Fig. 1: Intrauterine hyperglycaemia during late gestation leads to sarcopenia and causes mitochondrial abnormalities and insulin resistance in skeletal muscle in F1 males at 8 weeks.
A GDM male offspring were composed of more adiposity and less muscle (nCTR= 12, nGDM = 8, each “n” refers to a single mouse, two-tailed t test); B GDM male offspring consumed less oxygen and produced less carbon dioxide (n = 8, 2-way ANOVA); C No difference in gripping force between two groups was found (nCTR= 13, nGDM = 8, two-tailed t test); D Endurance exercise capacity test was demonstrated to be poor in GDM male offspring (nCTR= 5, nGDM = 6, two-tailed t test); E QUA and TA weights normalised to body weight were significantly lighter in GDM male offspring (nCTR= 6, nGDM = 5, two-tailed t test); F TEM of SOL (a, b) showed swollen mitochondria with vacuoles, SDH staining of QUA (c, d) and GAS (e, f) revealed smaller staining area in GDM male offspring. Immunofluorescence of TA (g, h) showed composition of specific metabolic type of myofibers; G CSA of TA in GDM male offspring was smaller (n = 15); H: Myofiber type distribution according to immunofluorescent staining in TA showed glycolytic myofibers (MHCIIb) significantly increased, while oxidative myofibers (MHCI and MHCIIa) tended to decrease (n = 11, multiple t tests); I Genes related to mitochondrial biogenesis and oxidative metabolism by RT-qPCR were found to be inhibited in GDM male offspring soleus (nCTR= 5, nGDM = 4, multiple t tests); J Representative western blotting images showed insulin signalling proteins were inhibited to be phosphorylated in GDM male offspring muscle at basal and insulin stimulation (n = 3, multiple t tests); Data are expressed as the mean ± SEM. Significance of the differences: *p < 0.05, **p < 0.01, ***p < 0.001.
