PMID- 36063867
OWN - NLM
STAT- MEDLINE
DCOM- 20221114
LR  - 20221130
IS  - 1095-6840 (Electronic)
IS  - 0016-6480 (Linking)
VI  - 329
DP  - 2022 Dec 1
TI  - The effect of genistein on IGF-1, PlGF, sFLT-1 and fetoplacental development.
PG  - 114122
LID - S0016-6480(22)00147-2 [pii]
LID - 10.1016/j.ygcen.2022.114122 [doi]
AB  - The mechanisms by which genistein, a phytoestrogen, affects fetoplacental 
      development adversely are still poorly understood. It is reported that genistein 
      ingestion modulates thyroid functions, leptin hormone, C-reactive protein, and 
      thyroxin kinase activities. In this study, we evaluated changes in serum and 
      placental insulin-like growth factor-I (IGF-1), placental growth factor (PIGF), 
      and soluble fms-like tyrosine kinase-1 (sFLT-1) in pregnant rats exposed to 
      genistein using ELISA. According to the treatments, Rats were divided into 
      control, 2 mg genistein, and 4 mg genistein groups. Genistein groups were 
      administered with the doses orally from gestational day (GD) one onwards until 
      sacrifice, while the control group received an equal volume of distilled water 
      the vehicle. At GD-12, GD-16, and GD-20, serum samples and placenta homogenates 
      were prepared from maternal blood samples and the placenta and were analysed to 
      determine the concentration of IGF-1, sFLT-1, and PIGF. Serum IGF-1 and PIGF were 
      both increased in all genistein groups at GD-12 and GD-16, and at GD-20 in the 
      4 mg group. However, serum IGF-1and PIGF levels were decreased in the placenta 
      from all genistein groups at GD-20. Placenta sFLT-1 levels increased at both 
      GD-16 and GD-20 in genistein-treated rat serum. An initial decrease in placental 
      sFLT-1 at GD-12 was followed by an increase at GD-16 and finally a decrease at 
      GD-20 in all genistein-treated rats. The sFL-1/PlGF ratio in placenta samples of 
      genistein-exposed rats was decreased at GD-16 and increased at GD-20, while the 
      reverse was recorded in the serum sample at the same gestational periods. The 
      fetoplacental growth disruption mechanism of genistein can be partly explained by 
      its interference with placental growth factor signalling.
CI  - Copyright (c) 2022 Elsevier Inc. All rights reserved.
FAU - Awobajo, F O
AU  - Awobajo FO
AD  - Department of Physiology. Faculty of Basic Medical Sciences, College of Medicine 
      University of Lagos, Nigeria. Electronic address: fawobajo@unilag.edu.ng.
FAU - Medobi, E F
AU  - Medobi EF
AD  - Department of Physiology. Faculty of Basic Medical Sciences, College of Medicine 
      University of Lagos, Nigeria.
FAU - Abdul, M W
AU  - Abdul MW
AD  - Department of Physiology. Faculty of Basic Medical Sciences, College of Medicine 
      University of Lagos, Nigeria.
FAU - Aminu, B B
AU  - Aminu BB
AD  - Department of Physiology. Faculty of Basic Medical Sciences, College of Medicine 
      University of Lagos, Nigeria.
FAU - Ojimma, C T
AU  - Ojimma CT
AD  - Department of Physiology. Faculty of Basic Medical Sciences, College of Medicine 
      University of Lagos, Nigeria.
FAU - Dada, O G
AU  - Dada OG
AD  - Department of Physiology. Faculty of Basic Medical Sciences, College of Medicine 
      University of Lagos, Nigeria.
LA  - eng
PT  - Journal Article
DEP - 20220905
PL  - United States
TA  - Gen Comp Endocrinol
JT  - General and comparative endocrinology
JID - 0370735
RN  - 0 (Biomarkers)
RN  - DH2M523P0H (Genistein)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - 144589-93-5 (Placenta Growth Factor)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1)
SB  - IM
MH  - Animals
MH  - Female
MH  - Pregnancy
MH  - Rats
MH  - Biomarkers/metabolism
MH  - *Genistein/pharmacology
MH  - Insulin-Like Growth Factor I/metabolism
MH  - Placenta/metabolism
MH  - Placenta Growth Factor/metabolism/pharmacology
MH  - *Pre-Eclampsia/metabolism
MH  - Vascular Endothelial Growth Factor A/metabolism
MH  - Vascular Endothelial Growth Factor Receptor-1/metabolism/pharmacology
OTO - NOTNLM
OT  - Foetal development
OT  - Genistein
OT  - Growth factor
OT  - Placental
OT  - sFLT-1
COIS- Declaration of Competing Interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2022/09/06 06:00
MHDA- 2022/11/09 06:00
CRDT- 2022/09/05 19:22
PHST- 2021/08/11 00:00 [received]
PHST- 2022/08/03 00:00 [revised]
PHST- 2022/08/27 00:00 [accepted]
PHST- 2022/09/06 06:00 [pubmed]
PHST- 2022/11/09 06:00 [medline]
PHST- 2022/09/05 19:22 [entrez]
AID - S0016-6480(22)00147-2 [pii]
AID - 10.1016/j.ygcen.2022.114122 [doi]
PST - ppublish
SO  - Gen Comp Endocrinol. 2022 Dec 1;329:114122. doi: 10.1016/j.ygcen.2022.114122. 
      Epub 2022 Sep 5.