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Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring I

ABSTRACT: Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring I

PROVIDER: PRJNA994877 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25280119_1.fastq.gz	Fastqsanger.gz
	SRR25280119_2.fastq.gz	Fastqsanger.gz
	SRR25280120_1.fastq.gz	Fastqsanger.gz
	SRR25280120_2.fastq.gz	Fastqsanger.gz
	SRR25280121_1.fastq.gz	Fastqsanger.gz

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Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring I

Project description:Kupffer cells (KCs) are tissue-resident macrophages which colonize the developing liver early during embryogenesis1. Throughout development and adulthood, KCs have distinct core functions that are essential for liver and organismal homeostasis, such as supporting fetal erythropoiesis as well as postnatal erythrocyte recycling and liver metabolism2. KCs acquire their tissue-specific transcriptional signature immediately after colonizing the liver, mature together with the tissue, and adapt to the tissue’s function1,3,4. However, whether perturbation of macrophage core functions during development may contribute to or cause disease at postnatal stages is poorly understood. Here, we utilize a maternal obesity model to disturb KC functions during gestation. We show that offspring born to obese mothers develop fatty liver disease that is accompanied by a local pro-inflammatory response, a phenotype that is augmented if the offspring is kept on control diet after birth. Further, transcriptional analyses reveal that KCs undergo developmental programming through the maternal high-fat diet, which lasts until adulthood. The offspring’s KC developmental programming is irreversible despite the switch to control diet and leads to increased lipid uptake in hepatocytes mediated via paracrine factors stemming from KCs. The transcriptional programming of KCs and the fatty liver disease phenotype are rescued by genetic depletion of hypoxia-inducible factor alpha (Hif1a) in macrophages during gestation. These results demonstrate that macrophages rely on an undisturbed development to fulfil their core functions and support organ homeostasis during adulthood, and establish developmental programming of KCs as a therapeutic strategy for metabolic disorders, such as fatty liver disease.

2023-08-22 | GSE237393 | GEO

Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring II

2023-08-22 | GSE237405 | GEO

Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring [snMultiome sequencing]

Project description:Kupffer cells (KCs) are tissue-resident macrophages which colonize the liver early during embryogenesis. KCs start to acquire a tissue-specific transcriptional signature immediately after colonizing the liver, mature together with the tissue, and adapt to the tissue’s functions. Throughout development and adulthood, KCs have distinct core functions that are essential for liver and organismal homeostasis, such as supporting fetal erythropoiesis as well as postnatal erythrocyte recycling and liver metabolism. However, whether perturbations of macrophage core functions during development contribute to or cause disease at postnatal stages is poorly understood. Here, we utilize a mouse model of maternal obesity to perturb KC functions during gestation. We show that offspring exposed to maternal obesity develop fatty liver disease, driven by aberrant developmental programming of KCs that persists into adulthood. Programmed KCs mediate lipid uptake by hepatocytes through apolipoprotein secretion. KC depletion in neonates born to obese mothers, followed by replenishment with exogenous monocytes, rescues the fatty liver disease. The transcriptional programming of KCs and the fatty liver disease phenotype are also rescued by genetic depletion of hypoxia-inducible factor alpha (Hif1a) in macrophages during gestation. These results establish developmental perturbation of KC functions as a cause for the development of fatty liver disease in adult life and, thereby, place fetal-derived macrophages as intergenerational messengers within the concept of developmental origins of health and diseases.

2024-12-04 | GSE283082 | GEO

Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring

Project description:Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring

| PRJNA994896 | ENA

Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring II

Project description:Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring II

| PRJNA994895 | ENA

Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring [snMultiome sequencing]

Project description:Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring [snMultiome sequencing]

| PRJNA1191826 | ENA

Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-22 | GSE237408 | GEO

Multi-omics data integration reveals sex-dependent hippocampal programming by maternal high-fat diet during lactation in adult mouse offspring

Project description:Early-life exposure to high-fat diet (HF) can program metabolic and cognitive alterations in adult offspring. Although the hippocampus plays a crucial role in memory and metabolic homeostasis, few studies reported the impact of maternal HF on this structure. We assessed the effects of maternal HF during lactation on physiological, metabolic and cognitive parameters in young adult offspring mice. To identify early-programming mechanisms in hippocampus, we developed a multi-omics strategy in male and female offspring. Maternal HF induced a transient increased body weight at weaning, a mild glucose intolerance only in 3-month-old male mice with no change in plasma metabolic parameters in adult male and female offspring. Behavioral alterations revealed by Barnes maze test were observed both in 6-month-old male and female mice. Multi-omics strategy unveiled sex-specific transcriptomic and proteomic modifications in the hippocampus of adult offspring. These studies, that were confirmed by regulon analysis, showing that, although genes whose expression was modified by maternal HF were different between sexes, the main pathways affected were similar with mitochondria and synapses as main hippocampal targets of maternal HF. The effects of maternal HF reported here may help to better characterize sex-dependent molecular pathways involved in cognitive disorders and neurodegenerative diseases.

2024-01-26 | PXD045639 | Pride

Developmental programming by maternal obesity alters offspring lifespan and immune function in a diet- and sex-specific manner

Project description:Maternal obesity is a growing health concern that predisposes offspring to metabolic dysfunction, immune system alterations, and neurodegenerative disorders. To investigate the intergenerational effects of maternal obesity, we used Drosophila melanogaster models exposed to high-sugar (HSD) and high-fat diets (HFD). We found that maternal diet-induced obesity significantly altered offspring lifespan, immune function, and neuronal health in a sex- and diet-specific manner. Male offspring were particularly susceptible, exhibiting reduced lifespan, impaired climbing ability, and increased axonal degeneration, especially following maternal HFD exposure. Transcriptomic analyses revealed age-dependent and diet-specific changes, with males showing pronounced alterations at 50 days of age. Developmental programming of hemocytes (macrophage-like cells) played a crucial role in these outcomes, as knockdown of key immune pathways such as Relish and Upd3 in hemocytes further influenced lifespan in a diet-specific manner. These findings highlight the complex interplay between maternal diet and immune function, underscoring the importance of immune cells in mediating the long-term health consequences of maternal obesity. Our study provides new insights into conserved mechanisms linking maternal metabolic health to offspring outcomes and emphasizes the continued need for animal models to understand intergenerational health impacts.

2024-12-23 | GSE284632 | GEO

Sex-Dependent Programming of Glucose and Fatty Acid Metabolism in Mouse Offspring by Maternal Protein Restriction

Project description:Analysis of glucose and Lipid metabolism in male and female offspring after protein restriction of the mother Male offspring showed features of metabolic syndrome after receiving a high fat diet, regardless of the diet of the dam. Glucose and lipid metabolism in male offspring was unaltered. Insulin sensitivity and hepatic fatty acid storage in female offspring of low-protein-fed dams changed in such a way that it resembled the male pattern of insulin sensitivity and hepatic fatty acid storage. Microarray analysis on hepatic gene expression patterns confirmed these findings. We therefore conclude that in mice, maternal protein restriction does not change the response of glucose and fatty acid metabolism to a high fat diet in male offspring, but does program metabolism in female offspring in such a way that it resembles male metabolism. Our findings might have implications for potential future gender-specific treatment of the features of metabolic diseases.

2012-02-08 | GSE15940 | GEO

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