ATP Synthase β-subunit Abnormality in Pancreas Islets of Rats with Polycystic Ovary Syndrome and Type 2 Diabetes Mellitus
10.1007/s11596-017-1717-9
- Author:
LI WEI
1
;
LI SAI-JIAO
;
YIN TAI-LANG
;
YANG JING
;
CHENG YAN
Author Information
1. Department of Gynecology and Obstetrics
- Keywords:
polycystic ovarian syndrome;
type 2 diabetes mellitus;
ATP synthase β-subunit;
pancreas islet
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2017;37(2):210-216
- CountryChina
- Language:Chinese
-
Abstract:
This study investigated the abnormal expression of ATP synthase β-subunit (ATPsyn-β) in pancreas islets of rat model of polycystic ovary syndrome (PCOS) with type 2 diabetes mellitus (T2DM),and the secretion function changes after up-regulation of ATP5b.Sixty female SD rats were divided into three groups randomly and equally.The rat model of PCOS with T2DM was established by free access to the high-carbohydrate/high-fat diet,subcutaneous injections of DHEA,and a single injection of streptozotocin.The pancreas was removed for the detection of the ATPsyn-β expression by immunohistochemical staining,Western blotting and reverse transcription-PCR (RT-PCR).The pancreas islets of the rats were cultured,isolated with collagenase Ⅴ and purified by gradient centrifugation,and the insulin secretion after treatment with different glucose concentrations was tested.Lentivirus ATP5b was successfully constructed with the vector of GV208 and transfected into the pancreas islets for the over-expression of ATPsyn-β.The insulin secretion and intracellular ATP content were determined after transfection of the PCOS-T2DM pancreas islets with Lenti-ATP5b.The results showed that the expression of ATPsyn-β protein and mRNA was significantly decreased in the pancreas of PCOS-T2DM rats.The ATP content in the pancreas islets was greatly increased and the insulin secretion was improved after the up-regulation of ATPsyn-β in the pancreas islets transfected with lenti-ATP5b.These results indicated that for PCOS,the ATPsyn-β might be one of the key factors for the attack of T2DM.
