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Environmental Cadmium Exposure Exacerbated Bone Loss in NAFLD Mice

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Date 2023 Dec 15
PMID 38100013
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Abstract

Due to rapid urbanization and industrialization, Cadmium (Cd) contamination is widespread. Meanwhile, the prevalence of nonalcoholic fatty liver disease (NAFLD) has been increasing. Cd is linked to bone damage. However, the osteotoxicity of environmental Cd exposure in NAFLD remains unclear. Therefore, this study aimed to investigate the effects and potential mechanisms of Cd on bone metabolism in NAFLD mice. NAFLD mice were treated with 50 mg/L cadmium chloride in drinking water for 12 weeks. Bone microstructures were scanned by Micro-CT. Liver lipid droplets and fibrosis were measured by histopathological staining. Insulin tolerance tests were performed in mice. RT-PCR and Western blot were performed to analyse hepatic inflammation factors. Results show no damage in healthy mice exposed to Cd. However, Cd exacerbated liver fibrosis and significantly reduced cancellous bone mineral density and decreased the number and thickness of trabecular bone in NAFLD mice. Additionally, the morphology of trabecular bone transformed from a plate structure to a rod structure in NAFLD mice after Cd exposure. The underlying mechanism appears to be related to the Cd-induced direct or indirect toxicity. Exacerbated liver fibrosis, increased inflammatory factors (TGF-β and IL-1β), and reduced lecithin-cholesterol acyltransferase (LCAT) and insulin-like growth factor-1 (IGF-1) might contribute to bone damages. Collectively, our study illustrates that despite lower dosing Cd exposure did not induce bone damages in healthy mice, Cd caused bone loss in NAFLD mice. Therefore, it is recommended that individuals with metabolic disorders should avoid working in Cd pollution environment and consuming cadmium-contaminated food and water.

References
1.
He X, Gao J, Hou H, Qi Z, Chen H, Zhang X . Inhibition of Mitochondrial Fatty Acid Oxidation Contributes to Development of Nonalcoholic Fatty Liver Disease Induced by Environmental Cadmium Exposure. Environ Sci Technol. 2019; 53(23):13992-14000. DOI: 10.1021/acs.est.9b05131. View

2.
Choudhury H, Harvey T, Thayer W, Lockwood T, Stiteler W, Goodrum P . Urinary cadmium elimination as a biomarker of exposure for evaluating a cadmium dietary exposure--biokinetics model. J Toxicol Environ Health A. 2001; 63(5):321-50. DOI: 10.1080/15287390152103643. View

3.
Horiguchi H, Aoshima K, Oguma E, Sasaki S, Miyamoto K, Hosoi Y . Latest status of cadmium accumulation and its effects on kidneys, bone, and erythropoiesis in inhabitants of the formerly cadmium-polluted Jinzu River Basin in Toyama, Japan, after restoration of rice paddies. Int Arch Occup Environ Health. 2010; 83(8):953-70. DOI: 10.1007/s00420-010-0510-x. View

4.
Osada M, Izuno T, Kobayashi M, Sugita M . Relationship between environmental exposure to cadmium and bone metabolism in a non-polluted area of Japan. Environ Health Prev Med. 2011; 16(6):341-9. PMC: 3206976. DOI: 10.1007/s12199-010-0204-8. View

5.
Brzoska M, Majewska K, Kupraszewicz E . Effects of low, moderate and relatively high chronic exposure to cadmium on long bones susceptibility to fractures in male rats. Environ Toxicol Pharmacol. 2011; 29(3):235-45. DOI: 10.1016/j.etap.2010.01.005. View