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    • Routine administration of exogenous GC is pertinent during l

    2022-06-16

    Routine administration of exogenous GC is pertinent during late gestation, particularly in women who are at risk of delivering a preterm infant, aiming at ensuring proper neonatal outcome and survival (Kamath-Rayne et al., 2012). Unfortunately, despite its beneficial roles in foetal survival, various studies have reported programmed metabolic disorders such as IR, atherogenic dyslipidemia, increased body weight and type 2 diabetes in mothers (Holness and Sugden, 2001; Gomes et al., 2014) and later life of offsprings that were exposed to prenatal GC exposure (O’Regan et al., 2004). Dipeptidyl peptidase IV (DPP-4) is also a newly identified adipokine that is located on the surface of various fgfr inhibitor and exists in plasma and body fluids (Lambeir et al., 2003). Initially, it was believed that DPP-4 only play a predominant role in glucose metabolism by degrading incretins; glucagon like peptide-1 (GLP-1), glucose-dependent insulinotrophic peptide (GIP) (Zhong et al., 2013). Recent reports have also documented its role in pathogenesis of inflammation and cardiometabolic disorder (CMD) (Wronkowitz et al., 2014; Zhong et al., 2015). Glycogen synthase kinase 3 (GSK3) is a serine/threonine protein kinase that is involved in the storage of glucose into glycogen. Increased GSK3 activity is an early event in the development of IR where glycogen synthesis is impaired in type 2 diabetes (Eldar-Finkelman et al., 1999; Nikoulina et al., 2000) and inhibition of GSK3 in Zucker diabetic fatty rats leads to an improvement in both insulin action and glucose uptake (Cline et al., 2002). Furthermore, GCs has also been reported to cause impaired insulin action through GSK-3-dependent (Ruzzin et al., 2005) and independent (Vaughan et al., 2015) pathways. Plasma endoglin levels have been positively correlated with basal glycemia in patients with diabetes and hypertension, and with glycated haemoglobin in all patients with diabetes (Blázquez-Medela et al., 2010). Endoglin, also known as CD105, is one of the key proteins that is synthesized and released by the placenta. It is highly expressed on the vascular endothelium and syncytiotrophoblast and is known to play a role in angiogenesis and in the regulation of the vascular tone through its interaction with endothelial nitric oxide synthase (eNOS) (Robinson and Johnson et al., 2007; Smith and Wear, 2009).
    Materials and methods
    Results
    Discussion Regardless of obvious beneficial effects of GC on acceleration of foetal lung and cardiomyocytes maturation (Kamath-Rayne et al., 2012; Rog-Zielinska et al., 2015), the current study revealed that GC exposure during late pregnancy induces IR and altered foetal outcome. This finding is in line with previous studies in animals (O’Regan et al., 2004; Gomes et al., 2014) as well as in humans (Di Dalmazi et al., 2012). However, IR which is the predominant mechanism involved in the diabetogenic effects of GC based therapy is an independent risk factor for CVD and has been strongly associated with vascular inflammation (Paneni et al., 2013). From the findings of this study, it is observed that GC exposure in pregnant rats resulted in IR that is accompanied by reduced body weight gain, increased liver weight, decreased visceral adiposity and uterine fat suggesting that the IR induced by gestational GC exposure is independent of body weight gain, visceral and uterine fat accumulation that is expected in pregnancy but associated with liver inflammation and hypertrophy. However, the reduced body weight may be as a result of reduced food intake as observed in this study. Decreased body weight and food intake shown in this study are consistent with previous study that reported that gestational GC exposure led to weight loss (Gomes et al., 2014) and reduced food intake in animal studies (Holness and Sugden, 2001). In addition, gestational GC-induced adverse birth outcome in the present study is in consonance with previous findings in experimental animals (Schwitzgebel et al., 2009). Adverse prenatal environment such as exposure to excess GC have been reported to lead to metabolic imprinting including intrauterine growth restriction (IUGR) characterized by low birth weight and negative impact on the placenta that is needed to sustain foetal growth which are predictive of increased development of CMD such as IR, type 2 diabetes, obesity and hypertension in later life of offsprings (Seckl, 2004; Cunningham et al., 2010).