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  • Furthermore increased plasma levels of

    2021-09-16

    Furthermore, increased plasma levels of endoglin have been associated with diabetic complications (Valbuena-Diez et al., 2012). The involvement of soluble endoglin in a number of widespread pathologies demonstrates that endoglin is not only marker of endothelial integrity but also a causative factor for endothelial dysfunction. Investigators have also suggested that soluble endoglin levels may be used to assess the progression and treatment efficacy of cardiovascular diseases related to endothelial dysfunction (Rathouska et al., 2015). In consonance with our finding that gestational GC exposure led to increase atherogenic dyslipidemia and impaired nitric oxide biosynthesis that is associated with increase endoglin, report exist that endoglin levels increase during the early stages of atherosclerosis due to damaged endothelial EPZ004777 australia and then decrease during the later stages of the atherosclerotic process (Li et al., 2000). In another study, the endoglin levels of patients with hypertension and/or type 2 diabetes as well as target-organ damage such as retinopathy, were significantly higher than in the controls (Blázquez-Medela et al., 2010). In addition, endoglin was shown to act synergistically with soluble Flt-1 (sFlt-1), the natural antagonist of vascular endothelial growth factor (VEGF), to induce maternal endothelial dysfunction and severe preeclampsia in animal studies (Venkatesha et al., 2006). Therefore, the observed gestational GC-induced systemic and hepatic inflammation and oxidative stress together with alteration in foetal outcome (decreased foetal and placenta weights) may be due in part to the elevated endoglin in gestational GC-exposed rats. Earlier studies have reported contrasting findings on the effect of GC exposure on DPP-4 activity such as diminished DPP-4 activity on cultured human dermal fibroblasts (Sorrell et al., 2003), increased DPP-4 activity in thymocyte of male rats (Kraml et al., 2003) and unaltered circulating DPP-4 activity in asthmatic patients (Van Der Velden et al., 1999). However, it is interesting to note that the diabetogenic effect of GC exposure during late pregnancy was accompanied by elevated DPP-4 activity in this study. The report of Quarta and coworkers support the involvement of DPP-4 in GC-induced gluco-metabolic dysfunction because mice treated with glucagon-like peptide-1 (GLP-1) had improved glucose homeostasis while GC-exposed mice had impaired glucose homeostasis (Quarta et al., 2017). Elevated DPP-4 activity has been strongly associated with diabetes mellitus, IR (Röhrborn et al., 2015), metabolic syndrome (Lamers et al., 2011) and inflammation (Zhong et al., 2015). However, report has it that GC exposure increases DPP-4activity in thymocyte homogenates (Kraml et al., 2003) but to the best of our knowledge, this is the first study that report elevated DPP-4 activity in GC-exposed rats during late pregnancy. However, one of the most remarkable findings from this study is that gestational GC exposure in female rats caused elevated DPP-4 activity suggesting that the glucose dysregulation induced by gestational GC exposure is DPP-4 dependent in female rats. Glycogen synthase kinase-3 (GSK-3), a multi-tasking and housekeeping enzyme that has widespread influences on many cellular functions, plays an important role in energy metabolism, however, it is constitutively active in resting cells (Guo et al., 2016). It constitutes part of the insulin signalling pathway and has been reported to be involved in the pathogenesis of IR and diabetes mellitus (Nikoulina et al., 2000). Nevertheless, there has been conflicting documents on the role of GSK-3 in GC-induced IR. There are reports that GC-induced IR can either be associated or not associated with GSK-3 (Ruzzin et al., 2005; Vaughan et al., 2015) although GC has been reported to induce pancreatic β-cell apoptosis through GSK-3-dependent pathway that was accompanied by oxidative stress (Guo et al., 2016). Another study showed that GSK-3 is involved in oxidative stress-induced GC insensitivity in chronic obstructive pulmonary disease patients (Ngkelo et al., 2015).