期刊
REPRODUCTIVE SCIENCES
卷 26, 期 2, 页码 223-232出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/1933719118766253
关键词
gestational diabetes mellitus; insulin resistance; trophoblasts; 1, 25-dihydroxyvitamin D3; mammalian target of rapamycin
资金
- National Natural Science Foundation of China [81671483]
- National Key Technologies R&D Program of China [2015BAI13B06]
Gestational diabetes mellitus (GDM) is the primary cause of maternal and fetal morbidity and mortality. Insulin resistance (IR) is pivotal to GDM pathogenesis, and mammalian target of rapamycin (mTOR) is a critical regulator of GDM. An increasing amount of evidence indicates that vitamin D deficiency is a risk factor for GDM. However, there are few reports on the effect of IR on GDM placentas. The present study aims to verify that 1,25-dihydroxyvitamin D3 (1,25(OH)(2)D-3) can ameliorate trophoblast IR by suppressing mTOR signaling. An IR BeWo cell model was established in the presence of high insulin and glucose medium. The IR level and mTOR activation with or without 1,25(OH)(2)D-3 treatment were evaluated. The IR cells exhibited excessive mTOR signaling activation, upregulated inflammatory factor levels, and extensive lipid infiltration. However, 1,25(OH)(2)D-3 reversed mTOR activation and reduced the IR level and lipid infiltration. In addition, 1,25(OH)(2)D-3 treatment in GDM placental explants blocked the aberrant, increased levels of leptin, TNF-, and IL-6. Therefore, 1,25(OH)(2)D-3 treatment protects trophoblasts against high IR mainly through suppressing mTOR signaling, and this mechanism may serve as a potential therapy for patients with GDM.
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