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Role of placental fibrinogen-like protein 1 in gestational diabetes.

. 2020 Apr;218:73-80. Epub 2020 Jan 10
Lin Kang 1 , Hung-Yuan Li 2 , Horng-Yih Ou 3 , Pensee Wu 4 , Shu-Huei Wang 5 , Chih-Jen Chang 6 , Shin-Yu Lin 7 , Chao-Liang Wu 8 , Hung-Tsung Wu 9
Lin Kang 1 , Hung-Yuan Li 2 , Horng-Yih Ou 3 , Pensee Wu 4 , Shu-Huei Wang 5 , Chih-Jen Chang 6 , Shin-Yu Lin 7 , Chao-Liang Wu 8 , Hung-Tsung Wu 9
+ et al

[No authors listed]

Author information
  • 1 Department of Obstetrics and Gynecology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
  • 2 Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
  • 3 Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
  • 4 Institute for Science & Technology in Medicine, Keele University, Keele, United Kingdom.
  • 5 Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan.
  • 6 Department of Family Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
  • 7 Department of Obstetrics and Gynecology, National Taiwan University Hospital, Taipei, Taiwan.
  • 8 Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
  • 9 Graduate Institute of Metabolism and Obesity Sciences, Taipei Medical University, Taipei, Taiwan. Electronic address: wuht0716@tmu.edu.tw.

摘要


In view of the increasing prevalence of gestational diabetes mellitus (GDM) and the increased risks of delivering a macrosomic infant, developing preeclampsia, and suffering a perinatal death due to GDM, GDM has emerged as a growing public health problem. Although the placenta was suggested to play a crucial role in the pathology of GDM, the mechanisms that induce the development of GDM are still obscure. Fibrinogen-like protein (FGL)-1 is a hepatokine that plays an important role in hepatogenesis, as well as in nonalcoholic fatty liver disease and diabetes. Although FGL-1 is also expressed by the placenta, the pathophysiological role of FGL-1 in GDM is still unknown. In this study, FGL-1 levels were evaluated in 45 subjects with (n = 16) or without (n = 29) GDM. We found that FGL-1 was mainly expressed by placental trophoblasts, and FGL-1 expression was significantly higher in subjects with GDM. FGL-1 increased trophoblast proliferation through an extracellular signal-regulated kinase 1/2-dependent pathway. In addition, plasma concentrations of FGL-1 were higher in subjects with GDM, and the increased circulating FGL-1 might contribute to systemic insulin resistance. FGL-1 disrupted the gluconeogenic action of insulin in HepG2 cells, and decreased insulin-induced glucose uptake by L6 myotubes. Taken together, placental FGL-1 possibly plays a role in the impairment of insulin function in the development of GDM, and it might be a novel biomarker for diagnosing GDM.