Publication: METHYLMERCURY ALTERATION IN THERMOGENESIS IS DIET DEPENDENT IN CAENORHABDITIS ELEGANS
| dc.contributor.author | Varney, Abigail | |
| dc.contributor.author | Radzimirski, Anthony | |
| dc.contributor.author | Caito, Samuel | |
| dc.date.accessioned | 2024-07-23T12:36:41Z | |
| dc.date.issued | 2024-04-18 | |
| dc.description.abstract | Thermogenesis is the process by which adipocytes metabolize triglycerides (TAG) to release energy as heat. This process is disrupted in metabolic syndrome, leading to increased TAG levels and weight gain. Methylmercury (MeHg) is an environmental toxin that has both neurotoxic and metabolic effects. We have previously shown that MeHg disrupts lipid homeostasis, leading to increased TAG content and storage sites in Caenorhabditis elegans. Furthermore, we have shown that TAG content in response to MeHg is dependent on their Escherichia coli diet. Worms fed a low lipid containing strain (HT115) showed less lipid dysregulation than worms fed a high lipid containing strain (OP50). As we have seen accumulation of TAG in response to MeHg, we hypothesized that MeHg could reduce thermogenesis in C. elegans. Worms were treated with environmentally relevant doses of MeHg, fed either OP50 or HT115, and were grown to adulthood at 15 or 25˚C. Worms were then placed at 4˚C for 48 hours and scored for survival. Untreated worms maintained at 15˚C and fed either diet were able to survive the temperature shift. MeHg significantly decreased survival of worms fed OP50 diet following the 15 to 4˚C shift, suggesting that thermoregulation was inhibited by MeHg. In contrast, MeHg had minimal effects on the survival of worms fed HT115 diet following the 15 to 4˚C shift. Shifting worms from 25 to 4˚C is lethal to all worms fed OP50. However, the HT115 diet prevented lethality in untreated or MeHg treated worms shifted from 25 to 4˚C. These data suggest that the HT115 diet is protective and can induce thermogenesis. Heat generation derives from mitochondria. HT115 fed worms had improved mitochondrial health in response to MeHg than OP50 fed worms. Taken together, our data suggests that MeHg-dependent mitochondrial damage is diet dependent leading to alterations in thermogenesis. | |
| dc.identifier.uri | https://dspace.husson.edu/handle/20.500.14298/131 | |
| dc.language.iso | en_US | |
| dc.title | METHYLMERCURY ALTERATION IN THERMOGENESIS IS DIET DEPENDENT IN CAENORHABDITIS ELEGANS | |
| dc.type | Abstract | |
| dspace.entity.type | Publication | |
| relation.isAuthorOfPublication | 98ab36f9-976c-4de4-902f-f2bc3ed2e33f | |
| relation.isAuthorOfPublication.latestForDiscovery | 98ab36f9-976c-4de4-902f-f2bc3ed2e33f |