Redistribution of tissue zinc pools during lactation and dyshomeostasis during marginal zinc deficiency in mice

McCormick, Nicholas H.; King, Janet C.; Krebs, Nancy F.; Soybel, David I.; Kelleher, Shannon L.

doi:10.1016/j.jtemb.2014.06.002

Cited by 10 publications

(6 citation statements)

References 43 publications

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“…In this study, mild ZD under basal conditions did not significantly alter the protein balance in skeletal muscle supporting prior studies showing that in the nonstressed state, the ZM phenotype is seemingly normal (McCormick et al. ; Dempsey et al. ; Croxford et al.…”

Section: Discussionsupporting

confidence: 88%

Marginal dietary zinc deprivation augments sepsis‐induced alterations in skeletal muscle TNF‐α but not protein synthesis

Crowell

Kelleher

Soybel

et al. 2016

Physiological Reports

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Severe zinc deficiency is associated with an increased systemic inflammatory response and mortality after sepsis. However, the impact of mild zinc deficiency, which is more common in populations with chronic illnesses and sepsis, is unknown. In this study, we hypothesized that marginal dietary Zn deprivation (ZM) would amplify tissue inflammation and exacerbate the sepsis‐induced decrease in muscle protein synthesis. Adult male C57BL/6 mice were fed a zinc‐adequate (ZA) or ZM diet (30 or 10 mg Zn/kg, respectively) over 4 weeks, peritonitis was induced by cecal ligation and puncture (CLP), and mice were examined at either 24 h (acute) or 5 days (chronic) post‐CLP. Acute sepsis decreased the in vivo rate of skeletal muscle protein synthesis and the phosphorylation of the mTOR substrate 4E‐BP1. Acutely, sepsis increased TNF‐α and IL‐6 mRNA in muscle, and the increase in TNF‐α was significantly greater in ZM mice. However, muscle protein synthesis and 4E‐BP1 phosphorylation returned to baseline 5 days post‐CLP in both ZA and ZM mice. Protein degradation via markers of the ubiquitin proteasome pathway was increased in acute sepsis, yet only MuRF1 mRNA was increased in chronic sepsis and ZM amplified this elevation. Our data suggest that mild zinc deficiency increases TNF‐α in muscle acutely after sepsis but does not significantly modulate the rate of muscle protein synthesis.

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Section: Discussionsupporting

confidence: 88%

Marginal dietary zinc deprivation augments sepsis‐induced alterations in skeletal muscle TNF‐α but not protein synthesis

Crowell

Kelleher

Soybel

et al. 2016

Physiological Reports

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“…There is consistent evidence in animal models that maternal dietary zinc deficiency during pregnancy reduces fetal growth [16,17,18,19]. From the studies that measured maternal zinc intake during pregnancy reviewed here, a possible relationship between low zinc intake (≤54% of the recommended 11 mg/day) and decreased infant birthweight may exist in human populations.…”

Section: Discussionmentioning

confidence: 77%

“…The importance of zinc to the growth of the fetus is demonstrated by the active transport of zinc across the placenta into the fetal circulation resulting in higher cord blood concentrations compared to those in the maternal circulation [11,12,13,14]. Rodent models of severe maternal zinc deficiency show increased rates of fetal loss and congenital malformations in the surviving fetuses [15] as well as reduced fetal growth [16,17,18], lower implantation rates and impaired placental growth [19], all highlighting the teratogenic effects of zinc deficiency in pregnancy.…”

Section: Introductionmentioning

confidence: 99%

Association between Maternal Zinc Status, Dietary Zinc Intake and Pregnancy Complications: A Systematic Review

et al. 2016

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Adequate zinc stores in the body are extremely important during periods of accelerated growth. However, zinc deficiency is common in developing countries and low maternal circulating zinc concentrations have previously been associated with pregnancy complications. We reviewed current literature assessing circulating zinc and dietary zinc intake during pregnancy and the associations with preeclampsia (PE); spontaneous preterm birth (sPTB); low birthweight (LBW); and gestational diabetes (GDM). Searches of MEDLINE; CINAHL and Scopus databases identified 639 articles and 64 studies were reviewed. In 10 out of 16 studies a difference was reported with respect to circulating zinc between women who gave birth to a LBW infant (≤2500 g) and those who gave birth to an infant of adequate weight (>2500 g), particularly in populations where inadequate zinc intake is prevalent. In 16 of our 33 studies an association was found between hypertensive disorders of pregnancy and circulating zinc; particularly in women with severe PE (blood pressure ≥160/110 mmHg). No association between maternal zinc status and sPTB or GDM was seen; however; direct comparisons between the studies was difficult. Furthermore; only a small number of studies were based on women from populations where there is a high risk of zinc deficiency. Therefore; the link between maternal zinc status and pregnancy success in these populations cannot be established. Future studies should focus on those vulnerable to zinc deficiency and include dietary zinc intake as a measure of zinc status.

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“…Diets were fed ad libitum for 4 weeks prior to the experiments. Feeding the ZM diet for this length of time to mice alters whole-body Zn balance by affecting fertility, testicular Zn concentration, sperm activity, and Zn concentration in milk of lactating female 22–24 . Although this specific ZM diet does not appear to alter plasma Zn levels 22–25 , it has been reported to lower hepatic Zn content in the non-stressed state 22 .…”

Section: Methodsmentioning

confidence: 99%

Immune and metabolic responses in early and late sepsis during mild dietary zinc restriction

Crowell

Phillips

Kelleher

et al. 2017

Journal of Surgical Research

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Background Mild dietary zinc (Zn) deficiency is wide-spread in human populations, but its influence on recovery following acute illness is poorly understood. In a mouse model of abdominal sepsis (cecal-ligation-puncture, CLP), systemic immune responses and liver metabolism were monitored in early (24 hr) and late (5 day) phases, under control conditions and during mild dietary Zn restriction. Methods Mice were fed diets adequate (ZA) or marginally deficient (ZM) in zinc (30 vs 10 mg zinc/kg diet) for 4 weeks, before undergoing laparotomy alone (nonseptic control) or CLP (septic). Results Among nonseptic mice, the ZM state was not associated with differences in inflammation or metabolic responses. Among septic mice, mortality did not differ between the ZA and ZM groups. In the early phase, the ZM state amplified increases in plasma IL-6, TNF-α and IL-10, while dampening the IFN-γ response. In the late phase, subtle but significant ZM-associated increases were observed in plasma IL-5 and IFN-γ levels, and hepatic protein synthesis, the latter of which appeared to be mTOR-independent and was associated with increased hepatic TNF-α mRNA content. Conclusions Without increasing mortality, the ZM state is associated with a more disordered acute systemic inflammatory response and persistence or enhancement of acute phase responses within the liver parenchyma.

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Redistribution of tissue zinc pools during lactation and dyshomeostasis during marginal zinc deficiency in mice

Cited by 10 publications

References 43 publications

Marginal dietary zinc deprivation augments sepsis‐induced alterations in skeletal muscle TNF‐α but not protein synthesis

Marginal dietary zinc deprivation augments sepsis‐induced alterations in skeletal muscle TNF‐α but not protein synthesis

Association between Maternal Zinc Status, Dietary Zinc Intake and Pregnancy Complications: A Systematic Review

Immune and metabolic responses in early and late sepsis during mild dietary zinc restriction

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