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INPP4B protects from metabolic disease and obesity associated prostate neoplasia.

ABSTRACT: INPP4B protects from metabolic disease and obesity associated prostate neoplasia.

PROVIDER: PRJNA555198 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9702110_1.fastq.gz	Fastqsanger.gz
	SRR9702110_2.fastq.gz	Fastqsanger.gz
	SRR9702103_1.fastq.gz	Fastqsanger.gz
	SRR9702103_2.fastq.gz	Fastqsanger.gz
	SRR9702104_1.fastq.gz	Fastqsanger.gz

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INPP4B protects from metabolic disease and obesity associated prostate neoplasia.

Project description:A high fat diet and obesity have been linked to the development of metabolic dysfunction and the promotion of multiple cancers in mice and men. The causative cellular signals are multifactorial and not completely understood. Previous studies have shown that metabolic dysfunction leads to activation of the AKT and PKC pathways. Both signaling pathways are inhibited by the dual specificity phosphatase, INPP4B, which dephosphorylates PI(3,4)P2, an activator of AKT, and PI(4,5)P2, an activator of the PLC/PKC pathway. We established that INPP4B signaling protects mice from metabolic dysfunction. Inpp4b-/- male mice had accelerated activation of SREBF1 in liver which, along with the high fat diet, caused increased expression and activity of PPARG and other lipogenic pathways leading non-alcoholic fatty liver disease (NAFLD), type II diabetes, expansion and inflammation of WAT, and systemic and localized prostate inflammation that drives the development of high-grade prostatic intraepithelial neoplasia (PIN).

2021-02-04 | GSE134466 | GEO

KDM4B epigenetically protects against obesity and metabolic dysfunction

Project description:KDM4B epigenetically protects against obesity and metabolic dysfunction

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Estrogen Receptor α Protects Against Obesity-Induced Metabolic Dysfunction by Regulating VAT Tregs

Project description:Estrogens are important for metabolic health. Individuals with low levels of circulating estrogens, including men and postmenopausal women, exhibit an elevated risk for developing obesity-associated metabolic syndromes. Chronic low-grade inflammation in the visceral adipose tissue (VAT) is a major contributor to metabolic dysfunction during obesity. Regulatory T cells (Tregs) in the VAT limit tissue inflammation and protect against obesity-associated metabolic disease. In this study, we identify opposing roles of estrogen receptor α (ERα) in regulating VAT Tregs in female mice under steady-state and obese conditions. At steady state, ERα restrained the age-dependent clonal expansion of specific VAT Treg subsets expressing the IL-33 receptor ST2. However, during obesity, ERα-deficiency predisposed females to the loss of ST2+ VAT Tregs, exacerbating VAT inflammation and insulin resistance. These findings indicate that ERα signaling protects against obesity-induced metabolic diseases by preserving metabolically protective ST2+ VAT Treg subsets, and the loss of this protection may contribute to the heightened metabolic risk in estrogen-deficient individuals.

2026-02-13 | GSE294200 | GEO

Estrogen Receptor α Protects Against Obesity-Induced Metabolic Dysfunction by Regulating VAT Tregs (oVAT)

2026-02-13 | GSE312696 | GEO

Deficiency of Irx5 protects mice from obesity and associated metabolic abnormalities

Project description:Deficiency of Irx5 protects mice from obesity and associated metabolic abnormalities

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Endothelial Overexpression protects Metabolic Homeostasis and the Development of Obesity and cardiovascular disease

Project description:Endothelial Overexpression protects Metabolic Homeostasis and the Development of Obesity and cardiovascular disease

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Estrogen Receptor α Protects Against Obesity-Induced Metabolic Dysfunction by Regulating VAT Tregs

Project description:Estrogen Receptor α Protects Against Obesity-Induced Metabolic Dysfunction by Regulating VAT Tregs

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Estrogen Receptor α Protects Against Obesity-Induced Metabolic Dysfunction by Regulating VAT Tregs (oVAT)

Project description:Estrogen Receptor α Protects Against Obesity-Induced Metabolic Dysfunction by Regulating VAT Tregs (oVAT)

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Endothelial Overexpression protects Metabolic Homeostasis and the Development of Obesity and cardiovascular disease

Project description:Introduction: Obesity is a major risk factor associated with multiple pathological conditions including diabetes and cardiovascular disease. Endothelial dysfunction is an early predictor of obesity. However, little is known regarding how early endothelial changes trigger obesity. In the present work we report a novel endothelial-mediated mechanism essential for regulation of metabolic homeostasis, driven by c-Myc. Methods: We used conditional overexpression (EC-Myc OE) mouse models to investigate the role of endothelial-specific c-Myc in metabolic homeostasis during high-fat diet exposure. Body weight, metabolic parameters and cardiovascular function were collected over time and tissue samples collected at endpoint for biochemical, pathology and RNA-sequencing analysis. Results: In the present study we demonstrate that Overexpression of endothelial c-Myc attenuated diet-induced obesity and visceral fat accumulation and prevented the development of glucose tolerance and cardiac dysfunction. Transcriptome analysis of skeletal muscle suggests that the protective effects promoted by endothelial c-Myc overexpression are associated with the expression of genes known to increase weight loss, energy expenditure and glucose tolerance. Discussion: Our results show a novel important role for endothelial c-Myc in regulating metabolic homeostasis and suggests its potential targeting in preventing obesity and associated complications such as diabetes type-2 and cardiovascular dysfunction.

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KDM4B epigenetically protects against obesity and metabolic dysfunction [gene expression]

Project description:KDM4B (lysine demethylase 4B) in adipose tissues plays a critical role in energy balance, oxidation, lipolysis and thermogenesis. Loss of KDM4B in mice resulted in obesity associated with reduced energy expenditure and impaired adaptive thermogenesis. Mechanistically, we determined that KDM4B directly controls the expression of multiple metabolic genes.

2019-05-22 | GSE102289 | GEO

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