Fructooligosaccharide (FOS) and Galactooligosaccharide (GOS) Improve Neuroinflammation and Cognition By Up-regulating IRS/PI3K/AKT Signaling Pathway in Diet-induced Obese Mice

Paiva, Igor Henrique Rodrigues de; Silva, Rodrigo Soares da; Mendonça, Ingrid Prata; Duarte-Silva, Eduardo; Souza, José Roberto Botêlho de; Peixoto, Christina Alves

doi:10.1007/s11481-023-10069-8

Cited by 6 publications

(3 citation statements)

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“…To the best of our knowledge, this is the first demonstration of such an effect in an animal model of ASD. Similar cognitive improvements have been observed in other prebiotic intervention studies with different neurological conditions [29,65,66]. Additionally, beneficial effects on social deficits were observed at an early stage, while the positive impact on spatial working memory required more time.…”

Section: Discussionsupporting

confidence: 84%

“…Mice were fed a combination of two prebiotics, galacto-oligosaccharide (GOS) and fructo-oligosaccharide (FOS), at an early developmental stage. The choice of prebiotic fibers was based on their established ability to modulate the immune system [29][30][31], a central factor in the gut-brain axis and implicated in ASD pathology. Specifically, these dietary fibers have been shown to suppress allergic reactions [32], diminish the incidence of infections [33], enhance immune competence [34,35], and reduce inflammation [36].…”

Section: Introductionmentioning

confidence: 99%

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Prebiotic diet normalizes aberrant immune and behavioral phenotypes in a mouse model of autism spectrum disorder

Prince,

Peralta Marzal,

Markidi

et al. 2024

Acta Pharmacol Sin

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Autism spectrum disorder (ASD) is a cluster of neurodevelopmental disorders characterized by deficits in communication and behavior. Increasing evidence suggests that the microbiota-gut-brain axis and the likely related immune imbalance may play a role in the development of this disorder. Gastrointestinal deficits and gut microbiota dysfunction have been linked to the development or severity of autistic behavior. Therefore, treatments that focus on specific diets may improve gastrointestinal function and aberrant behavior in individuals with ASD. In this study, we investigated whether a diet containing specific prebiotic fibers, namely, 3% galacto-oligosaccharide/fructo-oligosaccharide (GOS/FOS; 9:1), can mitigate the adverse effects of in utero exposure to valproic acid (VPA) in mice. Pregnant BALB/cByJ dams were injected with VPA (600 mg/kg, sc.) or phosphate-buffered saline (PBS) on gestational day 11 (G11). Male offspring were divided into four groups: (1) in utero PBS-exposed with a control diet, (2) in utero PBS-exposed with GOS/FOS diet, (3) in utero VPA-exposed with a control diet, and (4) in utero VPA-exposed with GOS/FOS diet. Dietary intervention started from birth and continued throughout the duration of the experiment. We showed that the prebiotic diet normalized VPA-induced alterations in male offspring, including restoration of key microbial taxa, intestinal permeability, peripheral immune homeostasis, reduction of neuroinflammation in the cerebellum, and impairments in social behavior and cognition in mice. Overall, our research provides valuable insights into the gut-brain axis involvement in ASD development. In addition, dietary interventions might correct the disbalance in gut microbiota and immune responses and, ultimately, might improve detrimental behavioral outcomes in ASD.

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Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Prebiotic diet normalizes aberrant immune and behavioral phenotypes in a mouse model of autism spectrum disorder

Prince,

Peralta Marzal,

Markidi

et al. 2024

Acta Pharmacol Sin

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“…Inhibition of central iNOS ameliorated not only glucose metabolism, but also macrophage activation induced inflammation in hypothalamus of HFD-induced obesity mice [ 136 ]. In addition, 18 or 20 w of HFD consumption also can significantly enhance the expression of COX-2 in the hippocampus of the mice [ 142 , 143 ]. An increased activity of COX-2-PEG2 signaling pathway has been considered to play a key role in impairing hippocampal neuronal function and cognition [ 144 , 145 ].…”

Section: Obesity-induced Neuroinflammation: Phenotypes and Mechanismsmentioning

confidence: 99%

Obesity-induced blood-brain barrier dysfunction: phenotypes and mechanisms

Feng,

Fang,

et al. 2024

J Neuroinflammation

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Obesity, a burgeoning global health issue, is increasingly recognized for its detrimental effects on the central nervous system, particularly concerning the integrity of the blood-brain barrier (BBB). This manuscript delves into the intricate relationship between obesity and BBB dysfunction, elucidating the underlying phenotypes and molecular mechanisms. We commence with an overview of the BBB’s critical role in maintaining cerebral homeostasis and the pathological alterations induced by obesity. By employing a comprehensive literature review, we examine the structural and functional modifications of the BBB in the context of obesity, including increased permeability, altered transport mechanisms, and inflammatory responses. The manuscript highlights how obesity-induced systemic inflammation and metabolic dysregulation contribute to BBB disruption, thereby predisposing individuals to various neurological disorders. We further explore the potential pathways, such as oxidative stress and endothelial cell dysfunction, that mediate these changes. Our discussion culminates in the summary of current findings and the identification of knowledge gaps, paving the way for future research directions. This review underscores the significance of understanding BBB dysfunction in obesity, not only for its implications in neurodegenerative diseases but also for developing targeted therapeutic strategies to mitigate these effects.

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