Methylmercury displays pro-adipogenic properties in rainbow trout preadipocytes

Tinant, Gilles; Neefs, Ineke; Das, Krishna; Rees, Jean-François; Larondelle, Yvan; Debier, Cathy

doi:10.1016/j.chemosphere.2020.127917

Cited by 7 publications

(3 citation statements)

References 76 publications

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“…We are unaware of other studies of the effects of mercury on PPAR -γ (or other PPARs) in birds, but effects in other taxa have been inconsistent. For example, mercury increased PPAR -γ expression in nematodes 26 , rat adipocytes 65 , and fish brain cells 66 , while it decreased it in mouse fibroblasts and adipocytes 23 , 67 , and had no effect in fish preadipocytes 53 . Interestingly, Corder et al 68 found liver expression of PPAR -γ and target genes for FAT/CD36, FABPpm, and cytosolic FABP in migratory gray catbirds ( Dumetella carolinensis ) to remain similar across the annual cycle, indicating increased expression of PPAR -γ and fatty acid transporters may not be needed for the liver to meet the metabolic demands of migration.…”

Section: Discussionmentioning

confidence: 99%

“…We are unaware of any prior studies of the effects of mercury on fatty acid transporters in birds, but fatty acid transporters in other taxa have shown mixed responses. For example, exposure of fish to MeHg increased expression of cytosolic FABP in preadipocytes 53 and muscles 54 , while it decreased FABPpm expression in preadipocytes 53 , hepatocytes 55 , and kidney cells 45 . FAT/CD36 expression was reduced in adipocytes of mice exposed to mercury chloride 23 .…”

Section: Discussionmentioning

confidence: 99%

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Short-term mercury exposure disrupts muscular and hepatic lipid metabolism in a migrant songbird

Seewagen¹,

Elowe

Gerson

et al. 2022

Sci Rep

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Methylmercury (MeHg) is a global pollutant that can cause metabolic disruptions in animals and thereby potentially compromise the energetic capacity of birds for long-distance migration, but its effects on avian lipid metabolism pathways that support endurance flight and stopover refueling have never been studied. We tested the effects of short-term (14-d), environmentally relevant (0.5 ppm) dietary MeHg exposure on lipid metabolism markers in the pectoralis and livers of yellow-rumped warblers (Setophaga coronata) that were found in a previous study to have poorer flight endurance in a wind tunnel than untreated conspecifics. Compared to controls, MeHg-exposed birds displayed lower muscle aerobic and fatty acid oxidation capacity, but similar muscle glycolytic capacity, fatty acid transporter expression, and PPAR expression. Livers of exposed birds indicated elevated energy costs, lower fatty acid uptake capacity, and lower PPAR-γ expression. The lower muscle oxidative enzyme capacity of exposed birds likely contributed to their weaker endurance in the prior study, while the metabolic changes observed in the liver have potential to inhibit lipogenesis and stopover refueling. Our findings provide concerning evidence that fatty acid catabolism, synthesis, and storage pathways in birds can be dysregulated by only brief exposure to MeHg, with potentially significant consequences for migratory performance.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Short-term mercury exposure disrupts muscular and hepatic lipid metabolism in a migrant songbird

Seewagen¹,

Elowe

Gerson

et al. 2022

Sci Rep

View full text Add to dashboard Cite

show abstract

“…The effects of MeHg on driving adipocyte differentiation seems to be conserved across species. In primary pre-adipocytes from rainbow trout ( Oncorhynchus mykiss ) exposed to MeHg for 6 days, there was an accumulation of neutral lipids as well as the upregulation of genes that are markers of mature adipocytes, including perilipin 2, apolipoprotein Eb, fatty acid synthase, and fatty acid binding protein [ 237 ].…”

Section: Introductionmentioning

confidence: 99%

Association between Heavy Metals, Metalloids and Metabolic Syndrome: New Insights and Approaches

Martins

Ferrer

Tinkov

et al. 2023

Toxics

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Metabolic syndrome (MetS) is an important public health issue that affects millions of people around the world and is growing to pandemic-like proportions. This syndrome is defined by the World Health Organization (WHO) as a pathologic condition characterized by abdominal obesity, insulin resistance, hypertension, and hyperlipidemia. Moreover, the etiology of MetS is multifactorial, involving many environmental factors, including toxicant exposures. Several studies have associated MetS with heavy metals exposure, which is the focus of this review. Environmental and/or occupational exposure to heavy metals are a major risk, contributing to the development of chronic diseases. Of particular note, toxic metals such as mercury, lead, and cadmium may contribute to the development of MetS by altering oxidative stress, IL-6 signaling, apoptosis, altered lipoprotein metabolism, fluid shear stress and atherosclerosis, and other mechanisms. In this review, we discuss the known and potential roles of heavy metals in MetS etiology as well as potential targeted pathways that are associated with MetS. Furthermore, we describe how new approaches involving proteomic and transcriptome analysis, as well as bioinformatic tools, may help bring about an understanding of the involvement of heavy metals and metalloids in MetS.

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Heavy metal-induced lipogenic gene aberration, lipid dysregulation and obesogenic effect: a review

et al. 2022

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Methylmercury displays pro-adipogenic properties in rainbow trout preadipocytes

Cited by 7 publications

References 76 publications

Short-term mercury exposure disrupts muscular and hepatic lipid metabolism in a migrant songbird

Short-term mercury exposure disrupts muscular and hepatic lipid metabolism in a migrant songbird

Association between Heavy Metals, Metalloids and Metabolic Syndrome: New Insights and Approaches

Heavy metal-induced lipogenic gene aberration, lipid dysregulation and obesogenic effect: a review

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