Epigenetic repression of AT2 receptor is involved in β cell dysfunction and glucose intolerance of adult female offspring rats exposed to dexamethasone prenatally

MDH1 and MDH2 Promote Cell Viability of Primary AT2 Cells by Increasing Glucose Uptake

“…The activity of the NADPH-generating enzyme was positively correlated with the backfat thickness of live pigs [ 23 ]. The results of the study showed that the correlation coefficients between MDH and backfat thickness and lean meat percentage were 0.36 and −0.612, respectively [ 24 ]. The study found that using NADPH-producing enzyme activity as an early selection index to select lean pigs has more advantages than using backfat thickness as a selection index and control body fat deposition [ 25 ].…”

The Angiotensin AT2Receptor: From a Binding Site to a Novel Therapeutic Target

“…These findings were confirmed by a follow up study in which treatment of pregnant mice with PD123319 led to a reduced number of b-cells in neonates and an impairment of their insulin secretory function (Leung et al, 2014). Prenatal exposure to dexamethasone is known as well to impair b-cell function in offspring, which interestingly could be restored by AT 2 R overexpression in an in vitro model (Kou et al, 2020). In line with this, STZ-diabetic, C21-treated rat neonates had lower blood glucose, better insulin secretory function, and higher islet-cell mass than nontreated controls (Wang L et al, 2017), which could be due to AT 2 R-mediated improved b-cell function or protection of islets from STZ toxicity as shown in adult rats (Shao et al, 2014).…”

Epigenetic programming mediates abnormal gut microbiota and disease susceptibility in offspring with prenatal dexamethasone exposure

“…Series of our previous animal experiments showed that PDE could lead to offspring multi-organ developmental programming and susceptibility to various diseases, such as osteoporosis, 46 depression 62 and abnormal glucose metabolism, 63 through “multi-axis, multi-organ, and multi-target” effects. 64 , 65 , 66 In the present study, our study focused on the gut-liver axis and confirmed that the abnormal gut microbiota induced by PDE renders cholestatic liver injury in female adult offspring rats.…”