Fig. 5: Intrauterine hyperglycaemia during late gestation caused metabolic disorders, sarcopenia, and mitochondrial abnormalities in the skeletal muscle of 16-week-old F2 males.
A Growth curves of F2 male offspring showed GC and GG male were much heavier than others from 10 weeks old on (nCC= 21, nGC = 41, nCG = 34, nGG = 20, 2-way ANOVA); B Evident impaired GTT was observed in the GC and GG male mice compared to CC, CG had higher glucose level at 60 and 120 min compared to CC (nCC= 10, nGC = 14, nCG = 10, nGG = 9, 2-way ANOVA). AUC, area under the curve (ordinary one-way ANOVA); a.u., arbitrary units; C ITT line chart showed GC was mostly insulin resistant compared to other groups, CG had higher glucose level at 30 and 60 min compared to CC. AUC demonstrated GC male showed impaired ITT compared to CC and GG (nCC= 10, nGC = 8, nCG = 8, nGG = 10, 2-way ANOVA, AUC, ordinary one-way ANOVA); D Less muscle was detected in GC, more fat was detected in GC and CG males in body composition analysis (nCC= 18, nGC = 25, nCG = 17, nGG = 15, ordinary one-way ANOVA); E No difference was detected in gripping force among F2 generation (nCC= 11, nGC = 24, nCG = 24, nGG = 10, ordinary one-way ANOVA); F Compared to CC male, four muscle weights in GC as well as GAS and soleus of CG males were significantly lighter (nCC= 18, nGC = 25, nCG = 18, nGG = 17, ordinary one-way ANOVA); G TEM of SOL in the GC and CG groups exhibited severe mitochondrial abnormalities; H Quantification of mRNA levels of Ppargc1α in the soleus showed a decrease in F2 generation (nCC= 5, nGC = 5, nCG = 6, nGG = 6, ordinary one-way ANOVA); Data are expressed as the mean ± SEM. Significance of the differences: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 vs. CC; #p < 0.05, ##p < 0.01, ###p < 0.001, ####p < 0.0001 vs. GC; &p < 0.05, &&p < 0.01 vs. CG.
