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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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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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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.

2024-05-31 | GSE267493 | GEO

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

Deficiency of Irx5 protects mice from obesity and associated metabolic abnormalities

Project description:Here we aim to decipher the actions of Irx5 in the regulation of obesity and metabolic abnormalities. We employed a mouse model homozygous for an Irx5-knockout (Irx5KO) allele and conducted droplet based single-cell RNA sequencing (Drop-seq) in the hypothalamic arcuate-median eminence (ARC-ME), which is the main control center for sensing and integrating feeding regulatory signals.

2022-09-19 | GSE201736 | GEO

Deletion of intestinal Hdac3 remodels the lipidome of enterocytes and protects mice from diet-induced obesity

Project description:Deletion of intestinal Hdac3 remodels the lipidome of enterocytes and protects mice from diet-induced obesity

2020-01-13 | PXD015738 | Pride

RAP1 protects from obesity, diabetes and metabolic syndrome through its extra telomeric role regulating gene expression (old mouse liver)

Project description:RAP1 is one of the components of shelterin, the capping complex at chromosome ends or telomeres. Unlike other shelterins, however, RAP1 is not essential for preventing telomere fusions. RAP1 also binds along chromosome arms, where it is proposed to regulate gene expression. To investigate the non-telomeric roles of RAP1 in vivo, we generated a RAP1 whole-body knock-out mouse model. Unexpectedly, these mice presented an early onset of obesity, which was particularly severe in females and was aggravated under a high-fat diet. Rap1-deficient mice showed abnormal accumulation of fat in abdominal depots and developed signs of type II diabetes and metabolic syndrome, including hepatic steatosis and high fasting plasma levels of insulin, glucose, cholesterol, and alanine transaminase. Gene expression analyses of the liver and visceral white fat from Rap1-deficient mice before the onset of obesity indicated deregulation of key metabolic transcriptional programs including fatty acid metabolism, PPARa signalling and glucose metabolism. Transcriptome and Western blotting analyses in liver further identified Ppara and Pgc1a and their target genes as the key metabolic pathways affected by Rap1 deletion. Finally, we show here that RAP1 binds to Ppara and Pgc1a loci and modulates their transcription. These findings underscore an unprecedented role for a telomere-binding protein in the regulation of metabolism. 2 condition experiment: WT versus Rap1 knockout. Tissue: liver. 3 biological replicates per genotype. Mice were 30 weeks old.

2013-06-21 | E-GEOD-43173 | biostudies-arrayexpress

RAP1 protects from obesity, diabetes and metabolic syndrome through its extra telomeric role regulating gene expression (young mouse liver)

Project description:RAP1 is one of the components of shelterin, the capping complex at chromosome ends or telomeres. Unlike other shelterins, however, RAP1 is not essential for preventing telomere fusions. RAP1 also binds along chromosome arms, where it is proposed to regulate gene expression. To investigate the non-telomeric roles of RAP1 in vivo, we generated a RAP1 whole-body knock-out mouse model. Unexpectedly, these mice presented an early onset of obesity, which was particularly severe in females and was aggravated under a high-fat diet. Rap1-deficient mice showed abnormal accumulation of fat in abdominal depots and developed signs of type II diabetes and metabolic syndrome, including hepatic steatosis and high fasting plasma levels of insulin, glucose, cholesterol, and alanine transaminase. Gene expression analyses of the liver and visceral white fat from Rap1-deficient mice before the onset of obesity indicated deregulation of key metabolic transcriptional programs including fatty acid metabolism, PPARa signalling and glucose metabolism. Transcriptome and Western blotting analyses in liver further identified Ppara and Pgc1a and their target genes as the key metabolic pathways affected by Rap1 deletion. Finally, we show here that RAP1 binds to Ppara and Pgc1a loci and modulates their transcription. These findings underscore an unprecedented role for a telomere-binding protein in the regulation of metabolism. 2 condition experiment: WT versus Rap1 knockout. Tissue: liver. 4 biological replicates per genotype. Mice were 10 weeks old.

2013-06-21 | E-GEOD-43171 | biostudies-arrayexpress

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