安格普特4
妊娠期糖尿病
内科学
胰岛素抵抗
内分泌学
细胞凋亡
蛋白激酶B
促炎细胞因子
PI3K/AKT/mTOR通路
糖尿病
化学
癌症研究
医学
生物
炎症
怀孕
生物化学
妊娠期
基因
遗传学
作者
M Li,X-J Yang,G Y Zhang,D. Su,Lei Lan,Rui Li
出处
期刊:PubMed
日期:2018-08-01
卷期号:22 (16): 5056-5062
被引量:8
标识
DOI:10.26355/eurrev_201808_15697
摘要
To explore ANGPTL4 expressions in patients with gestational diabetes mellitus (GDM) and its underlying mechanism.We first detected serum expressions of ANGPTL4 in GDM patients and healthy pregnancies. Subsequently, effects of ANGPTL4 knockdown on apoptosis, proliferation, and cell cycle in 3T3-L1 cells were determined, respectively. Effects of ANGPTL4 on glucose uptake and adipocyte differentiation were also evaluated, respectively. The cytokine secretion in adipocytes transfected with sh-ANGPTL4 was detected by quantitative Reverse Transcriptase-Polymerase Chain Reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Furthermore, effects of ANGPTL4 knockdown on NF-kB and Akt pathway were detected by Western blot.ANGPTL4 was down-regulated in serum of GDM patients. In vitro experiments suggested that down-regulated ANGPTL4 inhibited apoptosis and promoted proliferation of 3T3-L1 cells. Meanwhile, down-regulated ANGPTL4 significantly inhibited glucose uptake and Akt pathway. However, ANGPTL4 expression did not affect cell cycle and adipocyte differentiation. Detection of inflammatory cytokines suggested that down-regulated ANGPTL4 resulted in increased expressions of inflammatory cytokines and activation of NF-kB pathway.ANGPTL4 is down-regulated in GDM and may participate in the GDM development by promoting insulin resistance and secretion of inflammatory cytokines.
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