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β-cell adaptation in mice expressing exclusively lamin C counteracts glucose intolerance associated with aging, obesity and diabetes

ABSTRACT: β-cell adaptation in mice expressing exclusively lamin C counteracts glucose intolerance associated with aging, obesity and diabetes

PROVIDER: PRJNA504768 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8178090.fastq.gz	Fastqsanger.gz
	SRR8178091.fastq.gz	Fastqsanger.gz
	SRR8178092.fastq.gz	Fastqsanger.gz
	SRR8178093.fastq.gz	Fastqsanger.gz
	SRR8178094.fastq.gz	Fastqsanger.gz

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β-cell adaptation in mice expressing exclusively lamin C counteracts glucose intolerance associated with aging, obesity and diabetes (LamineA-C_RNASeq)

Project description:β-cell adaptation in mice expressing exclusively lamin C counteracts glucose intolerance associated with aging, obesity and diabetes (LamineA-C_RNASeq)

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β-cell adaptation in mice expressing exclusively lamin C counteracts glucose intolerance associated with aging, obesity and diabetes (LamineA-C_RRBS)

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β-cell adaptation in mice expressing exclusively lamin C counteracts glucose intolerance associated with aging, obesity and diabetes (LamineA-C_RNASeq)

Project description:Lamin A, lamin C and progerin, produced by alternative RNA processing of LMNA gene, are intermediate filaments involved in nuclear and chromatin architecture. We investigate the ability of LMNALCS/LCS mice to adapt insulin level to physiological and physiopathologic conditions. The metabolic status of young vs old mice shows that old LMNALCS/LCS mice are obese but glucose tolerant due to an increased β cell mass and insulin secretion. By combining RNAseq and RRBS analysis, we observed a transcriptional disregulation of genes related to translation and mitochondria, confirmed by functionnal analysis, suggesting that LMNALCS/LCS mice set up a transcriptional program to adapt β cell mass and function to insulin demand. To investigate this point, we challenged young mice by inducing T1DM and T2DM. In these contexts, we show that LMNALCS/LCS mice are able to normalize their fasting glycemia by both increasing insulin secretion and regenerating β cells.

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β-cell adaptation in mice expressing exclusively lamin C counteracts glucose intolerance associated with aging, obesity and diabetes (LamineA-C_RRBS)

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β-cell adaptation in mice expressing exclusively lamin C counteracts glucose intolerance associated with aging, obesity and diabetes

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2019-11-09 | GSE122361 | GEO

Lamin and Lamin B receptor knockout

Project description:influence of lamin B rereceptor knockout and lamin A/C knockout on gene expression in cultured myoblast cells and in striated muscle tissue knockout samples are obtained by mating of heterozygous animals. Homozygous KO and wt animals of one litter are compared. Two boilogical replicates of KO samples are processed in parallel. wt samples are used as controls. One wt sample is processed per KO litter. Where appropriate two wt samples are used as biological replicates.

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Lamin and Lamin B receptor knockout

Project description:influence of lamin B rereceptor knockout and lamin A/C knockout on gene expression in cultured myoblast cells and in striated muscle tissue

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Changes in subcutaneous white adipose tissue cellular composition and molecular programs underlie glucose intolerance in persons with HIV

Project description:Subcutaneous adipose tissue (SAT) is a critical regulator of systemic metabolic homeostasis. Persons with HIV (PWH) have an increased risk of metabolic diseases and have significant alterations in SAT immune cells compared with the general population. We generated a comprehensive SAT atlas from 59 PWH with a spectrum of metabolic diseases to characterize cellular compositional and transcriptional changes associated with glucose intolerance and demographic characteristics. In PWH, glucose intolerance was associated with increased lipid-associated macrophages, CD4+ and CD8+ T effector memory cells, and decreased perivascular macrophages. We observed a coordinated intercellular regulatory program enriched for genes related to inflammation and lipid-processing with glucose intolerance that was also present in diabetic HIV-negative persons. Finally, CD4+ tissue resident cells were most strongly associated with altered whole tissue expression of genes related to lipid and glucose metabolism. These data provide a comprehensive assessment of SAT immune cells that may contribute to glucose intolerance.

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Endothelial TFEB improves glucose intolerance via upregulation of IRS1 and IRS2

Project description:Endothelial TFEB improves glucose intolerance via upregulation of IRS1 and IRS2

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