Circulating leptin and angiogenic factors in preeclampsia patients.
Leptin, one of adipocytokines, plays a wide range of important roles in reproductive biology. We have previously reported that low hypo-adiponectinemia might be involved in the pathophysiology of overweight preeclampsia (PE) patients. Moreover, recent reports have underscored the importance of circulating angiogenic factors in the pathophysiology of PE. Here, we examined whether leptin in conjunction with adiponectin and/or angiogenic factors plays some role in the pathophysiology of PE. We performed a cross-sectional study in 34 PE patients and normal pregnancies matched for gestational age and body mass index as controls. We measured serum concentrations of leptin, adiponectin, the angiogenic factors vascular endothelial growth factor (VEGF), placental growth factor, and the soluble VEGF receptors sFlt-1 and sFlk-1. We observed that leptin levels in PE patients were significantly higher compared with those in controls, but did not observe significant differences between normal- and overweight patients in both groups. We also showed a significant negative correlation between leptin and adiponectin in controls, but not in PE patients. There was a significant correlation between leptin and sFlt-1 in PE patients, while there were significant differences of body mass index, mean blood pressure and proteinuria between high and low leptin/sFlt-1 ratio group in PE patients. Moreover, there was a significant difference of leptin level between IUGR and normal growth group in PE patients. These results suggest that the circulating increased leptin might be derived mainly from the placenta and regulated by the placental hypoxic condition, whereas adiponectin might be derived mainly from adipose tissue; and that leptin might play some role through insulin resistance, autonomic activation, or direct effect on endothelium with other angiogenic factors in pathophysiology of PE compared with the exaggerated release of adiponectin from adipose tissue.
Nakatsukasa
Hideki
H
Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Masuyama
Hisashi
H
Takamoto
Norio
N
Hiramatsu
Yuji
Y
D052242:Adiponectin / Q000097:blood; D000328:Adult; D043925:Angiogenesis Inducing Agents / Q000097:blood*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007333:Insulin Resistance / Q000502:physiology; D020738:Leptin / Q000097:blood* / Q000502:physiology; D008565:Membrane Proteins / Q000097:blood; D050177:Overweight / Q000097:blood / Q000150:complications; D011225:Pre-Eclampsia / Q000097:blood* / Q000209:etiology; D011247:Pregnancy; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000097:blood
C499918:ADIPOQ protein, human; D052242:Adiponectin; D043925:Angiogenesis Inducing Agents; D020738:Leptin; D008565:Membrane Proteins; C098069:PIGF protein, human; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; C501162:FLT1 protein, human; D040281:Vascular Endothelial Growth Factor Receptor-1; D040301:Vascular Endothelial Growth Factor Receptor-2