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Maternal emulsifier consumption programs offspring metabolic and neuropsychological health

ABSTRACT: Maternal emulsifier consumption programs offspring metabolic and neuropsychological health

PROVIDER: PRJNA967660 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24445724_1.fastq.gz	Fastqsanger.gz
	SRR24445724_2.fastq.gz	Fastqsanger.gz
	SRR24445725_1.fastq.gz	Fastqsanger.gz
	SRR24445725_2.fastq.gz	Fastqsanger.gz
	SRR24445726_1.fastq.gz	Fastqsanger.gz

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Maternal emulsifier consumption programs offspring metabolic and neuropsychological health

Project description:Modern lifestyle is associated with a major consumption of ultra-processed foods (UPF) due to their practicality and palatability. The ingestion of emulsifiers, a main additive in UPFs, has been related to gut inflammation, microbiota dysbiosis, adiposity and obesity. Maternal unbalanced nutritional habits during embryonic and perinatal stages perturb offspring’s long-term metabolic health, thus increasing obesity and associated comorbidity risk. However, whether maternal emulsifier consumption influences developmental programming in the offspring remains unknown. Here we show that, in mice, maternal consumption of dietary emulsifiers (1% CMC and 1% P80 in drinking water), during gestation and lactation, perturbs the development of hypothalamic energy balance regulation centers of the progeny, leads to metabolic impairments, cognition deficits and induces anxiety-like traits in a sex-specific manner. Our findings support the notion that maternal consumption of emulsifiers, common additives of UPFs, causes mild metabolic and neuropsychological malprogramming in the progeny. Our data call for nutritional advice during gestation.

2023-07-31 | GSE231769 | GEO

Dietary emulsifier consumption alters gene expression in the amygdala and paraventricular nucleus of the hypothalamus in mice

Project description:Purpose: The goal of the current study was to test whether emulsifier consumption is associated with changes in gene expression in the amygdala and PVN Methods: Adult male C57BL/6J mice received drinking water containing either 1% sodium carboxymethylcellulose (CMC), 1% polysorbate-80 (P80) or water without emulsifier for 12 weeks. PVN and amygdala gene expression was generated by RNA-Seq using an Illumina NextSeq 500. FastQ quality filter was used to filter low quality sequences and Tophat, Bowtie, Cufflinks, and Cuffdiff were used for RNA-Seq analysis. qRT–PCR validation was performed using 6 differential genes of interest. Results: A total of 243 genes were differentially expressed in the amygdala and PVN of emulsifier-treated mice compared to controls. There was minimal overlap of differentially expressed genes in CMC- and P80-treated animals, suggesting that each emulsifier acts via distinct molecular mechanisms to produce an anxiety-like phenotype. Furthermore, gene ontology and pathway analysis revealed that various stress, metabolic, and immune terms and pathways were altered in emulsifier conditions. RNA-seq data was validated with qRT–PCR data (R2= 0.8815). Conclusions: These findings are the first to demonstrate that emulsifier consumption changes gene expression in brain regions that are critical for stress responding, providing possible molecular mechanisms that may underly the observed anxiety-like phenotype

2022-01-27 | GSE194260 | GEO

Dietary emulsifier consumption accelerates type 1 diabetes development in NOD mice

Project description:Dietary emulsifier consumption accelerates type 1 diabetes development in NOD mice

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Human intestinal microbiome determines individualized inflammatory response to dietary emulsifier carboxymethylcellulose consumption

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Maternal Brown Fat Thermogenesis Programs Glucose Tolerance in the Male Offspring

Project description:Maternal Brown Fat Thermogenesis Programs Glucose Tolerance in the Male Offspring

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Maternal Brown Fat Thermogenesis Programs Glucose Tolerance in the Male Offspring

Project description:We tested if minor changes in maternal non-shivering thermogenesis during pregnancy can severely alter the phenotype of the offspring already in the next generation. Therefore, male offspring of dams lacking the uncoupling protein 1 (UCP1-KO) in the thermogenic brown adipose tissue were analysed. Genome-wide expression profiling identified several alterations in the hepatic transcriptomic landscape, demonstrating that even minor differences in the demand for maternal thermogenesis profoundly and permanently alter hepatic gene activity in the adult offspring. Liver gene expression data of offspring from WT and UCP1-KO dams.

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Maternal Brown Fat Thermogenesis Programs Glucose Tolerance in the Male Offspring

Project description:We tested if minor changes in environmental temperature during pregnancy can severely alter the phenotype of the offspring already in the next generation. Genome-wide expression profiling of liver samples obtained from adult male mice offspring identified several alterations in the hepatic transcriptomic landscape, thus demonstrating that even minor differences in the demand for maternal thermogenesis profoundly and permanently alter hepatic gene activity in the adult offspring. Liver gene expression data of offspring from dams that were kept at different ambient temperatures (30°C, 23°C, 18°C, 10°C) only during pregnancy.

2020-11-09 | GSE145142 | GEO

Maternal and offspring

Project description:Cecal microbiome of C-, WD- and REV-dams at weaning and in their offspring (C-offspring, WD-offspring, and REV-offspring, respectively) at 4 months.

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Maternal hematopoietic TNF, via milk chemokines, programs hippocampal development and memory

Project description:TNF is a proinflammatory cytokine with established roles in host defense and immune system organogenesis. Here we report a novel physiological function of TNF that extends its effect beyond the host into the developing offspring. A partial/complete maternal TNF-deficit, specifically in hematopoietic cells, resulted in reduced milk levels of chemokines IP-10, MCP-1/-3/-5, and MIP-1β, which in turn, augmented offspring postnatal hippocampal proliferation, leading to improved adult spatial memory. These effects were reproduced by the postpartum administration of a clinically used anti-TNF agent. Chemokines, fed to suckling pups of TNF-deficient mothers, restored both postnatal proliferation and adult spatial memory to normal levels. This work identifies a TNF-dependent “lactrocrine” pathway that programs offspring hippocampal development and memory. The level of ambient TNF is known to be downregulated by physical activity/exercise and adaptive stress; thus, we propose that the maternal TNF-milk chemokine pathway evolved to promote offspring adaptation to post-weaning environmental challenges/competition. Examined transcriptomes of TNF wild type offspring of TNF wild type or heterozygouse mothers

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