Marginal Zinc Deficiency in Mice Increased the Number of Abnormal Sperm and Altered the Expression Level of Spermatogenesis-Related Genes

Peng, Cheng; Cheng, Qian; Liu, Youjiao; Zhang, Zhaoyu; Wang, Ziqiong; Ma, Haitao; Wang, Lei; Wang, Chunhong

doi:10.1007/s12011-021-02979-6

Cited by 9 publications

(3 citation statements)

References 56 publications

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“…Consistent with the symptoms of piglet diarrhea models [29,30], ETEC k88-infected mice also exhibited more significant body weight losses, diarrhea scores, and intestinal barrier damage and inflammatory reactions. In addition, marginal zinc-deficient mice exhibited severe symptoms of serum zinc deficiency, which is in agreement with previous studies on mice [31].…”

Section: Discussionsupporting

confidence: 92%

Marginal Zinc Deficiency Aggravated Intestinal Barrier Dysfunction and Inflammation through ETEC Virulence Factors in a Mouse Model of Diarrhea

Wang¹,

Chen²,

Gan³

et al. 2022

Veterinary Sciences

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Zinc is both essential and inhibitory for the pathogenesis of enterotoxigenic Escherichia coli (ETEC). However, the accurate effects and underlying mechanism of marginal zinc deficiency on ETEC infection are not fully understood. Here, a marginal zinc-deficient mouse model was established by feeding mice with a marginal zinc-deficient diet, and ETEC k88 was further administrated to mice after antibiotic disruption of the normal microbiota. Marginal zinc deficiency aggravated growth impairment, diarrhea, intestinal morphology, intestinal permeability, and inflammation induced by ETEC k88 infection. In line with the above observations, marginal zinc deficiency also increased the intestinal ETEC shedding, though the concentration of ETEC in the intestinal content was not different or even decreased in the stool. Moreover, marginal zinc deficiency failed to change the host’s zinc levels, as evidenced by the fact that the serum zinc levels and zinc-receptor GPR39 expression in jejunum were not significantly different in mice with ETEC challenge. Finally, marginal zinc deficiency upregulated the relative expression of virulence genes involved in heat-labile and heat-stable enterotoxins, motility, cellular adhesion, and biofilm formation in the cecum content of mice with ETEC infection. These findings demonstrated that marginal zinc deficiency likely regulates ETEC infection through the virulence factors, whereas it is not correlated with host zinc levels.

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Section: Discussionsupporting

confidence: 92%

Marginal Zinc Deficiency Aggravated Intestinal Barrier Dysfunction and Inflammation through ETEC Virulence Factors in a Mouse Model of Diarrhea

Wang¹,

Chen²,

Gan³

et al. 2022

Veterinary Sciences

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“…Similarly, other studies had also found that the exposure of C57BL/6J mice to DEHP resulted in a higher liver index [ 36 ]. Furthermore, histopathological analyses showed that DEHP caused a large reduction in spermatogenic cells, abnormal morphology, which was consistent with the findings of previous research [ 37 , 38 ]. ZnSO 4 and OPZCL restored the morphology of spermatozoa and improved the reproductive capacity of ICR male mice.…”

Section: Discussionsupporting

confidence: 92%

Oyster Peptide-Zinc Complex Ameliorates Di-(2-ethylhexyl) Phthalate-Induced Testis Injury in Male Mice and Improving Gut Microbiota

Lu,

Huang,

Chen

et al. 2023

Foods

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Di-(2-ethylhexyl) phthalate (DEHP) is a widely used plasticizer, which can cause damage to male reproductive organs, especially the atrophy of the testis. Meanwhile, DEHP can also lead to a decrease in testicular zinc content, but the role of zinc remains unclear. This study aims to prepare oyster peptide-zinc complex (OPZC) to alleviate DEHP-induced reproductive damage in mice. OPZC was successfully obtained through electron microscopy, X-ray diffraction, and thermogravimetric analysis, with stable structure and high water-solubility. Low dose oyster peptide-zinc complex (OPZCL) significantly reduced the reproductive damage caused by DEHP in mice. Further research had shown that OPZCL restored the content of serum hormones and the activity of oxidative stress kinases to normal, while also normalizing testicular zinc and selenium levels. In addition, it also recovered the disorder of gut microbiota, reduced the proportion of Bacteroides, increased the abundance of Ligilactobacillus, and restored the proportion of Acidobacterota, Chloroflexi, and Proteobacteria. Therefore, OPZCL can relieve the reproductive damage caused by DEHP in mice by restoring testicular zinc homeostasis and the composition of intestinal microbiota, indicating that OPZCL has a potential protective effect on male reproductive health.

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“…25) The activity of SOD enzyme in serum of female Zinc-deficient mice of F0 generation decreased, which confirmed that zinc deficiency would affect SOD enzyme activity. 26,27) Previous literatures have reported that zinc ion can improve the catalytic efficiency and stability of SOD enzyme. 28,29) F0 generation male mice did not show glucose tolerance impairment after the low zinc diet intervention, which may be due to the marginal zinc deficiency of mice, which is relatively mild and does not cause the disorder of glucose metabolism.…”

Section: Discussionmentioning

confidence: 99%

Effects of Zinc Deficiency in Male Mice on Glucose Metabolism of Male Offspring

Yang

et al. 2022

CHEMICAL & PHARMACEUTICAL BULLETIN

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As an essential metal, zinc is central to insulin biosynthesis and energy metabolism. Zinc can not only maintain the activity of insulin, but also has insulin-like effect. When zinc is sufficient, the body needs less insulin. Zinc can correct abnormal glucose tolerance and even replace insulin to improve glucose metabolism disorder in diabetic rats. However, the effect of paternal zinc deficiency on glucose metabolism of offspring is still unclear. In the present study, sixteen 8-week-old male mice were randomly allocated into low-zinc group and control group (8 mice in each group), which were fed with low zinc and standard diet for 6 weeks, respectively. The mice were mated with female mice fed with standard diet to get the first generation of mice (F1) to explore the effect zinc deficiency on the glucose metabolism of offspring. Glucose tolerance, insulin sensitivity and insulin secretion in mice were determined by oral glucose tolerance test (OGTT), insulin tolerance test (ITT) and glucose stimulated insulin secretion test (GSIS), respectively. Compared with the control group, the fasting blood glucose levels of F1 generation male mice in the low zinc group increased at 15 and 30 min after glucose injection. The blood glucose of F1 generation male mice in the low zinc group of mice decreased at 60, 90, 120, 180, 240 min after insulin injection. Compared with the control group, serum insulin of F1 generation male mice in the low zinc group decreased at 15 min after glucose injection (all p values <0.05). However F1 female mice in the low zinc group did not show abnormal glucose metabolism. Marginal zinc deficiency in male mice can cause abnormal glucose homeostasis in male offspring, but not in female offspring.

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Marginal Zinc Deficiency in Mice Increased the Number of Abnormal Sperm and Altered the Expression Level of Spermatogenesis-Related Genes

Cited by 9 publications

References 56 publications

Marginal Zinc Deficiency Aggravated Intestinal Barrier Dysfunction and Inflammation through ETEC Virulence Factors in a Mouse Model of Diarrhea

Marginal Zinc Deficiency Aggravated Intestinal Barrier Dysfunction and Inflammation through ETEC Virulence Factors in a Mouse Model of Diarrhea

Oyster Peptide-Zinc Complex Ameliorates Di-(2-ethylhexyl) Phthalate-Induced Testis Injury in Male Mice and Improving Gut Microbiota

Effects of Zinc Deficiency in Male Mice on Glucose Metabolism of Male Offspring

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