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

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.