamma genes, and decreased activity of natural killer cells (NK) and T cytotoxic T cells. The effect of zinc deficiency on thymulin activity and IL-2 mRNA was seen within eight to twelve weeks of the institution of zinc-deficient diet in human volunteers, whereas lymphocyte zinc decreased in 20 weeks and plasma zinc decreased in 24 weeks after instituting zinc-deficient diet. We hypothesized that decreased thymulin activity, which is known to proliferate Th1 cells, decreased the proliferation differentiation of Th1 cells. This resulted in decreased generation of IL-2 and IFN-gamma. We observed no effect in Th2 cell function; thus, zinc deficiency resulted in an imbalance of Th1 to Th2 function resulting in decreased cell-mediated immunity. Zinc therapy may be very useful in many chronic diseases. Zinc supplementation improves cell-mediated immunity, decreases oxidative stress, and decreases generation of chronic inflammatory cytokines in humans. Development of sensitive immunological biomarkers may be more sensitive than an assay of zinc in plasma and peripheral blood cells for diagnosis of marginal zinc deficiency in human.

Coenzyme Q10 status, glucose parameters, and antioxidative capacity in college athletes

BackgroundGlycemia is related to energy production during exercise. Coenzyme Q10 is an antioxidant that participates in adenosine triphosphate synthesis in mitochondria. The aim of this study was to investigate the level of coenzyme Q10, glucose parameters, and antioxidant capacity in athletes.MethodsThis study was designed as a cross-sectional study. Well-trained college athletes (n = 43) and age-gender matched healthy subjects (n = 25) were recruited from a college. The levels of glucose parameters, oxidative stress, antioxidant enzymes activity, Trolox equivalent antioxidant capacity (TAC), and coenzyme Q10 status were measured in the present study.ResultsThe athletes had a significantly lower level of white blood cells (WBC) coenzyme Q10 than the healthy subjects (0.34 ± 0.24 vs. 0.65 ± 0.43 nmol/g, p < 0.01); however, no significant difference was detected in plasma coenzyme Q10 between the two groups. Regarding the glucose parameters, the athletes had significantly higher values for HbA1c (5.5 ± 0.3 vs. 5.3 ± 0.3%, p < 0.05) and quantitative insulin sensitivity check index (QUICKI, 0.37 ± 0.03 vs. 0.34 ± 0.03, p < 0.05), and lower homeostatic model assessment-insulin resistance (HOMA-IR, 1.5 ± 0.8 vs. 2.9 ± 3.8, p < 0.05) than the healthy subjects. A higher level of TAC was found in the athletes (serum, 5.7 ± 0.3 vs. 5.4 ± 0.2 mM Trolox; erythrocyte, 10.5 ± 0.6 vs. 10.0 ± 0.5 mM Trolox, p < 0.05). In addition, WBC coenzyme Q10 status was significantly correlated with catalase activity (r = 0.56, p < 0.01), GPx activity (r = 0.56, p < 0.01), serum TAC (r = 0.54, p < 0.01), fasting glucose (β = − 1.10, p < 0.01), HbA1c (β = − 0.82, p < 0.01), HOMA-IR (β = − 1.81, p < 0.01), and QUICK (β = 0.08, p < 0.01).ConclusionsAthletes may suffer from a marginal coenzyme Q10 deficiency, and the level was related to glycemic control and antioxidant capacity. Further interventional studies are needed to clarify an adequate dose of coenzyme Q10 supplementation in athletes to optimize their coenzyme Q10 status and athletic performance or recovery during exercise.

Serum biotin level during pregnancy is associated with fetal growth and preterm delivery.

Background : Biotin is a water-soluble vitamin that plays various biological roles through histone modification, such as immune functions and fetal growth. Mammalian maternal biotin deficiency during gestation induces fetal growth restriction. Preterm infants are known to be marginal biotin deficiency. However, studies on the biotin status of pregnant women under various conditions are lacking. Method : This was a retrospective case control study to analyze serum biotin concentration during pregnancy and cord blood in normal pregnancy, preterm delivery and small-for-gestational-age (SGA). Results : Twenty pregnant women with normal term delivery, 35 with preterm delivery, 24 with SGA, and 10 non-pregnant adult women were enrolled. Serum biotin concentrations of pregnant women remained low from first to third trimester. The levels of serum biotin in cord blood showed a significant positive correlation with gestational age, and that of pregnant women showed a weak positive correlation with gestational age. The maternal serum biotin levels during second and third trimester of SGA group were significantly lower than those of normal term delivery. Conclusion : This study suggests that maternal biotin deficiency during pregnancy might be the risk of preterm labor or fetal growth restriction. Further studies are required to clarify the roles of biotin in perinatal medicine. J. Med. Invest. 67 : 170-173, February, 2020.

Effects of dietary arachidonic acid in European sea bass (Dicentrarchus labrax) distal intestine lipid classes and gut health.

The use of low fishmeal/fish oil in marine fish diets affects dietary essential fatty acids (EFAs) composition and concentration and, subsequently, may produce a marginal deficiency of those fatty acids with a direct impact on the fish intestinal physiology. Supplementation of essential fatty acids is necessary to cover the requirements of the different EFAs, including the ones belonging to the n-6 series, such as arachidonic acid (ARA). ARA, besides its structural role in the configuration of the lipid classes of the intestine, plays an important role in the functionality of the gut-associated immune tissue (GALT). The present study aimed to test five levels of dietary ARA (ARA0.5 (0.5%), ARA1 (1%), ARA2 (2%), ARA4 (4%), and ARA6 (6%)) for European sea bass (Dicentrarchus labrax) juveniles in order to determine (a) its effect in selected distal intestine (DI) lipid classes composition and (b) how these changes affected gut bacterial translocation rates and selected GALT-related gene expression pre and post challenge. No differences were found between distal intestines of fish fed with the graded ARA levels in total neutral lipids and total polar lipids. However, DI of fish fed with the ARA6 diet presented a higher (P < 0.05) level of phosphatidylethanolamine (PE) and sphingomyelin (SM) than those DI of fish fed with the ARA0.5 diet. In general terms, fatty acid profiles of DI lipid classes mirrored those of the diet dietary. Nevertheless, selective retention of ARA could be observed in glycerophospholipids when dietary levels are low (diet ARA0.5), as reflected in the higher glycerophospholipids-ARA/dietary-ARA ratio for those animals. Increased ARA dietary supplementation was inversely correlated with eicosapentaenoic acid (EPA) content in lipid classes, when data from fish fed with the diets with the same basal composition (diets ARA1 to ARA6). ARA supplementation did not affect intestinal morphometry, goblet cell number, or fish survival, in terms of gut bacterial translocation, along the challenge test. However, after the experimental infection with Vibrio anguillarum, the relative expression of cox-2 and il-1β were upregulated (P < 0.05) in DI of fish fed with the diets ARA0.5 and ARA2 compared with fish fed with the rest of the experimental diets. Although dietary ARA did not affect fish survival, it altered the fatty acid composition of glycerophospholipids and the expression of pro-inflammatory genes after infection when included at the lowest concentration, which could be compromising the physical and the immune functionality of the DI, denoting the importance of ARA supplementation when low FO diets are used for marine fish.

Biotin deficiency in hyperemesis gravidarum

The aim of this study was to determine the serum biotin levels in patients with hyperemesis gravidarum (HG). Ninety pregnant women with HG (mild (n = 30), moderate (n = 30) and severe (n = 30)), and 80 pregnant women without HG were included for this study. In both groups, serum biotin levels were measured. There were no statistically significant differences in demographic and clinical characteristics between the HG groups and the control group except for PUQE scores. Serum biotin levels in all hyperemesis gravidarum groups were statistically significantly lower than control group. Negative statistically significant correlation between hyperemesis gravidarum severity and serum biotin levels was noted. This is the first study that shows low serum biotin levels in women with hyperemesis gravidarum.Impact statementWhat is already known on this subject? Almost 80% of pregnant women have nausea and vomiting. If nausea and vomiting became severe and the symptoms combined with weight loss and ketonuria; the diagnosis should be hyperemesis gravidarum (HG). The etiopathogenetic factors of this unwanted condition have not been exactly known. Biotin is an essential water-soluble vitamin. Biotin catabolism increases in pregnancy. Marginal biotin deficiency occurs in approximately 50% of the gestations despite the “normal” biotin intake on the diet.What do the results of this study add? Current study results elucidated that serum biotin levels were lower in HG cases compared to non HG cases. This study is the first study that reports the association between low serum level of biotin and HG.What are the implications of these findings for clinical practice and/or further research? Further research is needed to show the importance of biotin supplementation in women with hyperemesis gravidarum.

Direct observation of delithiation as the origin of analog memristance in LixNbO2

The discovery of analog LixNbO2 memristors revealed a promising new memristive mechanism wherein the diffusion of Li+ rather than O2− ions enables precise control of the resistive states. However, directly correlating lithium concentration with changes to the electronic structure in active layers remains a challenge and is required to truly understand the underlying physics. Chemically delithiated single crystals of LiNbO2 present a model system for correlating lithium variation with spectroscopic signatures from operando soft x-ray spectroscopy studies of device active layers. Using electronic structure modeling of the x-ray spectroscopy of LixNbO2 single crystals, we demonstrate that the intrinsic memristive behavior in LixNbO2 active layers results from field-induced degenerate p-type doping. We show that electrical operation of LixNbO2-based memristors is viable even at marginal Li deficiency and that the analog memristive switching occurs well before the system is fully metallic. This study serves as a benchmark for material synthesis and characterization of future LixNbO2-based memristor devices and suggests that valence change switching is a scalable alternative that circumvents the electroforming typically required for filamentary-based memristors.

Folate and Vitamin B12 Status in Women of Reproductive Age in Rural Areas in Haryana, Northern India (P10-117-19)

ObjectivesTo conduct a household and biomarker survey to assess the baseline prevalence of folate deficiency and insufficiency and vitamin B12 deficiency in women of reproductive age prior to the start of a wheat flour fortification program in the Ambala District in Haryana, India. MethodsA multistage cluster probability household and biomarker survey was conducted. Participants were women of reproductive age (18–49 y) who were not pregnant and resided in rural areas of two subdistricts in Ambala District in Haryana. Venous blood samples were collected among 866 women. Plasma, serum, and red blood cells (RBC) were separated by centrifugation, processed, and stored at <-80°C until analysis. RBC and serum folate concentrations were measured using microbiologic assay and serum vitamin B12 was measured via chemiluminescence. Serum folate deficiency was defined as serum folate <7 nmol/L and RBC folate deficiency and insufficiency were defined as RBC folate <305 nmol/L and <748 nmol/L, respectively. Vitamin B12 deficiency was defined as vitamin B12 <200 pg/mL and vitamin B12 marginal deficiency was defined as vitamin B12 ≥200 and <300 pg/mL. ResultsThe geometric mean concentrations for serum folate, RBC folate, and serum vitamin B12 were 12.3 (95% confidence interval [CI]: 11.8, 12.9) nmol/L, 544 (95% CI: 516, 573) nmol/L, and 190 (95% CI: 176, 206) pg/mL, respectively. The prevalence of folate deficiency was 11.3% (95% CI: 9.2, 13.9) for serum folate and 9.7% (95% CI: 7.8, 12.0) for RBC folate, and the prevalence of RBC folate insufficiency was 78.6% (95% CI: 74.8, 82.5). A total of 58.3% (95% CI: 54.2, 62.5) of women were vitamin B12 deficient (<200 pg/mL) and an additional 22.9% (95% CI: 19.7, 26.1) were marginally deficient for vitamin B12. ConclusionsThe magnitude of folate insufficiency and vitamin B12 deficiency in this Northern Indian population is a substantial public health concern. The findings from the survey help establish the baseline for a planned wheat flour fortification program aimed at reducing these micronutrient deficiencies. Funding SourcesCenters for Disease Control and Prevention.

Relationship Between Status of Methyl Donor Nutrients and Malignancy Cancer Stages in Taiwanese NSCLC Patients (P24-027-19)

ObjectivesLung cancer patients may suffer from one-carbon malnutrition due to insufficient dietary intake or one-carbon enzymes genotypic diversity. However, the correlation of one-carbon metabolites and lung cancer risk, malignant progression is still unclear. Our objective was to examine methyl donor status and tumor stages. MethodsThe cross-sectional recruited 32 non-small cell lung cancer (NSCLC) patients in National Taiwan University Hospital (NTUH), Taiwan. Nutrition, clinical pathological and biochemical data were collected. Long-term nutritional intake was evaluated by one-carbon semi-quantitative dietary frequency questionnaire, biochemical values were analyzed by Liquid chromatography–mass spectrometry (LC/MS), Tumor information was collected by department of pathology in NTUH. ResultsData revealed that marginal deficiency rate of dietary folate intake was 26.4%, over UL value (>1000mcg) was 9.4%. Energy adjusted folate, free-choline and betaine intake had significantly positive correlation (r = 0.519, r = 0.336, r = 0.388, P < 0.05); Energy adjusted folate and vitamin B12 intake had positive correlation (r = 0.184). According to TNM stages, we classified NSCLC tumor stages and found that increasing energy adjusted folate intake was significantly positive correlated with late stage (P = .001). The adjusted dietary folate in late stages was significantly higher than early stage (P < 0.05). The clinical value of plasma marginal folate deficiency rate was 12.5%, plasma marginal high of homocysteine rate was 15.6%. Plasma free-choline and betaine levels had significantly positive correlation (r = 0.495, P = 0.023). Otherwise, plasma folate and betaine, free-choline levels had negative correlation (r = −0.166, r = −0.075), and plasma folate levels had positive correlation with vitamin B12 (r = 0.353). The plasma folate levels had significantly positive correlation with energy adjusted folate intake (r = 0.464, P = 0.034). Increasing plasma folate level was positive correlated with late tumor stage (r = 0.108). ConclusionsIn summary, higher one-carbon nutrients intake status may be associated with tumor lymphatic metastasis stages of NSCLC patients. Funding SourcesMinistry of Science and Technology.

Defining the plasma folate concentration associated with the red blood cell folate concentration threshold for optimal neural tube defects prevention: a population-based, randomized trial of folic acid supplementation

For women of reproductive age, a population-level red blood cell (RBC) folate concentration below the threshold 906nmol/L or 400 ng/mL indicates folate insufficiency and suboptimal neural tube defect (NTD) prevention. A corresponding population plasma/serum folate concentration threshold for optimal NTD prevention has not been established. The aim of this study was to examine the association between plasma and RBC folate concentrations and estimated a population plasma folate insufficiency threshold (pf-IT) corresponding to the RBC folate insufficiency threshold (RBCf-IT) of 906 nmol/L. We analyzed data on women of reproductive age (n=1673) who participated in a population-based, randomized folic acid supplementation trial in northern China. Of these women, 565 women with anemia and/or vitamin B-12 deficiency were ineligible for folic acid intervention (nonintervention group); the other 1108 received folic acid supplementation for 6 mo (intervention group). We developed a Bayesian linear model to estimate the pf-IT corresponding to RBCf-IT by time from supplementation initiation, folic acid dosage, methyltetrahydrofolate reductase (MTHFR) genotype, body mass index (BMI), vitamin B-12 status, or anemia status. Using plasma and RBC folate concentrations of the intervention group, the estimated median pf-IT was 25.5 nmol/L (95% credible interval: 24.6, 26.4). The median pf-ITs were similar between the baseline and postsupplementation samples (25.7 compared with 25.2 nmol/L) but differed moderately (±3-4 nmol/L) by MTHFR genotype and BMI. Using the full population-based baseline sample (intervention and nonintervention), the median pf-IT was higher for women with vitamin B-12 deficiency (34.6 nmol/L) and marginal deficiency (29.8 nmol/L) compared with the sufficient group (25.6 nmol/L). The relation between RBC and plasma folate concentrations was modified by BMI and genotype and substantially by low plasma vitamin B-12. This suggests that the threshold of 25.5 nmol/L for optimal NTD prevention may be appropriate in populations with similar characteristics, but it should not be used in vitamin B-12 insufficient populations. This trial was registered at clinicaltrials.gov as NCT00207558.

Early Developmental Marginal Zinc Deficiency Affects Neurogenesis Decreasing Neuronal Number and Altering Neuronal Specification in the Adult Rat Brain.

During pregnancy, a decreased availability of zinc to the fetus can disrupt the development of the central nervous system leading to defects ranging from severe malformations to subtle neurological and cognitive effects. We previously found that marginal zinc deficiency down-regulates the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and affects neural progenitor cell (NPC) proliferation. This study investigated if marginal zinc deficiency during gestation in rats could disrupt fetal neurogenesis and affect the number and specification of neurons in the adult offspring brain cortex. Rats were fed a marginal zinc deficient or adequate diet throughout gestation and until postnatal day (P) 2, and subsequently the zinc adequate diet until P56. Neurogenesis was evaluated in the offspring at embryonic day (E)14, E19, P2, and P56 measuring parameters of NPC proliferation and differentiation by Western blot and/or immunofluorescence. At E14 and E19, major signals (i.e., ERK1/2, Sox2, and Pax6) that stimulate NPC proliferation and self-renewal were markedly downregulated in the marginal zinc deficient fetal brain. These alterations were associated to a lower number of Ki67 positive cells in the ventricular (VZs) and subventricular zones (SVZs). Following the progression of NPCs into intermediate progenitor cells (IPCs) and into neurons, Pax6, Tbr2 and Tbr1 were affected in the corresponding areas of the brain at E19 and P2. The above signaling alterations led to a lower density of neurons and a selective decrease of glutamatergic neurons in the young adult brain cortex exposed to maternal marginal zinc deficiency from E14 to P2. Current results supports the concept that marginal zinc deficiency during fetal development can disrupt neurogenesis and alter cortical structure potentially leading to irreversible neurobehavioral impairments later in life.

Zinc Nutritional Status in Patients with Cystic Fibrosis.

Background: Zinc is an essential nutrient for all forms of life and its deficiency affects the normal growth and development of human beings. Objective: The main aim was to investigate zinc nutritional status by serum zinc concentration (SZC) and dietary zinc intake and their association in cystic fibrosis (CF) patients. Methods: A cross-sectional study was conducted in CF patients. Anthropometric measurements and respiratory and pancreatic tests were conducted. Hypozincemia was determined by SZC while using atomic absorption spectrophotometry and dietary zinc deficiency by prospective 72-h dietary surveys. Results: Mean SZC (87.2 ± 16.7 μg/dL) and dietary zinc intake (97 ± 26.9% Dietary Reference Intake) were normal. Three of 17 patients with CF (17.6%) had hypozincemia and four (23.5%) had a dietary zinc deficiency. No patient with dietary zinc deficiency had hypozincemia. A positive and significant association was observed between SZC and Z-score of BMI-for-age (p = 0.048) and weight-for-height (p = 0.012) and between dietary zinc intake and energy intake (EI, p = 0.036) and Z-score of weight-for-high (p = 0.029). Conclusion: SZC was associated with the nutritional status, expressed as BMI (Body Mass Index) and weight-for-height Z score, and dietary zinc intake with EI and weight-for-height Z-score. No patient with hypozincemia had dietary zinc deficiency. This situation should alert us to a marginal zinc deficiency and it may explain why there were no overlapping cases between the two groups. We suggest that probably 41% of the cases in this study would be at elevated risk of zinc deficiency and a zinc supplementation may be considered.

Zinc Deficiency and Arsenic Exposure Can Act Both Independently or Cooperatively to Affect Zinc Status, Oxidative Stress, and Inflammatory Response.

The negative health impact of zinc deficiency overlaps significantly with arsenic exposure, and is associated with increased risk for chronic diseases. Arsenic contamination in the groundwater often co-exists in regions of the world that are prone to zinc deficiency. Notably, low zinc status shares many hallmarks of arsenic exposure, including increased oxidative stress and inflammation. Despite their common targets and frequent co-distribution in the population, little is known regarding the interaction between zinc deficiency and arsenic exposure. In this study, we tested the effect of arsenic exposure at environmentally relevant doses in combination with a physiologically relevant level of zinc deficiency (marginal zinc deficiency) on zinc status, oxidative damage, and inflammation. In cell culture, zinc-deficient THP-1 monocytes co-exposed with arsenic resulted in further reduction in intracellular zinc, as well as further increase in oxidative stress and inflammatory markers. In ananimal study, zinc-deficient mice had further decrease in zinc status when co-exposed to arsenic. Zinc deficiency, but not arsenic exposure, resulted in an increase in baseline transcript abundance of inflammatory markers in the liver. Upon lipopolysaccharide challenge to elicit an acute inflammatory response, arsenic exposure, but not zinc deficiency, resulted in an increase in proinflammatory response. In summary, zinc deficiency and arsenic exposure can function independently or cooperatively to affect zinc status, oxidant stress, and proinflammatory response. The results highlight the need to consider both nutritional status and arsenic exposures together when considering their impact on health outcomes in susceptible populations.

Effects of wet season mineral nutrition on chital deer distribution in northern Queensland

Abstract ContextTo predict the success of an invasive species, it is important to understand the habitat factors that influence its distribution and abundance. In northern Queensland, chital deer (Axis axis) is an introduced ungulate that occupies specific areas over periods of several decades. AimsThe aim was to compare mineral concentrations in the soil and food plants of areas that chital occupy in high and low densities, and to assess mineral levels in blood sera. MethodsFaecal counts were used to identify areas of high and low chital density. Samples of soil and food plants were analysed from high- and low-density areas to determine the concentrations of 10 minerals from 32 collection sites. Laboratory examination was conducted on serum collected from 46 culled chital to evaluate mineral concentrations. Key resultsChital density varied markedly, with higher mineral concentrations found in soil and food plants in areas of high chital density compared with low-density locations. Average-ranked analyses indicated soil phosphorus levels were significantly (1.5×) higher in areas of high chital density, together with levels of Na (3.4×), Mg (2.3×), Mn (2.1×) and Fe (1.3×) in grasses that comprise more than 90% of the wet season (November to March) diet. Based on minimum requirements for ruminants, the concentrations of Na and Zn in grasses were suboptimal for chital. Serum Zn concentrations suggest a marginal deficiency in most of the animals sampled. ConclusionsMineral requirements of ungulates are such that deficiencies in availability of key nutrients may be sufficient to influence density and distribution. If there are deficiencies, the principal determinants of habitat selection are likely to be P in soil, and Na and Zn in food plants. Deficiencies of both Na and Zn in the diet may limit growth and reproductive output. Implications Mineral adequacy in the diet of chital may be a determinant of their current distribution and a predictor of the habitats they may successfully colonise in the future. Recognition of mineral nutrition as a habitat predictor may aid in the management of chital as a keystone species where it is native on the Indian subcontinent, and as an invasive species where it has become naturalised.

Novel metabolic disturbances in marginal vitamin B6-deficient rat heart

Vitamin B6 deficiency is associated with cardiovascular disease (CVD). Although plasma biomarkers have been proposed, no studies have yet directly profiled heart tissue, and the mechanisms have to be fully defined. Thus, in order to provide better insight into vitamin B6-deficient effects on cardiac functions, we sought to identify the metabolic profile in heart tissue consequent to change in dietary vitamin B6 levels by applying metabolomics. Heart tissues of rats fed a basal diet containing a marginal vitamin B6-deficient, vitamin B6-recommended or vitamin B6-supplemented level were analyzed by metabolomics analysis. Among over 500 detected metabolites, imidazole metabolites including carnosine, anserine, homocarnosine and histamine exhibited the highest decrease upon vitamin B6 deficiency (>−45%, P<.01), along with their precursors β-alanine, γ-aminobutyric acid (GABA) and 1-methylhistidine. Ornithine was the only metabolite exhibiting an increased level in the vitamin B6-deficient group. Vitamin B6 deficiency significantly attenuated the activity of heart tissue glutamate decarboxylase (GAD), although there was undetectable activity of aspartate decarboxylase (ADC), suggesting that the involvement of vitamin B6 in imidazole metabolite synthesis occurs partly through GABA production by regulating GAD rather than through a straightforward β-alanine production pathway via ADC in the heart. Notably, vitamin B6 deficiency significantly attenuated citric acid cycle metabolite levels, suggesting cardiac energy metabolism impairment. This study provides a new link between vitamin B6 and cardiac functions, in which marginal vitamin B6 deficiency impairs imidazole and energy metabolism in heart. This newly revealed cardiac metabolic profile may reveal novel molecular targets or foodstuffs for CVD prevention.

Marginal iron deficiency enhances liver triglyceride accumulation in rats fed a high-sucrose diet

We investigated whether marginal iron-deficiency (MID) without anemia influences liver lipid accumulation in rats. Ingestion of a MID diet in which the iron concentration was half of AIN-93 formulation (iron-adequate, IA) for 3weeks decreased liver iron concentration without anemia. We then evaluated the influence of the MID diet on liver lipid accumulation in combination with a high-sucrose (HS) diet and confirmed that the HS-MID diet successfully decreased liver iron concentration without anemia. Additionally, a significant increase in liver triglyceride concentration was found, accompanied by upregulation of hepatic fatty acid synthase expression in the rats fed the HS-MID diet compared to those in the rats fed an HS-IA diet, although no difference was observed in plasma transaminase activity and hepatic interleukin-1β expression. These results suggest that MID enhances de novo lipid synthesis via upregulation of lipogenic gene expression in combination with sucrose in the diet. Abbreviations: ALT, alanine aminotransferase; AST, aspartate aminotransferase; HS, high sucrose; IA, iron adequate; ID, iron deficiency; MID, marginal irondeficiency; NAFLD, non-alcoholic fatty liver disease.