Fig. 3: In vivo and in vitro experiments in myoblasts demonstrated that high glucose concentrations impaired mitochondrial transcription and function by inhibiting Ppargc1α transcription. | Nutrition & Diabetes

Fig. 3: In vivo and in vitro experiments in myoblasts demonstrated that high glucose concentrations impaired mitochondrial transcription and function by inhibiting Ppargc1α transcription.

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

Fig. 3

A Oxygen consumption rate (OCR) was decreased in GDM male myoblast (n = 8, 2-way ANOVA); B Analysis of the OCR produced during basal respiration, ATP-linked process, maximal respiration, proton leakage and nonmitochondrial oxidation showed only OCR in mitochondria was decreased in GDM male myoblast (n = 24, multiple t tests); C Representative mRNA levels of genes related to mitochondrial biogenesis and metabolism were also inhibited in GDM foetal isolated primary myoblasts determined by RT-qPCR (n = 5, multiple t tests); D Representative mRNA levels of genes mentioned above were time-dependently down-regulated on C2C12 incubation in high glucose (n = 3, multiple t tests); E Representative mRNA levels of genes mentioned above were lower in C2C12 after Ppargc1α silencing (n = 6, multiple t tests); F Representative mRNA levels of genes mentioned above were higher in C2C12 after Ppargc1α overexpression (n = 5, multiple t tests); G TEM showed Ppargc1α positively regulated the formation of mitochondria in C2C12 myoblasts. The data are expressed as the mean ± SEM. Significance of the differences: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

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