4.7 Article

Methylmercury drives lipid droplet formation and adipokine expression during the late stages of adipocyte differentiation in 3T3-L1 cells

Journal

TOXICOLOGY
Volume 486, Issue -, Pages -

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.tox.2023.153446

Keywords

Methylmercury; Autophagy; Adipocytes; Differentiation

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Chronic exposure to methylmercury is associated with obesity and metabolic syndromes. This study investigated the effects of continuous exposure to 0.5μM methylmercury on adipocyte differentiation in 3T3-L1 cells. The results showed that methylmercury enhanced triglyceride content and the expression of adipocyte differentiation markers, particularly during the later stages of differentiation.
Chronic exposure to methylmercury (MeHg) is positively associated with obesity and metabolic syndromes. However, the effect of MeHg on adipogenesis has not been thoroughly investigated. This study investigated the effects of continuous exposure to 0.5 mu M MeHg on adipocyte differentiation in 3T3-L1 cells. Oil Red O staining and triglycerides (TG) assays demonstrated that MeHg enhanced the TG content in 3T3-L1 cells. MeHg enhanced the mRNA and protein expression of adipocyte differentiation markers including peroxisome proliferator-activated receptor gamma, adiponectin, and fatty acid-binding protein, and their expression levels were prominent during the late stages (days 6-8) after the induction of differentiation. In addition, 0.5 mu M MeHg promoted the expression of autophagy-related genes, including light chain 3 B-II and p62, after induction of differentiation. Treatment of 3T3-L1 cells with chloroquine (CQ), an autophagy inhibitor, during the early stages (days 0-2) after induction of differentiation inhibited cellular lipid accumulation in the presence of 0.5 mu M MeHg. However, treatment with CQ during the late stages (days 6-8) had little effect on the MeHg-induced increase in TG content and the expression of adipocyte differentiation markers. Although the underlying mechanisms in the late stages remain to be completely elucidated, but the present data suggest that autophagy and other mechanisms play critical roles in adipogenesis during MeHg-induced differentiation. Collectively, our results suggest that continuous exposure to MeHg induces TG accumulation and expression of genes related to adipogenesis, espe-cially during the late stages of 3T3-L1 differentiation, which may contribute to an improved understanding of MeHg-induced adipogenesis.

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