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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)

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

PROVIDER: PRJNA504770 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8178095_1.fastq.gz	Fastqsanger.gz
	SRR8178095_2.fastq.gz	Fastqsanger.gz
	SRR8178096_1.fastq.gz	Fastqsanger.gz
	SRR8178096_2.fastq.gz	Fastqsanger.gz
	SRR8178097_1.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

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

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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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