PMID- 30103849
OWN - NLM
STAT- MEDLINE
DCOM- 20191206
LR  - 20191217
IS  - 1448-5990 (Electronic)
IS  - 1031-3613 (Linking)
VI  - 31
IP  - 2
DP  - 2019 Jan
TI  - Amelioration by quercetin of insulin resistance and uterine GLUT4 and ERalpha gene 
      expression in rats with polycystic ovary syndrome (PCOS).
PG  - 315-323
LID - 10.1071/RD18222 [doi]
AB  - Insulin resistance (IR) and infertility are two major complications of polycystic 
      ovary syndrome (PCOS), which are the results of changes in certain parts of the 
      reproductive and metabolic systems. We aimed to observe the effect of quercetin 
      on dehydroepiandrosterone (DHEA)-induced PCOS and insulin resistance in rats. All 
      animals were divided into five groups and DHEA was used to induce PCOS. 
      Bodyweight and ovarian morphology of all groups were observed. Fasting blood 
      glucose and insulin levels were analysed. The homeostasis model assessment of 
      insulin resistance (HOMA-IR) method was used for IR level determination. The 
      expression of oestrogen receptor alpha (ERalpha) and glucose transporter 4 (GLUT4) genes 
      in the uterus was examined by real-time polymerase chain reaction. Liver 
      hexokinase (HK) and glucokinase (GK) activity was determined using 
      spectrophotometry. Quercetin significantly improved the IR state in PCOS rats. 
      PCOS resulted in a decrease in liver GK and an increase in liver HK specific 
      activity, whereas quercetin increased both liver HK and GK activity. Our data 
      also showed a significant reduction in uterine ERalpha and GLUT4 expression in the 
      PCOS group, which was increased by quercetin. A remarkable effect of quercetin 
      was the intensive reduction of PCOS-IR and significant induction of uterine GLUT4 
      and ERalpha gene expression; it could thus be a possible effective treatment for PCOS 
      and its complications, IR and infertility.
FAU - Neisy, Asma
AU  - Neisy A
AD  - Biochemistry Department, School of Medicine, Shiraz University of Medical 
      Sciences, Shiraz, 7134845794 Iran.
FAU - Zal, Fatemeh
AU  - Zal F
AD  - Biochemistry Department, School of Medicine, Shiraz University of Medical 
      Sciences, Shiraz, 7134845794 Iran.
FAU - Seghatoleslam, Atefeh
AU  - Seghatoleslam A
AD  - Biochemistry Department, School of Medicine, Shiraz University of Medical 
      Sciences, Shiraz, 7134845794 Iran.
FAU - Alaee, Sanaz
AU  - Alaee S
AD  - Reproductive Biology Department, School of Advanced Medical Sciences and 
      Technologies, Shiraz University of Medical Sciences, Shiraz, 7134845794 Iran.
LA  - eng
PT  - Journal Article
PL  - Australia
TA  - Reprod Fertil Dev
JT  - Reproduction, fertility, and development
JID - 8907465
RN  - 0 (Antioxidants)
RN  - 0 (Estrogen Receptor alpha)
RN  - 0 (Glucose Transporter Type 4)
RN  - 0 (Slc2a4 protein, rat)
RN  - 459AG36T1B (Dehydroepiandrosterone)
RN  - 9IKM0I5T1E (Quercetin)
SB  - IM
MH  - Animals
MH  - Antioxidants/*pharmacology
MH  - Dehydroepiandrosterone
MH  - Disease Models, Animal
MH  - Estrogen Receptor alpha/genetics/*metabolism
MH  - Female
MH  - Gene Expression/*drug effects
MH  - Glucose Transporter Type 4/genetics/*metabolism
MH  - Insulin Resistance/*physiology
MH  - Polycystic Ovary Syndrome/chemically induced/genetics/*metabolism
MH  - Quercetin/*pharmacology
MH  - Rats
MH  - Uterus/*drug effects/metabolism
EDAT- 2018/08/15 06:00
MHDA- 2019/12/18 06:00
CRDT- 2018/08/15 06:00
PHST- 2018/02/17 00:00 [received]
PHST- 2018/07/05 00:00 [accepted]
PHST- 2018/08/15 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
PHST- 2018/08/15 06:00 [entrez]
AID - RD18222 [pii]
AID - 10.1071/RD18222 [doi]
PST - ppublish
SO  - Reprod Fertil Dev. 2019 Jan;31(2):315-323. doi: 10.1071/RD18222.