Intrauterine hyperglycemia during late gestation caused mitochondrial dysfunction in skeletal muscle of male offspring through CREB/PGC1A signaling
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. Overall design: We firstly observed the adverse mitochondrial structure and function in GDM adult male mice. To explore the effect of intrauterine hyperglycemia on foetal skeletal muscle, we ran RNA-sequence on limb muscle of foetal mice at embryonic day 18.5. Then, we performed the gene expression profiling analysis using data obtained from RNA-seq of skeletal muscle of CTR or GDM feotal mice.