Dataset Information

Alterations in gut microbiota composition, plasma lipids, and brain activity, suggest inter-connected pathways influencing malnutrition-associated cognitive and neurodevelopmental changes.

ABSTRACT:

Malnutrition affects over 30 million children annually and has profound immediate and enduring repercussions, with nearly half of child deaths under five linked to malnutrition. Survivors face lasting consequences, including impaired neurocognitive development, leading to cognitive and behavioural deficits, impacting academic performance and socioeconomic outcomes. Despite extensive literature on malnutrition’s associations with infections, metabolism, microbiome and genomics, knowledge gaps persist around how these changes are mechanistically connected. The objective of this study was to identify gut microbiome mediated associations between Moderate Acute Malnutrition (MAM) and cognitive development. Despite limitations, this study provides evidence supporting the hypothesis that inter-connected pathways between the gut microbiome, microbial metabolism mediate plasma lipids, brain activity and cognitive functions. Causality between gut microbiome, plasma metabolite changes and MAM phenotype remains unclear, necessitating further research. However, these findings offer insights to optimize interventions for MAM-associated neurodevelopmental changes.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse phase, Liquid Chromatography MS - positive - reverse phase

PROVIDER: MTBLS10066 | MetaboLights | 2024-11-27

REPOSITORIES: MetaboLights

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	20220921_LEAP-NEG_S001_RT_shift.mzML	Mzml
	20220921_LEAP-NEG_S002_RT_shift.mzML	Mzml
	20220921_LEAP-NEG_S003_RT_shift.mzML	Mzml
	20220921_LEAP-NEG_S004_RT_shift.mzML	Mzml
	20220921_LEAP-NEG_S005_RT_shift.mzML	Mzml

Items per page:

1 - 5 of 1280

Similar Datasets

Project description:Background: The long-term high-fat, high-sugar diet exacerbates type 2 diabetes mellitus (T2DM)-related cognitive impairments. The negative impact of poor dietary patterns on brain development and neurological function may be related to gut microbiota disturbance. The role of phlorizin in mitigating glucose and lipid metabolism disorders is well documented. However, the protective effect of phlorizin on diabetes-related cognitive dysfunction is unclear. Therefore, the present study aimed to investigate the effect of dietary supplementation of phlorizin on high-fat and high-fructose diet (HFFD)-induced cognitive dysfunction and evaluate the crucial role of the microbiota-gut-brain axis. Results: Dietary supplementation of phlorizin for 14 weeks effectively prevented glucolipid metabolism disorder, spatial learning impairment, and memory impairment in HFFD mice. In addition, phlorizin improved the HFFD-induced decrease in synaptic plasticity, neuroinflammation, and excessive activation of microglia in the hippocampus. Transcriptomics analysis shows that the protective effect of phlorizin on cognitive impairment was associated with increased expression of neurotransmitters and synapse-related genes in the hippocampus. Phlorizin treatment alleviated colon microbiota disturbance, mainly manifested by an increase in gut microbiota diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria. The level of microbial metabolites, including SCFA, inosine 5'-monophosphate (IMP), and D (-)-beta-hydroxybutyric acid (BHB) were also significantly increased after phlorizin treatment. Moreover, integrating multiomics analysis observed tight connections between phlorizin-regulated genes, microbiota, and metabolites. Furthermore, removal of the gut microbiota via antibiotics treatment diminished the protective effect of phlorizin against HFFD-induced cognitive impairment, underscoring the critical role of the gut microbiota in mediating cognitive behavior. Importantly, supplementation with SCFA and BHB alone mimicked the regulatory effects of phlorizin on cognitive function. Conclusions: These results indicate that gut microbiota and their metabolites mediate the ameliorative effect of phlorizin on HFFD-induced cognitive impairment. Therefore, phlorizin can be used as an easy-to-implement nutritional therapy to prevent and alleviate metabolism-related neurodegenerative diseases by targeting the regulation of the microbiome-gut-brain axis.

Dataset Information

Alterations in gut microbiota composition, plasma lipids, and brain activity, suggest inter-connected pathways influencing malnutrition-associated cognitive and neurodevelopmental changes.

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets