The Relationship between Maternal Plasma Leptin Levels and Fetal Growth Restriction

Mise, Hiroko; Yura, Shigeo; Itoh, Hiroaki; Nuamah, Mercy A.; Takemura, Masanori; Sagawa, Norimasa; Fujii, Shingo

doi:10.1507/endocrj.k06-225

Cited by 53 publications

(50 citation statements)

References 30 publications

(44 reference statements)

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“…We observed a significant difference of leptin level between IUGR and normal growth group in PE patients; these data are consistent with a recent report [34] and suggested that placental insufficiency might affect leptin production in placenta. Moreover, the placental hypoxic condition, which results from inadequate trophoblast invasion of maternal spiral arteries in PE [3,4], has been demonstrated to cause not only the abnormal production of angiogenic factors, such as VEGF, PlGF, sFlt-1 and sEng [6][7][8][9][10][11], but also placental leptin production [35,36].…”

Section: Discussionsupporting

confidence: 92%

Circulating Leptin and Angiogenic Factors in Preeclampsia Patients

et al. 2008

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Abstract. 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.

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Section: Discussionsupporting

confidence: 92%

Circulating Leptin and Angiogenic Factors in Preeclampsia Patients

et al. 2008

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“…Humans have interstitial implantation compared with the superficial form with fewer invasive trophoblasts seen in Old World monkeys (46). CCK has been shown to regulate leptin levels (47), and leptin expression levels have been shown to change in the obstetrical syndromes of preeclampsia and intrauterine growth retardation (48). GH2 also increases its expression in patients with preeclampsia (49).…”

Section: Resultsmentioning

confidence: 99%

Distinct genomic signatures of adaptation in pre- and postnatal environments during human evolution

Uddin¹,

Goodman

Erez

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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The human genome evolution project seeks to reveal the genetic underpinnings of key phenotypic features that are distinctive of humans, such as a greatly enlarged cerebral cortex, slow development, and long life spans. This project has focused predominantly on genotypic changes during the 6-million-year descent from the last common ancestor (LCA) of humans and chimpanzees. Here, we argue that adaptive genotypic changes during earlier periods of evolutionary history also helped shape the distinctive human phenotype. Using comparative genome sequence data from 10 vertebrate species, we find a signature of human ancestry-specific adaptive evolution in 1,240 genes during their descent from the LCA with rodents. We also find that the signature of adaptive evolution is significantly different for highly expressed genes in human fetal and adult-stage tissues. Functional annotation clustering shows that on the ape stem lineage, an especially evident adaptively evolved biological pathway contains genes that function in mitochondria, are crucially involved in aerobic energy production, and are highly expressed in two energy-demanding tissues, heart and brain. Also, on this ape stem lineage, there was adaptive evolution among genes associated with human autoimmune and aging-related diseases. During more recent human descent, the adaptively evolving, highly expressed genes in fetal brain are involved in mediating neuronal connectivity. Comparing adaptively evolving genes from pre-and postnatal-stage tissues suggests that different selective pressures act on the development vs. the maintenance of the human phenotype.fetal ͉ human disease ͉ mitochondria ͉ placenta ͉ thyroid

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“…An inverse relation between leptin level and infant birth weight has been observed in some, though not all, previous studies. [21][22][23][24] Of note, Verhaeghe and colleagues found that, compared with glucose, insulin, adiponectin and tumour necrosis factor-α, leptin was the mediator that was most strongly (and negatively) associated with birth weight. 23 Placental dysfunction has been suggested as a unifying mechanism underlying both fetal growth restriction and elevated maternal leptin levels (through increased placental production of leptin), al though this model remains speculative.…”

Section: Discussionmentioning

confidence: 99%