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Intrauterine hyperglycemia during late gestation caused mitochondrial dysfunction in skeletal muscle of male offspring through CREB/PGC1A signaling

ABSTRACT: Intrauterine hyperglycemia during late gestation caused mitochondrial dysfunction in skeletal muscle of male offspring through CREB/PGC1A signaling

PROVIDER: PRJNA1074247 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27899710_1.fastq.gz	Fastqsanger.gz
	SRR27899710_2.fastq.gz	Fastqsanger.gz
	SRR27899711_1.fastq.gz	Fastqsanger.gz
	SRR27899711_2.fastq.gz	Fastqsanger.gz
	SRR27899712_1.fastq.gz	Fastqsanger.gz

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Intrauterine hyperglycemia during late gestation caused mitochondrial dysfunction in skeletal muscle of male offspring through CREB/PGC1A signaling

Project description:Short-term intrauterine hyperglycaemia significantly reduced lean mass in male offspring at 8 weeks, resulting in decreased exercise endurance and metabolic disorders. Disrupted organization and function of the mitochondria in skeletal muscle were also observed among them. Foetal exposure to hyperglycaemia decreased phosphorylated CREB and reduced the transcription of Ppargc1a.

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Intrauterine hyperglycemia during late gestation caused mitochondrial dysfunction in skeletal muscle of male offspring through CREB/PGC1A signaling

Project description:Short-term intrauterine hyperglycaemia inhibited the growth and reduced the lean mass of male offspring, leading to decreased endurance exercise capacity. The myofiber composition of the tibialis anterior muscle of GDM male offspring became more glycolytic and less oxidative. The morphology and function of mitochondria in the skeletal muscle of GDM male offspring were destroyed. A total of 993 upregulated and 653 downregulated genes were identified via RNA-seq. The transcription of specific genes related to metabolic processes and mitochondria according to RNA-seq was mostly inhibited.

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Intrauterine hyperglycemia exposure per se altered metabolic functions in F2 offspring via reprogramming F1 PGCs

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