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Article ; Online: Sex-specific effects of acute chlordane exposure in the context of steatotic liver disease, energy metabolism and endocrine disruption.

Luo, Jianzhu / Watson, Walter H / Gripshover, Tyler C / Qaissi, Zayna / Wahlang, Banrida

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

2023 Volume 180, Page(s) 114024

Abstract: Chlordane is an organochlorine pesticide (OCP) that is environmentally persistent. Although exposures to OCPs including chlordane have been associated with elevated liver enzymes, current knowledge on OCPs' contribution to toxicant-associated steatotic ... ...

Abstract	Chlordane is an organochlorine pesticide (OCP) that is environmentally persistent. Although exposures to OCPs including chlordane have been associated with elevated liver enzymes, current knowledge on OCPs' contribution to toxicant-associated steatotic liver disease (TASLD) and underlying sex-specific metabolic/endocrine disruption are still widely limited. Therefore, the objective of this study was to investigate the sex-dependent effects of chlordane in the context of TASLD. Age-matched male and female C57BL/6 mice were exposed to chlordane (20 mg/kg, one-time oral gavage) for two weeks. Female mice generally exhibited lower bodyfat content but more steatosis and hepatic lipid levels, consistent with increased hepatic mRNA levels of genes involved in lipid synthesis and uptake. Surprisingly, chlordane-exposed females demonstrated lower hepatic cholesterol levels. With regards to metabolic disruption, chlordane exposure decreased expression of genes involved in glycogen and glucose metabolism (Pklr, Gck), while chlordane-exposed females also exhibited decreased gene expression of HNF4A, an important regulator of liver identity and function. In terms of endocrine endpoints, chlordane augmented plasma testosterone levels in males. Furthermore, chlordane activated hepatic xenobiotic receptors, including the constitutive androstane receptor, in a sex-dependent manner. Overall, chlordane exposure led to altered hepatic energy metabolism, and potential chlordane-sex interactions regulated metabolic/endocrine disruption and receptor activation outcomes.
MeSH term(s)	Male ; Female ; Mice ; Animals ; Chlordan/toxicity ; Chlordan/metabolism ; Mice, Inbred C57BL ; Hydrocarbons, Chlorinated ; Fatty Liver/chemically induced ; Fatty Liver/metabolism ; Liver ; Hazardous Substances ; Lipids ; Energy Metabolism
Chemical Substances	Chlordan (12789-03-6) ; Hydrocarbons, Chlorinated ; Hazardous Substances ; Lipids
Language	English
Publishing date	2023-09-04
Publishing country	England
Document type	Journal Article
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2023.114024
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Article ; Online: Prognostic value and potential molecular mechanism of ITGB superfamily members in hepatocellular carcinoma.

Xie, Haixiang / Qin, Chongjiu / Zhou, Xin / Liu, Junqi / Yang, Kejian / Nong, Jusen / Luo, Jianzhu / Peng, Tao

Medicine

2023 Volume 102, Issue 33, Page(s) e34765

Abstract: We analyzed the prognostic value and potential molecular mechanisms of the members of integrin β (ITGB)superfamily in hepatocellular carcinoma (HCC) using data from The Cancer Genome Atlas (TCGA), cBioPortal, Gene Expression Profiling Interactive ... ...

Abstract	We analyzed the prognostic value and potential molecular mechanisms of the members of integrin β (ITGB)superfamily in hepatocellular carcinoma (HCC) using data from The Cancer Genome Atlas (TCGA), cBioPortal, Gene Expression Profiling Interactive Analysis (GEPIA), Human Protein Atlas (HPA) HPA, Search Tool for the Retrieval of Interacting Genes/Proteins, GeneMANIA, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), TIMER and Gene set enrichment analysis (GSEA) databases. ITGB4/5 mRNA was upregulated in HCC tissues in contrast to the normal liver tissues, whereas ITGB2/3/8 levels were lower in the former. ITGB4 was the most frequently mutated ITGB gene in HCC. Receiver operating characteristic curve (ROC) analysis showed that the expression levels of ITGB2/3/4/5/7/8 had significant diagnostic value in distinguishing HCC tissues from healthy liver tissues, ITGB8 had the highest diagnostic efficacy. The ITGB1/3/6/8 were also upregulated in the HCC tissues in contrast to healthy liver tissues. The expression of ITGB8 was verified by immunohistochemistry (IHC). Furthermore, ITGB6 and ITGB7 expression levels were strongly associated with the overall survival (OS) of HCC patients. The ITGB superfamily members exhibited homology and interactions in protein structure. In addition, ITGB6 together with ITGB7 were negatively related to the infiltration of multiple immune cell populations. GSEA results showed that ITGB6 was enriched in HCC migration and recurrence, whereas ITGB7 was significantly enriched in HIPPO, TOLL and JAK-STAT signaling pathways. In conclusion, ITGB6 and ITGB7 genes are possible to be prognostic biomarkers for HCC.
MeSH term(s)	Humans ; Integrins ; Carcinoma, Hepatocellular/genetics ; Prognosis ; Liver Neoplasms/genetics
Chemical Substances	Integrins
Language	English
Publishing date	2023-08-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	80184-7
ISSN	1536-5964 ; 0025-7974
ISSN (online)	1536-5964
ISSN	0025-7974
DOI	10.1097/MD.0000000000034765
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Article: Investigating the Acute Metabolic Effects of the N-Methyl Carbamate Insecticide, Methomyl, on Mouse Liver.

Groswald, Amy M / Gripshover, Tyler C / Watson, Walter H / Wahlang, Banrida / Luo, Jianzhu / Jophlin, Loretta L / Cave, Matthew C

Metabolites

2023 Volume 13, Issue 8

Abstract: Many pesticides have been identified as endocrine and metabolism-disrupting chemicals with hepatotoxic effects. However, data are limited for insecticides in the n-methyl carbamate class, including methomyl. Here, we investigate the liver and systemic ... ...

Abstract	Many pesticides have been identified as endocrine and metabolism-disrupting chemicals with hepatotoxic effects. However, data are limited for insecticides in the n-methyl carbamate class, including methomyl. Here, we investigate the liver and systemic metabolic effects of methomyl in a mouse model. We hypothesize that methomyl exposure will disrupt xenobiotic and intermediary metabolism and promote hepatic steatosis in mice. Male C57BL/6 mice were exposed daily to 0-5 mg/kg methomyl for 18 days. Mice were fed water and regular chow diet ad libitum. Metabolic phenotyping was performed, and tissue samples were collected. Effects were generally greatest at the highest methomyl dose, which induced
Language	English
Publishing date	2023-08-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662251-8
ISSN	2218-1989
ISSN	2218-1989
DOI	10.3390/metabo13080901
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Article: Sarcosine dehydrogenase as an immune infiltration-associated biomarker for the prognosis of hepatocellular carcinoma.

Xie, Haixiang / Yang, Kejian / Qin, Chongjiu / Zhou, Xin / Liu, Junqi / Nong, Jusen / Luo, Jianzhu / Wei, Yongguang / Hua, Huasheng / Han, Chuangye / Liao, Xiwen / Yang, Chengkun / Su, Hao / Zhu, Guangzhi / Ye, Xinping / Peng, Tao

Journal of Cancer

2024 Volume 15, Issue 1, Page(s) 149–165

Abstract: This study was aimed to investigate the prognostic value and clinical significance of sarcosine dehydrogenase (SARDH) in hepatocellular carcinoma (HCC) and to explore the underlying mechanisms. The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO) ...

Abstract	This study was aimed to investigate the prognostic value and clinical significance of sarcosine dehydrogenase (SARDH) in hepatocellular carcinoma (HCC) and to explore the underlying mechanisms. The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), HPA and CPTAC databases were adopted to analyze the expression of SARDH mRNA and protein between normal liver tissue and HCC, and examine their relationship with clinicopathological features. Kaplan-Meier analysis, Cox regression, as well as nomogram were adopted to explore the prognostic value of SARDH in HCC. Gene Ontology (GO), Kyoto Gene and Genome Encyclopedia (KEGG) together with Gene Set Enrichment Analysis (GSEA) were adopted to analyze the molecular mechanisms and biological functions of SARDH in HCC; while MethSurv, STRING, GeneMANIA, TIMER database data and single-sample gene set enrichment analysis (ssGSEA) algorithm were used for other bioinformatic analysis. Furthermore, immunohistochemistry was used to verify the expression of SARDH. Compared to normal liver tissue, SARDH expression was markedly lower in HCC. A lower SARDH expression was linked with Pathologic T stage (T3&T4), pathologic stage (Stage III&IV), and histologic grade (G3&4), which further indicates worse prognosis. Besides, results of bioinformatic analysis proved that SARDH expression was correlated with immune infiltration. In addition, SARDH hypermethylation was related to a poorer prognosis. SARDH expression was related to several key genes in the Ferroptosis pathway.
Language	English
Publishing date	2024-01-01
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.89616
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Article: MCM2 promotes the stemness and sorafenib resistance of hepatocellular carcinoma cells via hippo signaling.

Zhou, Xin / Luo, Jianzhu / Xie, Haixiang / Wei, Zhongliu / Li, Tianman / Liu, Junqi / Liao, Xiwen / Zhu, Guangzhi / Peng, Tao

Cell death discovery

2022 Volume 8, Issue 1, Page(s) 418

Abstract: Object: A large number of studies have suggested that stemness is an essential mechanism for drug resistance, metastasis and relapse in hepatocellular carcinoma (HCC). The aim of this study was to determine the impact of MCM2 on stemness and identify ... ...

Abstract	Object: A large number of studies have suggested that stemness is an essential mechanism for drug resistance, metastasis and relapse in hepatocellular carcinoma (HCC). The aim of this study was to determine the impact of MCM2 on stemness and identify potential mechanisms that complement the stemness regulatory network in HCC. Methods: MCM2 expression features and prognostic significance were analyzed in multiple cohorts, including TCGA LIHC dataset, GSE14520 dataset, Guangxi cohort, and GSE76427 dataset. Stemness-related molecules and phenotypes were examined to evaluate the impact of MCM2 on stemness. The expression levels of key molecules of the hippo signaling pathway together with downstream target genes were examined to evaluate the effect of MCM2 on hippo signaling. This was further demonstrated by rescue experiments with hippo signaling pathway inhibitors (super-TDU). Sorafenib-resistant cells were constructed to assess the effect of MCM2 on drug resistance. A xenotransplantation model of nude mice was constructed to validate the role of MCM2 in vivo. Results: MCM2, which is expressed at higher levels in HCC tissue than in normal liver tissues, is a good indicator for distinguishing tumor tissues from normal liver tissues and can help differentiate HCC patients at different BCLC stages. The annotation of the differentially expressed genes in the MCM2 high and low expression groups indicated that MCM2 may be associated with the hippo signaling pathway. In addition, the expression of MCM2 in HCC tissues was correlated with the expression of YAP1/TAZ, which are key molecules of the hippo signaling pathway. It indicated that manipulation of MCM2 expression affects hippo signaling and stemness, while the inhibition of hippo signaling significantly reversed the effect of MCM2 on stemness. Disruption of MCM2 expression significantly elevated the sensitivity of sorafenib-resistant cells to sorafenib, as evidenced by the decrease in IC50 and diminished sphere-forming capacity. The in vivo assays showed that MCM2 effectively enhanced the efficacy of sorafenib. Conclusion: MCM2 is a good prognostic marker. MCM2 enhances the stemness of HCC cells by affecting the Hippo signaling pathway, while the downregulation of MCM2 inhibits resistance towards sorafenib.
Language	English
Publishing date	2022-10-15
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-022-01201-3
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Article ; Online: The environmental pollutant, polychlorinated biphenyl 126, alters liver function in a rodent model of alcohol-associated liver disease.

Gripshover, Tyler C / Wahlang, Banrida / Head, Kimberly Z / Young, Jamie L / Luo, Jianzhu / Mustafa, Muhammad T / Kirpich, Irina A / Cave, Matthew C

Alcohol, clinical & experimental research

2022 Volume 47, Issue 1, Page(s) 60–75

Abstract: Background: The prevalence of alcohol-associated liver disease (ALD), a subtype of fatty liver disease (FLD), continues to rise. ALD is a major cause of preventable death. Polychlorinated biphenyl (PCB) 126 is an environmentally relevant, dioxin-like ... ...

Abstract	Background: The prevalence of alcohol-associated liver disease (ALD), a subtype of fatty liver disease (FLD), continues to rise. ALD is a major cause of preventable death. Polychlorinated biphenyl (PCB) 126 is an environmentally relevant, dioxin-like pollutant whose negative metabolic effects have been well documented. In human and animal studies, PCB has been associated with the severity of nonalcoholic fatty liver disease (NAFLD). However, few studies have investigated whether exposures to environmental toxicants can worsen ALD. Thus, the objective of the current study was to develop an alcohol-plus-toxicant model to study how an environmental pollutant, PCB 126, impacts rodent ALD pathology. Methods: Briefly, male C57BL/6J mice were exposed to 0.2 mg/kg PCB 126 or corn oil vehicle four days prior to ethanol feeding using the chronic-binge (10-plus-one) model. Results: Concentrations of macromolecules, including hepatic lipids, carbohydrates, and protein (albumin) were impacted. Exposure to PCB 126 exacerbated hepatic steatosis and hepatomegaly in mice exposed to the chemical and fed an ethanol diet. Gene expression and the analysis of blood chemistry showed a potential net increase and retention of hepatic lipids and reductions in lipid oxidation and clearance capabilities. Depletion of glycogen and glucose was evident, which contributes to disease progression by generating systemic malnutrition. Granulocytic immune infiltrates were present but driven solely by ethanol feeding. Hepatic albumin gene expression and plasma levels were decreased by ~50% indicating a potential compromise of liver function. Finally, gene expression analyses indicated that the aryl hydrocarbon receptor and constitutive androstane receptor were activated by PCB 126 and ethanol, respectively. Conclusions: Various environmental toxicants are known to modify or enhance FLD in high-fat diet models. Findings from the present study suggest that they interact with other lifestyle factors such as alcohol consumption to reprogram intermediary metabolism resulting in exacerbated ethanol-associated systemic malnutrition in ALD.
MeSH term(s)	Humans ; Male ; Mice ; Animals ; Polychlorinated Biphenyls/metabolism ; Polychlorinated Biphenyls/pharmacology ; Environmental Pollutants/metabolism ; Environmental Pollutants/pharmacology ; Rodentia ; Mice, Inbred C57BL ; Liver/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Liver Diseases, Alcoholic/metabolism ; Diet, High-Fat ; Ethanol/pharmacology ; Lipids/pharmacology ; Malnutrition/metabolism ; Malnutrition/pathology
Chemical Substances	3,4,5,3',4'-pentachlorobiphenyl (TSH69IA9XF) ; Polychlorinated Biphenyls (DFC2HB4I0K) ; Environmental Pollutants ; Ethanol (3K9958V90M) ; Lipids
Language	English
Publishing date	2022-12-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2993-7175
ISSN (online)	2993-7175
DOI	10.1111/acer.14976
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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
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Article ; Online: Multiomics Analysis of PCB126's Effect on a Mouse Chronic-Binge Alcohol Feeding Model.

Gripshover, Tyler C / Wahlang, Banrida / Head, Kimberly Z / Luo, Jianzhu / Bolatimi, Oluwanifemi E / Smith, Melissa L / Rouchka, Eric C / Chariker, Julia H / Xu, Jason / Cai, Lu / Cummins, Timothy D / Merchant, Michael L / Zheng, Hao / Kong, Maiying / Cave, Matthew C

Environmental health perspectives

2024 Volume 132, Issue 4, Page(s) 47007

Abstract: Background: Environmental pollutants, including polychlorinated biphenyls (PCBs) have been implicated in the pathogenesis of liver disease. Our group recently demonstrated that PCB126 promoted steatosis, hepatomegaly, and modulated intermediary ... ...

Abstract	Background: Environmental pollutants, including polychlorinated biphenyls (PCBs) have been implicated in the pathogenesis of liver disease. Our group recently demonstrated that PCB126 promoted steatosis, hepatomegaly, and modulated intermediary metabolism in a rodent model of alcohol-associated liver disease (ALD). Objective: To better understand how PCB126 promoted ALD in our previous model, the current study adopts multiple omics approaches to elucidate potential mechanistic hypotheses. Methods: Briefly, male C57BL/6J mice were exposed to Results: Principal component analysis showed that PCB126 uniquely modified the transcriptome in EtOH-fed mice. EtOH feeding alone resulted in Discussion: Previous work has demonstrated that PCB126 is a modifying factor in metabolic dysfunction-associated steatotic liver disease (MASLD), and our current work suggests that pollutants also modify ALD. PCB126 may, in part, be contributing to the malnutrition aspect of ALD, where metal deficiency is known to contribute and worsen prognosis. https://doi.org/10.1289/EHP14132.
MeSH term(s)	Male ; Mice ; Animals ; Multiomics ; Mice, Inbred C57BL ; Ethanol/toxicity ; Ethanol/metabolism ; Liver/metabolism ; Polychlorinated Biphenyls/toxicity ; Polychlorinated Biphenyls/metabolism ; Fatty Liver ; Liver Diseases, Alcoholic/etiology ; Liver Diseases, Alcoholic/metabolism ; Liver Diseases, Alcoholic/pathology ; Environmental Pollutants/toxicity ; Environmental Pollutants/metabolism ; Zinc/metabolism ; Tyrosine/metabolism
Chemical Substances	3,4,5,3',4'-pentachlorobiphenyl (TSH69IA9XF) ; Ethanol (3K9958V90M) ; Polychlorinated Biphenyls (DFC2HB4I0K) ; Environmental Pollutants ; Zinc (J41CSQ7QDS) ; Tyrosine (42HK56048U)
Language	English
Publishing date	2024-04-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	195189-0
ISSN	1552-9924 ; 0091-6765 ; 1078-0475
ISSN (online)	1552-9924
ISSN	0091-6765 ; 1078-0475
DOI	10.1289/EHP14132
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Article ; Online: SART3, regulated by p53, is a biomarker for diagnosis, prognosis and immune infiltration in hepatocellular carcinoma.

Nong, Jusen / Yang, Kejian / Li, Tianman / Lan, Chenlu / Zhou, Xin / Liu, Junqi / Xie, Haixiang / Luo, Jianzhu / Liao, Xiwen / Zhu, Guangzhi / Peng, Tao

Aging

2023 Volume 15, Issue 16, Page(s) 8408–8432

Abstract: Objective: This study aimed to investigate the role of squamous cell carcinoma antigen recognized by T cells 3 (SART3) in hepatocellular carcinoma (HCC).: Methods: SART3 expression and prognostic value were analyzed in TCGA and GEO datasets. The ... ...

Abstract	Objective: This study aimed to investigate the role of squamous cell carcinoma antigen recognized by T cells 3 (SART3) in hepatocellular carcinoma (HCC). Methods: SART3 expression and prognostic value were analyzed in TCGA and GEO datasets. The diagnostic value and prognostic significance of SART3 were determined using immunohistochemistry in the Guangxi cohort. The whole-exome mutation spectrum of SART3 was analyzed in high and low expression groups in both TCGA and Guangxi cohorts. The biological functions of the SART3 gene were validated through Results: SART3 expression was significantly higher in HCC tissues than in adjacent noncancerous liver tissues in TCGA, GEO and Guangxi cohorts. High expression of SART3 was significantly associated with poor prognosis in HCC patients. In TCGA and Guangxi cohorts, the expression of SART3 in the TP53 mutation group was significantly higher than that in the non-mutation group. Downregulation of SART3 expression significantly inhibited the migration and proliferation of HCC cells. SART3 may be involved mainly in immune infiltration of Th2 cells and macrophages in HCC. Additionally, SART3 can upregulate the expression of immune checkpoints (PD-L1 and TIM-3) and predict potential therapeutic agents for HCC. Conclusion: The findings of this study demonstrate the diagnostic and prognostic value of SART3 in HCC. SART3 may be associated with immune infiltration of Th2 cells and macrophages in HCC, highlighting its potential role in the development and progression of HCC.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular ; Tumor Suppressor Protein p53 ; Liver Neoplasms ; China ; Prognosis ; Biomarkers ; Antigens, Neoplasm ; RNA-Binding Proteins
Chemical Substances	Tumor Suppressor Protein p53 ; Biomarkers ; SART3 protein, human ; Antigens, Neoplasm ; RNA-Binding Proteins
Language	English
Publishing date	2023-08-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.204978
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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
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