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Evolutionary forces have wired our brains to prefer and consume energy-dense foods to aid in our survival. While effective during periods of limited access, the ubiquitous nature of high-fat food sources in society leads to obesity and numerous related health complications. Exacerbating this drive to consume more energy-dense, palatable foods is a devaluation of less appetitive, nutritionally-balanced foods. While this preference for calorically-rich foods is well known, significant gaps exist in our understanding of how this develops and leads to devaluation.

Laboratory mice are typically provided with ad libitum access to a well-balanced standard chow diet (SD) in which the macronutrient composition has been formulated for optimal growth. Introduction to ad libitum high fat diet (HFD), but not a high-sucrose diet, leads to rapid weight gain, at least in part due to excessive caloric intake. Interestingly, when mice are given a choice between ad libitum access to both SD and HFD, they strongly prefer consumption of the latter at the expense of the former. While this predilection for HFD over SD during prolonged exposure is well described, how rapidly this transition occurs under physiological or artificial hunger is less known. Removal of HFD from mice given the choice between HFD and SD, akin to a strict human diet, results in rapid weight loss due to the self-restricted consumption of SD. Additionally, mice fed a HFD will forgo SD consumption even in states of physiological or artificially-induced caloric deprivation. While this SD devaluation is robustly conserved between sex and subject and independent of fat mass accrual, the causative nature of this phenomenon is not well understood.

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Maternal gut Bifidobacterium breve modifies fetal brain metabolism in germ-free mice

Jorge Lopez-Tello, Raymond Kiu, Zoe Schofield, Cindy X.W. Zhang, ... Amanda N. Sferruzzi-Perri

Maternal gut Bifidobacterium breve modifies fetal brain metabolism in germ-free mice

 

Background

Recent advances have significantly expanded our understanding of the gut microbiome's influence on host physiology and metabolism. However, the specific role of certain microorganisms in gestational health and fetal development remains underexplored.

Objective

This study investigates the impact of Bifidobacterium breve UCC2003 on fetal brain metabolism when colonized in the maternal gut during pregnancy.

Methods

Germ-free pregnant mice were colonized with or without B. breve UCC2003 during pregnancy. The metabolic profiles of fetal brains were analyzed, focusing on the presence of key metabolites and the expression of critical metabolic and cellular pathways.

Results

Maternal colonization with B. breve resulted in significant metabolic changes in the fetal brain. Specifically, ten metabolites, including citrate, 3-hydroxyisobutyrate, and carnitine, were reduced in the fetal brain. These alterations were accompanied by increased abundance of transporters involved in glucose and branched-chain amino acid uptake. Furthermore, supplementation with this bacterium was associated with elevated expression of critical metabolic pathways such as PI3K-AKT, AMPK, STAT5, and Wnt-β-catenin signaling, including its receptor Frizzled-7. Additionally, there was stabilization of HIF-2 protein and modifications in genes and proteins related to cellular growth, axogenesis, and mitochondrial function.

Conclusions

The presence of maternal B. breve during pregnancy plays a crucial role in modulating fetal brain metabolism and growth. These findings suggest that Bifidobacterium could modify fetal brain development, potentially offering new avenues for enhancing gestational health and fetal development through microbiota-targeted interventions.

 

    Articles in Press

    Maternal gut Bifidobacterium breve modifies fetal brain metabolism in germ-free mice

    Jorge Lopez-Tello, Raymond Kiu, Zoe Schofield, Cindy X.W. Zhang, ... Amanda N. Sferruzzi-Perri

    Maternal gut Bifidobacterium breve modifies fetal brain metabolism in germ-free mice

     

    Background

    Recent advances have significantly expanded our understanding of the gut microbiome's influence on host physiology and metabolism. However, the specific role of certain microorganisms in gestational health and fetal development remains underexplored.

    Objective

    This study investigates the impact of Bifidobacterium breve UCC2003 on fetal brain metabolism when colonized in the maternal gut during pregnancy.

    Methods

    Germ-free pregnant mice were colonized with or without B. breve UCC2003 during pregnancy. The metabolic profiles of fetal brains were analyzed, focusing on the presence of key metabolites and the expression of critical metabolic and cellular pathways.

    Results

    Maternal colonization with B. breve resulted in significant metabolic changes in the fetal brain. Specifically, ten metabolites, including citrate, 3-hydroxyisobutyrate, and carnitine, were reduced in the fetal brain. These alterations were accompanied by increased abundance of transporters involved in glucose and branched-chain amino acid uptake. Furthermore, supplementation with this bacterium was associated with elevated expression of critical metabolic pathways such as PI3K-AKT, AMPK, STAT5, and Wnt-β-catenin signaling, including its receptor Frizzled-7. Additionally, there was stabilization of HIF-2 protein and modifications in genes and proteins related to cellular growth, axogenesis, and mitochondrial function.

    Conclusions

    The presence of maternal B. breve during pregnancy plays a crucial role in modulating fetal brain metabolism and growth. These findings suggest that Bifidobacterium could modify fetal brain development, potentially offering new avenues for enhancing gestational health and fetal development through microbiota-targeted interventions.

     

      You are what you eat

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