Fig. 3: Prenatal AE causes transgenerational defects in insulin secretion of male offspring.

a HOMA-β levels of F1 male offspring mice at 8 weeks of age (n = 6). b Serum insulin levels at 0, 15, and 30 min during insulin release test (IRT) after intraperitoneal glucose injection and the corresponding AUC in F1 male offspring at 8 weeks of age (n = 6). c Insulinogenic index during the IRT of F1 male offspring at 8 weeks of age (n = 6). d Islets isolated from Ctrl- and AE-F1 male offspring at 8 weeks of age were stimulated with 3.3 mM or 16.7 mM glucose and insulin secretion was assayed (n = 3). e HOMA-β levels of F1 male offspring mice at 32 weeks of age (n = 6). f Serum insulin levels at 0, 15, and 30 min of IRT after intraperitoneal glucose injection and the corresponding AUC in F1 male offspring at 32 weeks of age (n = 6). g Insulinogenic index during the IRT of F1 male offspring at 32 weeks of age (n = 6). h Islets isolated from Ctrl- and AE-F1 male offspring at 32 weeks of age were stimulated with 3.3 mM (Ctrl: n = 5; AE: n = 3) or 16.7 mM (Ctrl: n = 4; AE: n = 5) glucose and insulin secretion was assayed. i HOMA-β levels of F2 male offspring mice at 8 weeks of age (n = 6). j Serum insulin levels at 0, 15, and 30 min of IRT after intraperitoneal glucose injection and the corresponding AUC in F2 male offspring at 8 weeks of age (n = 5). k Insulinogenic index during the IRT of F2 male offspring at 8 weeks of age (n = 5). l Islets isolated from Ctrl- and AE-F2 male offspring at 8 weeks of age were stimulated with 3.3 mM (Ctrl: n = 5; AE: n = 4) or 16.7 mM (Ctrl: n = 5; AE: n = 5) glucose and insulin secretion was assayed. m Representative pancreatic sections were stained for INSULIN (green) and DAPI (blue), and insulin intensities, as well as pancreatic insulin contents, were quantified from 32-week-old F1 mice and 8-week-old F2 mice (n = 3‒5). Scale bars, 30 μm. Data are presented as mean ± SEM. *P < 0.05, **P < 0.01; significance is assessed by two-tailed unpaired Student’s t-test.