The impact of early pregnancy metabolic disorders on pregnancy outcome and the specific mechanism

Table 1 Metabolism-related genes and miscarriage

Gene	Target	Study model	Effect	Refs
SGLT1	SGLT1	C57BL/6 J mice Human Endometrial Stromal Cells	Reduce glycogen synthesis	[52]
PPARα	PPARs	C57BL/6 J mice	Inhibit fatty acid uptake and fatty acid transporter protein expression	[74]
COXs TBXA2R	PLA2α/COX-2	CD1 mice	Increase synthesis of prostaglandins, leading to uterine contractions	[84, 85]
GSTM1 GSTT1	Glutathione	Human blood samples	Increase oxidative stress	[112, 113]
NOS3	NO	Human blood samples	Decrease levels of NO cause vasoconstriction, which in turn leads to impaired placental perfusion and an increased risk of infarction	[124]
EMP2	FAK/Src/HIF-1α	C57BL/6 mice Human placenta samples	Inhibite angiogenesis and oxidative phosphorylation	[127]
ADIPOQ	Lipocalin	Human blood samples	Unknown	[129]
CFHrs1065489G > T	C3	Human blood samples	Homocysteine and prolactin levels	[131]
CFH rs1061170 TC	C3	Human blood samples	Uric acid and triglyceride levels	[131]

SGLT1 sodium-glucose co-transporter 1, PPAR Peroxisome proliferator activated receptor, COX cyclooxygenase, TBXA2R thromboxane A2 receptor, PLA2α phospholipase A2α, GST glutathione S-transferase, NOS3 nitric oxide synthase 3, EMP2 epithelial membrane protein 2, FAK focal adhesion kinase, Src steroid receptor coactivator, ADIPOQ Adiponectin

ISSN: 2047-783X