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Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway [II]

ABSTRACT: Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway [II]

PROVIDER: PRJNA482461 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7583970_1.fastq.gz	Fastqsanger.gz
	SRR7583970_2.fastq.gz	Fastqsanger.gz
	SRR7583971_1.fastq.gz	Fastqsanger.gz
	SRR7583971_2.fastq.gz	Fastqsanger.gz
	SRR7583964_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway

Project description:Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway

| PRJNA482452 | ENA

Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway [I]

Project description:Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway [I]

| PRJNA482455 | ENA

Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway [II]

Project description:To evaluate gene expression changes in response to low-density-lipoprotein related protein 1 (LRP1) depletion in endothelial cells, we performed mRNA-sequencing analysis with microvascular endothelial cells isolated from the liver LRP1 endothelial knockout mice and their littermate control wild type mice.

2021-06-11 | GSE117555 | GEO

Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway [I]

Project description:To evaluate gene expression changes in response to low-density-lipoprotein related protein 1 (LRP1) depletion in endothelial cells, we performed mRNA-sequencing analysis with microvascular endothelial cells isolated from the lung, heart and liver LRP1 endothelial knockout mice and their littermate control wild type mice.

2021-06-11 | GSE117554 | GEO

Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway

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

2021-06-11 | GSE117560 | GEO

Endothelium-specific depletion of LRP1 improves glucose homeostasis through inducing osteocalcin.

Project description:The vascular endothelium is present within metabolic organs and actively regulates energy metabolism. Here we show osteocalcin, recognized as a bone-secreted metabolic hormone, is expressed in mouse primary endothelial cells isolated from heart, lung and liver. In human osteocalcin promoter-driven green fluorescent protein transgenic mice, green fluorescent protein signals are enriched in endothelial cells lining aorta, small vessels and capillaries and abundant in aorta, skeletal muscle and eye of adult mice. The depletion of lipoprotein receptor-related protein 1 induces osteocalcin through a Forkhead box O -dependent pathway in endothelial cells. Whereas depletion of osteocalcin abolishes the glucose-lowering effect of low-density lipoprotein receptor-related protein 1 depletion, osteocalcin treatment normalizes hyperglycemia in multiple mouse models. Mechanistically, osteocalcin receptor-G protein-coupled receptor family C group 6 member A and insulin-like-growth-factor-1 receptor are in the same complex with osteocalcin and required for osteocalcin-promoted insulin signaling pathway. Therefore, our results reveal an endocrine/paracrine role of endothelial cells in regulating insulin sensitivity, which may have therapeutic implications in treating diabetes and insulin resistance through manipulating vascular endothelium.

| S-EPMC8421392 | biostudies-literature

Decreased IGF1R Attenuates Senescence and Improves Function in Pancreatic beta-Cells

Project description:Decreased IGF1R Attenuates Senescence and Improves Function in Pancreatic beta-Cells

| PRJNA955673 | ENA

Decreased IGF1R Attenuates Senescence and Improves Function in Pancreatic beta-Cells

Project description:We previously reported that increased expression of IGF1R in mouse and human beta-cells is a marker of older beta-cells; however, its contribution to age-related dysfunction and cellular senescence remains to be determined. In this study, we explored the direct role of IGF1R in beta-cell function and senescence using inducible beta-cell specific IGF1R knockdown (betaIgf1rKD) mice. Adult betaIgf1rKD mice showed improved glucose clearance and glucose-induced insulin secretion, accompanied by decreased p21Cip1 protein expression in beta-cells. RNASeq of islets isolated from these betaIgf1rKD mice revealed restoration of 3 signaling pathways known to be downregulated by aging: sulfide oxidation, autophagy, and mTOR signaling. Additionally, deletion of IGF1R in mouse beta-cells increased transcription of genes important for maintaining beta-cell identity and function, such as Mafa, Nkx6.1, and Kcnj11, while decreasing senescence-related genes, such as Cdkn2a, Il1b, and Serpine 1. These results suggest that IGF1R signaling plays a causal role in aging-induced beta-cell dysfunction.

2023-06-19 | GSE229709 | GEO

Global, neuronal, and beta-cell specific deletion of the insulin inhibitory receptor (inceptor) improves glucose homeostasis in diet-induced obese male mice

Project description:The insulin inhibitory receptor (inceptor) was recently identified as a key terminator of insulin and insulin-like growth factor 1 receptor (INSR/IGF1R) signaling in pancreatic 𝛽-cells12. Yet, the relevance of 𝛽-cell inceptor for glucose regulation through the INS1R/IGF1R axis has only been demonstrated for normoglycemic and insulin sensitive lean mice, questioning whether inceptor regulation of INS1R/IGF1R action also plays a role in glucose metabolism under conditions of diet-induced obesity and insulin resistance. Here we demonstrate that whole-body germline loss of inceptor improves glucose metabolism in diet-induced obese mice with only minimal effects on weight and body composition. To assess the effect in different tissues we performed proteomics in the global, neuronal and beta cell specific mouse knock-outs.

2024-01-17 | PXD046256 | Pride

Transcription profiling of mouse ventricles of IGF1R, IGF1R-caPI3K, IGF1R-dnPI3K, caPI3K, dnPI3K transgenic female mice at 3 months of age vs. non transgenic littermate controls

Project description:IGF1 and IGF1 receptors (IGF1R) are present in the adult heart and have been shown to be essential for myocardial performance. Insulin-like growth factor 1 (IGF1) is produced in numerous tissues particularly by the liver in response to growth hormone stimulation and is an important factor in the regulation of post-natal growth and development. We have generated and characterized transgenic mice over-expressing the IGF1R. We crossed IGF1R transgenic mice with dominant negative (dn)PI3K (p110) and with constitutively active (ca)PI3K(p110) transgenic mice. Expression profiling was performed on the ventricles of IGF1R, IGF1R-caPI3K, IGF1R-dnPI3K, caPI3K, dnPI3K transgenic female mice at 3 months of age. Non-transgenic littermates were used as controls.

2007-09-29 | E-GEOD-1143 | biostudies-arrayexpress

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