SynthesisEnvironmental health : a global access science source2025
A systematic review of exposure to endocrine disruptors and energy expenditure in mice.
Synthesis in Environmental health : a global access science source, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
5 authors.
Funding
Abstract
Exposure to endocrine disruptors (EDs) is associated with increased susceptibility to obesity and metabolic dysfunction in epidemiological and preclinical studies. Accumulating evidence supports that various EDs promote energy intake and fat storage, but little is known about how they affect energy expenditure (EE). This systematic review examined the effect of EDs on EE in murine models and on mitochondrial bioenergetics in cell-based studies. We included 12 in vivo studies, which assessed the effect of phytoestrogens, DDT, tolylfluanid, benzene, bisphenol A, bisphenol S, butyl-phthalate, deltamethrin, and the mixtures of 23 chemicals and of organophosphate flame retardants. DDT, tolylfluanid, benzene, and the mixtures of 23 chemicals and of flame retardants decreased; bisphenol A, bisphenol S, and butyl-phthalate had a neutral effect; and phytoestrogens and deltamethrin increased EE. The effects of some EDs were sexually dimorphic, dose-dependent, and interacted with diet. Nine cell-based studies were included and indicated that mitochondrial bioenergetics was impaired by tolylfluanid, bisphenol A, and DDT in muscle cells; by bisphenol AF, BDE-99, DDT, DDE, and the mixture of DDE, trans-nonachlor, and oxychlordane in adipocytes; by bisphenol A in hepatocytes; and by tributyltin in pluripotent cells. Our findings indicate that EDs affect EE in mice in a sexually dimorphic pattern and impair mitochondrial bioenergetics in cellular models which are representative of key tissues involved in energy balance. While further studies are needed to fully elucidate the impact of EDs on energy balance and mitochondrial function, this review underscores the plausibility of mitochondrial dysfunction and altered EE as key pathways linking ED exposure to metabolic diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.