Endothelin 1 and leptin in the pathophysiology of intrauterine growth restriction

Arslan, Murat; Yazici, Gürkan; Erdem, Ahmet; Erdem, Mehmet; Arslan, Emine; Himmetoğlu, Özdemir

doi:10.1016/s0020-7292(03)00332-1

Cited by 37 publications

(28 citation statements)

References 25 publications

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“…These findings may suggest that catecholamines are involved in the fetal adaptation to both hypoxia and undernutrition. In vascular tissue, expression of the precursor protein for endothelin-1 is increased by hypoxia-inducible factor-1 signaling (22), and the reported increase in fetal plasma endothelin-1 levels in response to hypoxia (1,16) may represent a specific adaptation to a reduced oxygen supply.…”

Section: Discussionmentioning

confidence: 99%

“…The redistribution of fetal cardiac output during hypoxia may be partially dependent on the reported increased circulating levels of several vasoactive factors, including norepinephrine (14,43) and endothelin-1 (1,19), but may also involve changes in the local vascular responses to these circulating factors. The effects of chronic hypoxia in utero on the regional vascular responses to these vasoconstrictors after birth are not yet known.…”

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confidence: 99%

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Differential effects of maternal hypoxia or nutrient restriction on carotid and femoral vascular function in neonatal rats

Williams

Campbell²,

McMillen³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

116

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Differential effects of maternal hypoxia or nutrient restriction on carotid and femoral vascular function in neonatal rats

Williams

Campbell²,

McMillen³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

116

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“…We chose to measure circulating levels of ET-1, NO x , sFlt-1, and PlGF given previous studies showing their importance in relation to the occurrence of fetal growth restriction and preeclampsia (1,7,8,17,18,25). For example, ET-1 is a potent vasoconstrictor that is known to be elevated in pregnancies complicated by preeclampsia or SGA (7,8), and when its vasoconstrictor actions are inhibited with the use of ET-1 antagonists, hypoxia-associated reductions in uteroplacental blood flow and fetal growth in rat models are completely abolished (27).…”

Section: Discussionmentioning

confidence: 99%

Lower uterine artery blood flow and higher endothelin relative to nitric oxide metabolite levels are associated with reductions in birth weight at high altitude

Julian

Galan²,

Wilson³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

102

107

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Moore LG. Lower uterine artery blood flow and higher endothelin relative to nitric oxide metabolite levels are associated with reductions in birth weight at high altitude. Am J Physiol Regul Integr Comp Physiol 295: R906 -R915, 2008. First published June 25, 2008 doi:10.1152/ajpregu.00164.2008.-Reduced uteroplacental blood flow is hypothesized to play a key role in altitude-associated fetal growth restriction. It is unknown whether reduced blood flow is a cause or consequence of reduced fetal size. We asked whether determinants of uteroplacental blood flow were altered prior to reduced fetal growth and whether vasoactive and/or angiogenic factors were involved. Women residing at low (LA; 1600 m, n ϭ 18) or high altitude (HA; 3100 m, n ϭ 25) were studied during pregnancy (20, 30, and 36 wk) and 4 mo postpartum (PP) using Doppler ultrasound. In each study, endothelin (ET-1), nitric oxide metabolites (NO x), soluble fms-like tyrosine kinase (sFlt-1) and placental growth factor (PlGF) levels were quantified. At HA, birth weights were lower (P Ͻ 0.01) and small-for-gestational age was more common (P Ͻ 0.05) compared with LA. HA was associated with lower uterine artery (UA) diameter (P Ͻ 0.01) and blood flow (P Ͻ 0.05). Altitude did not affect ET-1, sFlt-1 or PlGF; however, ET-1/NO x was greater and NOx lower during pregnancy and PP at HA vs. LA. ET-1/NO x was negatively associated with birth weight (20 wk, P Ͻ 0.01; 36 wk, P ϭ 0.05) at LA and HA combined. At HA, UA blood flow (30 wk) was positively associated with birth weight ( †). UA blood flow and ET-1/NO x levels accounted for 45% (20 wk) and 32% (30 wk) of birth weight variation at LA and HA combined, primarily attributed to effects at HA. We concluded that elevated ET-1/NO x and altered determinants of uteroplacental blood flow occur prior to altitude-associated reductions in fetal growth, and therefore, they are likely a cause rather than a consequence of smaller fetal size. fetal growth restriction; hypoxia; small-for-gestational age; uteroplacental oxygen delivery; pregnancy SMALL-FOR-GESTATIONAL AGE (SGA) is a common complication of pregnancy that raises the risk of morbidity and mortality during the perinatal period, as well as in later life (2, 11). Among the many determinants of SGA is the chronic hypoxia of residence at high altitude (Ն2,500 m; 8,200 ft). Birth weight declines progressively, and potently, with increasing altitude such that infants born to women permanently residing at elevations Ն2,500 m are at a greater risk of low birth weight than infants born at lower altitudes (13-15, 34). Altitudinal differences in gestational age, socioeconomic status, parity, maternal height, or the frequency of hypertensive complications do not explain the degree to which birth weight decreases with altitude, indicating that it is likely chronic hypoxia per se that is decreasing fetal growth (12,13,15). Despite the pervasive effect of high altitude on birth weight, the mechanisms by which hypoxia acts to reduce fetal growth are not well understood.A considera...

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“…In some of these studies, fetal leptin levels per kilogram of fetal weight, as well as fetal leptin levels before 34 weeks of gestation, were not significantly different in IUGR, indicating that leptin secretion is mainly associated with adipose tissue accumulation (61)(62)(63)(64). However, other investigators suggested that low fetal leptin levels in IUGR are associated with reduced placental production, since leptin levels dramatically decrease shortly after birth (73)(74)(75).…”

Section: The Role Of Adipose Tissuementioning

confidence: 98%

“…Several studies demonstrated lower circulating leptin concentrations in IUGR neonates at birth, due to reduced fat mass (58)(59)(60)(61)(62)(63)(64)(65)(66)(67)(68)(69)(70)(71)(72) and/or decreased placental production (73)(74)(75). In some of these studies, fetal leptin levels per kilogram of fetal weight, as well as fetal leptin levels before 34 weeks of gestation, were not significantly different in IUGR, indicating that leptin secretion is mainly associated with adipose tissue accumulation (61)(62)(63)(64).…”

Section: The Role Of Adipose Tissuementioning

confidence: 99%

Intrauterine growth restriction and adult disease: the role of adipocytokines

Briana¹,

Malamitsi‐Puchner²

2009

European Journal of Endocrinology

126

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Intrauterine growth restriction (IUGR) is the failure of the fetus to achieve his/her intrinsic growth potential, due to anatomical and/or functional disorders and diseases in the feto-placental-maternal unit. IUGR results in significant perinatal and long-term complications, including the development of insulin resistance/metabolic syndrome in adulthood.The thrifty phenotype hypothesis holds that intrauterine malnutrition leads to an adaptive response that alters the fetal metabolic and hormonal milieu designed for intrauterine survival. This fetal programming predisposes to an increased susceptibility for chronic diseases. Although the mechanisms controlling intrauterine growth are poorly understood, adipose tissue may play an important role in linking poor fetal growth to the subsequent development of adult diseases. Adipose tissue secretes a number of hormones, called adipocytokines, important in modulating metabolism and recently involved in intrauterine growth.This review aims to summarize reported findings concerning the role of adipocytokines (leptin, adiponectin, ghrelin, tumor necrosis factor (TNF), interleukin-6 (IL6), visfatin, resistin, apelin) in early life, while attempting to speculate mechanisms through which differential regulation of adipocytokines in IUGR may influence the risk for development of chronic diseases in later life.

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Endothelin 1 and leptin in the pathophysiology of intrauterine growth restriction

Abstract: These results suggest the intertwined roles of ET-1 and leptin in the pathophysiology of IUGR. Further studies concerning interaction between these peptides in different pregnancy conditions may provide important information about the actions of ET-1 and leptin on fetal growth.

Cited by 37 publications

References 25 publications

Differential effects of maternal hypoxia or nutrient restriction on carotid and femoral vascular function in neonatal rats

Differential effects of maternal hypoxia or nutrient restriction on carotid and femoral vascular function in neonatal rats

Lower uterine artery blood flow and higher endothelin relative to nitric oxide metabolite levels are associated with reductions in birth weight at high altitude

Intrauterine growth restriction and adult disease: the role of adipocytokines

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