Tertiary butylhydroquinone alleviates gestational diabetes mellitus in C57BL/KsJ‐Lep db/+ mice by suppression of oxidative stress. Issue 9 (3rd May 2019)

• Record Type: Journal Article
• Authors: Song, Hongbi; Xu, Yin; Yang, Xiaowu; Rong, Xiaoting; Wang, Ying; Wei, Na
• Is Part Of: Journal of cellular biochemistry. Volume 120:Issue 9(2019)
• Page Start: 15310
• Page End: 15319
• Publication Date: 2019-05-03
• Subjects: C57BL/KsJ‐Lep db/+ -- gestational diabetes mellitus -- nuclear factor erythroid 2‐related factor 2 -- oxidative stress -- tertiary butylhydroquinone; Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.28798
• Languages: English
• ISSNs: 0730-2312

Abstract

Abstract: Gestational diabetes mellitus (GDM) is a common disorder characterized by abnormal glucose metabolism during pregnancy, affecting 2% to 5% of pregnant women. Currently, clinical treatment for GDM is very limited. The present study was designed to investigate the effect and underlying molecular mechanism of tertiary butylhydroquinone (TBHQ) in a pregnant C57BL/KsJ‐Lep db/+ (referred to as db+) GDM mouse model. The results showed that nonpregnant db/+ mice did not show a diabetic phenotype, and TBHQ had no effect on glucose and insulin tolerance in these mice. Moreover, in db/+ pregnant mice exhibiting typical diabetes symptoms, such as hyperglycemia and hypoinsulinemia, TBHQ could remarkably decrease the blood glucose level, increase insulin level, and improve glucose and insulin intolerance. The results also revealed that TBHQ could inhibit oxidative stress in pregnant db/+ mice. Furthermore, TBHQ greatly improved offspring survival rate, glucose metabolism, and insulin tolerance. In addition, TBHQ inhibited oxidative stress by reducing malondialdehyde (MDA) and reactive oxygen species (ROS) levels and increased superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities. Moreover, we found that TBHQ activated the nuclear factor erythroid 2‐related factor 2 (Nrf2), thereby increasing the levels of Nrf2, and ultimately upregulating the expression of heme oxygenase 1 (NO‐1) and superoxide dismutase 2 (SOD2). In conclusion, our findings demonstrated that TBHQ alleviated GDM via Nrf2 activation. Abstract : In the present study, we first investigate the therapeutic potential of tertiary butylhydroquinone (TBHQ) on the db/+ genetic gestational diabetes mellitus (GDM) mouse model. The serum glucose and insulin levels before and during pregnancy are measured to evaluate the effect of TBHQ on GDM‐related symptoms. In addition, the potential underlying mechanism of TBHQ was also investigated.