A high fat, sugar, and salt Western diet induces motor‐muscular and sensory dysfunctions and neurodegeneration in mice during aging: Ameliorative action of metformin

Hong, Song; Nagayach, Aarti; Lü, Yan; Peng, Hongying; Duong, Quoc-Viet; Pham, Nicholas B.; Vuong, Christopher A.; Bazán, Nicolás G.

doi:10.1111/cns.13726

Cited by 8 publications

(2 citation statements)

References 115 publications

(314 reference statements)

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“…Neurodegeneration and myelin protein alterations were concomitantly observed, all indicative of a pathological state. Similar findings on peripheral sensory-motor dysfunctions and neurodegeneration in the context of reactive pro-inflammatory microglia have been reported in brain areas in a model of aging mice subjected to a western diet high-fat, high-sugar, and high-salt (30). Similarly, elderly rats subjected to a high-fat, high-sugar diet evidenced impaired spatial learning and working memory and increased anxiety-like behavior, associated with decreased neurogenesis and increased neuroinflammation fostered by astrogliosis (31).…”

Section: Discussionsupporting

confidence: 82%

High-fat and high-carbohydrate diets worsen the mouse brain susceptibility to damage produced by enterohemorrhagicEscherichia coliShiga toxin 2

Arenas-Mosquera,

Cerny,

Cangelosi

et al. 2024

Preprint

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BackgroundNutrition quality could be one of the reasons why, in the face of a Shiga toxin-producing enterohaemorrhagicEscherichia colioutbreak, some patients experience more profound deleterious effects than others, including unfortunate deaths. Thus, the aim of this study was to determine whether high-fat and/or high-carbohydrate diets could negatively modulate the deleterious action of Shiga toxin 2 on ventral anterior and ventral lateral thalamic nuclei and the internal capsule, the neurological centers responsible for motor activity.MethodsMice were fed a regular, high-fat, high-carbohydrate diet or a combination of both previous to the intravenous administration of Shiga toxin 2 or vehicle. Four days after intravenous administration, mice were subjected to behavioral tests and then sacrificed for histological and immunofluorescence assays to determine alterations in the neurovascular unit at the cellular and functional levels. Statistical analysis was performed using one-way analysis of variance followed by Bonferronipost hoctest. The criterion for significance was p = 0.0001 for all experiments.ResultsThe high-fat and the high-carbohydrate diets significantly heightened the deleterious effect of Stx2, while the combination of both diets yielded the worst results, including endothelial glycocalyx and oligodendrocyte alterations, astrocyte and microglial reactivity, neurodegeneration, and motor and sensitivity impairment.ConclusionsIn view of the results presented here, poor nutrition could negatively influence patients affected by Stx2 at a neurological level. Systemic effects, however, cannot be ruled out.

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Section: Discussionsupporting

confidence: 82%

High-fat and high-carbohydrate diets worsen the mouse brain susceptibility to damage produced by enterohemorrhagicEscherichia coliShiga toxin 2

Arenas-Mosquera,

Cerny,

Cangelosi

et al. 2024

Preprint

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“…Consistent with this, the lifespan extension effect of metformin is not seen in male rats 232 or aged female mice. 233 Nevertheless, metformin relieves many aging-related diseases in rodent models, including cognitive impairment and neurodegeneration, 229 , 234 – 237 depression, 238 chronic kidney disease, 239 thymus degeneration, 240 aging-related cataract, 228 aging-related hearing loss, 241 mitochondrial dysfunction in aged hearts, 230 adipose tissue senescence and metabolic abnormalities, 242 , 243 and aging-related developmental and metabolic phenotypes. 244 …”

Section: Epigenetic Regulation Of Agingmentioning

confidence: 99%

Epigenetic regulation of aging: implications for interventions of aging and diseases

Wang

Liu

et al. 2022

Sig Transduct Target Ther

151

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Aging is accompanied by the decline of organismal functions and a series of prominent hallmarks, including genetic and epigenetic alterations. These aging-associated epigenetic changes include DNA methylation, histone modification, chromatin remodeling, non-coding RNA (ncRNA) regulation, and RNA modification, all of which participate in the regulation of the aging process, and hence contribute to aging-related diseases. Therefore, understanding the epigenetic mechanisms in aging will provide new avenues to develop strategies to delay aging. Indeed, aging interventions based on manipulating epigenetic mechanisms have led to the alleviation of aging or the extension of the lifespan in animal models. Small molecule-based therapies and reprogramming strategies that enable epigenetic rejuvenation have been developed for ameliorating or reversing aging-related conditions. In addition, adopting health-promoting activities, such as caloric restriction, exercise, and calibrating circadian rhythm, has been demonstrated to delay aging. Furthermore, various clinical trials for aging intervention are ongoing, providing more evidence of the safety and efficacy of these therapies. Here, we review recent work on the epigenetic regulation of aging and outline the advances in intervention strategies for aging and age-associated diseases. A better understanding of the critical roles of epigenetics in the aging process will lead to more clinical advances in the prevention of human aging and therapy of aging-related diseases.

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Mechanism of metformin regulation in central nervous system: Progression and future perspectives

Cao¹,

Gong²,

Du³

et al. 2022

Biomedicine & Pharmacotherapy

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A high fat, sugar, and salt Western diet induces motor‐muscular and sensory dysfunctions and neurodegeneration in mice during aging: Ameliorative action of metformin

Abstract: This is an open access article under the terms of the Creat ive Commo ns Attri bution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 8 publications

References 115 publications

High-fat and high-carbohydrate diets worsen the mouse brain susceptibility to damage produced by enterohemorrhagicEscherichia coliShiga toxin 2

High-fat and high-carbohydrate diets worsen the mouse brain susceptibility to damage produced by enterohemorrhagicEscherichia coliShiga toxin 2

Epigenetic regulation of aging: implications for interventions of aging and diseases

Mechanism of metformin regulation in central nervous system: Progression and future perspectives

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