ArticleMetabolic brain disease2019
High fat diet deteriorates the memory impairment induced by arsenic in mice: a sub chronic in vivo study.
Article in Metabolic brain disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Understanding the contribution of toxicant exposures to Alzheimer's disease and related dementias.Current opinion in neurobiology · 2026Review
- Neuroprotection by Nauclea latifolia extract in arsenite & high-fat diet-induced brain stress.Environmental analysis, health and toxicology · 2025Article
- A long-term mild high-fat diet facilitates rabbit discrimination learning and alters glycerophospholipid metabolism.Neurobiology of learning and memory · 2025Article
- A high-fat diet exacerbates arsenic toxicity in various organs. A systematic review of toxicity and mechanism.Current research in toxicology · 2025Review
- Article
- Review
- Combination effects of a fatty diet and exercise on the depressive state and cardioprotection in apolipoprotein E knockout mice with a change inThe Journal of international medical research · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both arsenic (As) and obesity are associated with brain disorders. However, long term studies to evaluate their concomitant adverse effects on the brain functions are lacking. Present study was conducted to evaluate the long term co-exposure of As and high fat diet (HFD) on memory and brain mitochondrial function in mice. Male mice were randomly divided into 7 groups fed with HFD or ordinary diet (OD) and instantaneously exposed to As (25 or 50 ppm) in drinking water for, 4, 8, 12, 16 or 20 weeks. Step-down passive avoidance method was used for memory assessment and post exposure various parameters including mitochondrial damage, level of reactive oxygen species (ROS), malondialdeid (MDA) and glutathione (GSH) were determined. Results indicated that the retention latency decreased in As (25 and 50 ppm) and HFD received mice after 12 and 16 weeks respectively. Same results were observed at significantly shorter duration (8th week) when As was administered along with HFD as compared to control group. In the HFD alone fed mice increased the mitochondrial membrane damage, levels of ROS and MDA were observed while GSH contents decreased significantly. Concomitant administration of HFD and As amplified those mentioned toxic effects (p < 0.001). In conclusion, our findings demonstrated that the simultaneous HFD and As impaired memory at least three times more than exposing each one alone. These toxic effects could be due to the mitochondria originated oxidative stress along with the depleted antioxidant capacity of the brain of mice.
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