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  1. Article ; Online: Obesogenic polystyrene microplastic exposures disrupt the gut-liver-adipose axis.

    Zhao, Jingjing / Adiele, Ngozi / Gomes, Daniel / Malovichko, Marina / Conklin, Daniel J / Ekuban, Abigail / Luo, Jianzhu / Gripshover, Tyler / Watson, Walter H / Banerjee, Mayukh / Smith, Melissa L / Rouchka, Eric C / Xu, Raobo / Zhang, Xiang / Gondim, Dibson D / Cave, Matthew C / O'Toole, Timothy E

    Toxicological sciences : an official journal of the Society of Toxicology

    2024  Volume 198, Issue 2, Page(s) 210–220

    Abstract: Microplastics (MP) derived from the weathering of polymers, or synthesized in this size range, have become widespread environmental contaminants and have found their way into water supplies and the food chain. Despite this awareness, little is known ... ...

    Abstract Microplastics (MP) derived from the weathering of polymers, or synthesized in this size range, have become widespread environmental contaminants and have found their way into water supplies and the food chain. Despite this awareness, little is known about the health consequences of MP ingestion. We have previously shown that the consumption of polystyrene (PS) beads was associated with intestinal dysbiosis and diabetes and obesity in mice. To further evaluate the systemic metabolic effects of PS on the gut-liver-adipose tissue axis, we supplied C57BL/6J mice with normal water or that containing 2 sizes of PS beads (0.5 and 5 µm) at a concentration of 1 µg/ml. After 13 weeks, we evaluated indices of metabolism and liver function. As observed previously, mice drinking the PS-containing water had a potentiated weight gain and adipose expansion. Here we found that this was associated with an increased abundance of adipose F4/80+ macrophages. These exposures did not cause nonalcoholic fatty liver disease but were associated with decreased liver:body weight ratios and an enrichment in hepatic farnesoid X receptor and liver X receptor signaling. PS also increased hepatic cholesterol and altered both hepatic and cecal bile acids. Mice consuming PS beads and treated with the berry anthocyanin, delphinidin, demonstrated an attenuated weight gain compared with those mice receiving a control intervention and also exhibited a downregulation of cyclic adenosine monophosphate (cAMP) and peroxisome proliferator-activated receptor (PPAR) signaling pathways. This study highlights the obesogenic role of PS in perturbing the gut-liver-adipose axis and altering nuclear receptor signaling and intermediary metabolism. Dietary interventions may limit the adverse metabolic effects of PS consumption.
    MeSH term(s) Animals ; Mice ; Plastics/metabolism ; Plastics/pharmacology ; Polystyrenes/toxicity ; Polystyrenes/metabolism ; Microplastics/metabolism ; Microplastics/pharmacology ; Mice, Inbred C57BL ; Liver ; Non-alcoholic Fatty Liver Disease/metabolism ; Obesity/chemically induced ; Obesity/metabolism ; Weight Gain
    Chemical Substances Plastics ; Polystyrenes ; Microplastics
    Language English
    Publishing date 2024-01-16
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1420885-4
    ISSN 1096-0929 ; 1096-6080
    ISSN (online) 1096-0929
    ISSN 1096-6080
    DOI 10.1093/toxsci/kfae013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Can Zinc Supplementation Attenuate High Fat Diet-Induced Non-Alcoholic Fatty Liver Disease?

    Bolatimi, Oluwanifemi Esther / Head, Kimberly Z / Luo, Jianzhu / Gripshover, Tyler C / Lin, Qian / Adiele, Ngozi V / Watson, Walter H / Wilkerson, Caitlin / Cai, Lu / Cave, Matthew C / Young, Jamie L

    International journal of molecular sciences

    2023  Volume 24, Issue 2

    Abstract: The pathogenesis of non-alcoholic fatty liver disease (NAFLD), the most prevalent chronic liver disease, is associated with zinc deficiency. Previous studies show zinc supplementation improves steatosis and glucose metabolism, but its therapeutic effects ...

    Abstract The pathogenesis of non-alcoholic fatty liver disease (NAFLD), the most prevalent chronic liver disease, is associated with zinc deficiency. Previous studies show zinc supplementation improves steatosis and glucose metabolism, but its therapeutic effects in patients with established NAFLD remain unclear. We developed an in vivo model to characterize the effects of zinc supplementation on high-fat diet (HFD) induced NAFLD and hypothesized that the established NAFLD would be attenuated by zinc supplementation. Male C57BL/6J mice were fed a control diet or HFD for 12 weeks. Mice were then further grouped into normal and zinc-supplemented diets for 8 additional weeks. Body composition and glucose tolerance were determined before and after zinc supplementation. At euthanasia, plasma and liver tissue were collected for characterization and downstream analysis. As expected, 12 weeks of HFD resulted in reduced glucose clearance and altered body composition. Eight weeks of subsequent zinc supplementation did not alter glucose handling, plasma transaminases, steatosis, or hepatic gene expression. Results from our model suggest 8-week zinc supplementation cannot reverse established NAFLD. The HFD may have caused NAFLD disease progression beyond rescue by an 8-week period of zinc supplementation. Future studies will address these limitations and provide insights into zinc as a therapeutic agent for established NAFLD.
    MeSH term(s) Male ; Mice ; Animals ; Non-alcoholic Fatty Liver Disease/drug therapy ; Non-alcoholic Fatty Liver Disease/etiology ; Non-alcoholic Fatty Liver Disease/metabolism ; Diet, High-Fat/adverse effects ; Zinc/metabolism ; Mice, Inbred C57BL ; Liver/metabolism ; Dietary Supplements ; Glucose/metabolism ; Disease Models, Animal
    Chemical Substances Zinc (J41CSQ7QDS) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2023-01-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24021763
    Database MEDical Literature Analysis and Retrieval System OnLINE

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