Leptin and gestational weight gain: relation of maternal and cord blood leptin to birth weight

Shaarawy, Mohamed; El-Mallah, Samira Youssef

doi:10.1016/s1071-5576(99)00003-9

Cited by 27 publications

(26 citation statements)

References 17 publications

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“…The observed positive correlation between plasma leptin concentrations and the maternal BMI during pregnancy and gestational weight gain is in accordance with many [9,32,53] but not all previous studies in pregnancy [28,54]. The BMI in pregnancy is an imprecise measure of the amount of body fat stores and relates to the fetal weight as well as to placenta size, amniotic fluid and maternal fluid expansion.…”

Section: Discussionsupporting

confidence: 90%

“…Maternal leptin homeostasis does not seem to directly influence fetal plasma leptin concentrations, which in some [53,54,61] but not all [9,62] studies closely relates to birth weight and possibly also to maternal plasma leptin in the third trimester [53]. In our study birth weight was not related to maternal pregestational weight, overall weight gain and HbA 1 c in women with gestational diabetes, but inversely with maternal plasma leptin and maternal insulin resistance at 28 gestational weeks.…”

Section: Discussioncontrasting

confidence: 59%

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Increased plasma leptin in gestational diabetes

Kautzky‐Willer

Pacini²,

Tura³

et al. 2001

Diabetologia

170

127

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Leptin, a polypeptide hormone originating from adipocytes, contributes to body weight control and provides negative feedback between adipose tissue and the hypothalamic satiety centre. In animal models, leptin decreases food intake but increases energy expenditure and body temperature [1±3]. Furthermore, it is found to be higher in women than in men [4] and to influence the reproductive function [5]. In humans plasma leptin is highly correlated with body fat Diabetologia (2001) Abstract Aims/hypothesis. Insulin resistance as well as marked changes in body weight and energy metabolism are associated with pregnancy. Its impact on plasma leptin is not known and was determined in this longitudinal study in both diabetic and normal pregnancy. Methods. At 28 gestational weeks plasma concentrations of leptin and B-cell hormones were measured at fasting and after an oral glucose load (OGTT:75 g) in women with gestational diabetes and pregnant women with normal glucose tolerance and compared with women who were not pregnant (C).Results. Plasma leptin (ng/ml) was higher (p < 0.001) in women with gestational diabetes (24.9 1.6) than in women with normal glucose tolerance (18.2 1.5) and increased in both groups when compared with the non-pregnant women (8.2 1.3; p < 0.0005). No change in plasma leptin concentrations was induced by OGTT in any group. Basal insulin release was higher (p < 0.05) in women with gestational diabetes compared with the pregnant women with normal glucose tolerance. Marked insulin resistance was confirmed by a 20 % lower (p < 0.05) insulin sensitivity in subgroup analysis and a decrease of almost 40 % in fasting glucose/insulin ratio (p < 0.005) in women with gestational diabetes. Leptin correlated in women with gestational diabetes with basal plasma concentrations of glucose (p < 0.02), insulin (p < 0.004) and proinsulin (p < 0.01) as well as with BMI (p < 0.001) and overall pregnancy induced maternal weight gain (p < 0.009). With normalisation of blood glucose 8 weeks after delivery in women with gestational diabetes their plasma leptin decreased (p < 0.0005) to 17.3 1.9 ng/ml but did not completely normalize (p < 0.05 vs non-pregnant women). Conclusion/interpretation. Our data show that women with gestational diabetes without any change in plasma leptin upon oral glucose loading have increased plasma leptin concentrations during and after pregnancy, a clear association of plasma leptin with the respective concentration of glucose and insulin resistance as well as with changes in body weight, and a failure to normalize spontaneously BMI to the same extent as pregnant women with normal glucose tolerance when compared with matched control subjects. [Diabetologia (2001) 44: 164±172]

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Section: Discussionsupporting

confidence: 90%

Section: Discussioncontrasting

confidence: 59%

Increased plasma leptin in gestational diabetes

Kautzky‐Willer

Pacini²,

Tura³

et al. 2001

Diabetologia

170

127

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“…10 It has been documented that maternal serum leptin concentrations correlate positively with gestational age, gestational weight gain or maternal BMI, and subsequently placental leptin levels with birth weight in a study of 52 pregnant women from Egypt. 4 Here, maternal genotype variation at the LEPR Gln223Arg variant site showed no signi®cant association with foetal birth weight in either group, although birth weight increased in offspring of mothers with the variant allele in our UKaIrish population. No association was observed with gestational length.…”

Section: Resultsmentioning

confidence: 47%

“…This polymorphism is in strong linkage disequilibrium with four other LEPR polymorphisms, all of which showed no signi®cant association with BMI in white British males. 14 While maternal leptin levels have been signi®cantly associated with maternal weight gain, gestational length and birth weight, 4 the maternal LEPR Gln223Arg variant showed no signi®cant associations with any of these in either of our population groups. LEPR Gln223Arg does not appear to modulate maternal body weight and birth weight in our study, and more complex multiple gene investigation may be required to identify gene variants involved in modulating maternal and infant weight.…”

Section: Resultsmentioning

confidence: 66%

“…Mutations in OB have been identi®ed in morbidly obese patients, and have been shown to affect circulating leptin levels and cause earlyonset obesity. 3 Increases in placental leptin levels have been positively correlated with birth weight, 4 and LEPR mRNA has been shown to be increased in the rat uterus during pregnancy. 5 As leptin is involved in the regulation of body mass index (BMI), signalling via the LEPR may play a role in the regulation of maternal body weight during pregnancy and foetal growth.…”

Section: Introductionmentioning

confidence: 99%

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Maternal leptin receptor gene variant Gln223Arg is not associated with variation in birth weight or maternal body mass index in UK and South Asian populations

et al. 2001

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BACKGROUND:Leptin is an adipocyte secreted hormone involved in regulation of body weight and metabolism in man. Placenta leptin levels correlate positively with birth weight. It is therefore possible that variation in the leptin receptor gene (LEPR) may contribute to obesity and in¯uence birth weight. OBJECTIVE: This study investigates the in¯uence of the leptin receptor gene variant Gln223Arg (A?G, 668), on maternal body mass index (BMI), foetal gestational length and birth weight in a cohort of 455 healthy pregnant women of Asian Indian (India, Bangladesh, Pakistan) and UKaIrish origin. RESULTS: Maternal genotype distributions did not differ from those expected under Hardy ± Weinberg equilibrium conditions in either population of origin. Maternal genotype for the Gln223Arg leptin receptor gene polymorphism showed no signi®cant association with foetal birth weight (adjusted for gestational length) or with maternal BMI during ®rst trimester (adjusted for age) in either population group. CONCLUSION: These results suggest that the Gln223Arg variant in the maternal leptin receptor gene does not explain the association between placental leptin levels and birth weight, and is not associated with variation in maternal BMI in early pregnancy in our sample.

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Maternal serum leptin concentration during the second trimester of pregnancy: association with fetal chromosomal abnormalities

et al. 2002

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Recent studies suggest that leptin, the product of the obese gene, is produced by the placenta during pregnancy. The present study addressed the question whether second trimester maternal serum leptin could be altered by fetal Down syndrome or Edwards syndrome. Maternal serum leptin concentrations were measured in 18 pregnancies complicated with Down syndrome, six pregnancies complicated with Edwards syndrome and 183 uncomplicated pregnancies during the second trimester of pregnancy. The present results demonstrate that leptin concentrations in uncomplicated pregnancies slightly decrease from the 16th week of pregnancy, reaching a minimum of 18.8 ng/ml around the 20th week, and then rapidly increase to 28.2 ng/ml by the 24th week. Leptin correlation with maternal body weight decreases from r=0.695 at 16-17 week of gestation to r=0.544 at >22 weeks of gestation. There was no significant difference between the mean MoMs of Down syndrome- (0.926) or Edwards syndrome- (0.960) affected pregnancies and normal pregnancies (1.002). A weak correlation (r=0.18, p<0.02) was observed between corrected leptin MoMs and human chorionic gonadotrophin (hCG) MoMs in normal pregnancies. It is assumed that around the 20th week of pregnancy placental leptin production is activated or at least is accelerated and it is added to the amount of leptin produced by maternal adipose tissue. Fetal Down syndrome or Edwards syndrome does not seem to alter maternal leptin concentration and therefore leptin cannot be used as a marker for these chromosomal abnormalities in the early second trimester of pregnancy.

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Leptin and gestational weight gain: relation of maternal and cord blood leptin to birth weight

Abstract: Elevated serum leptin is associated with maternal adiposity and risk of developing large for gestational age infants.

Cited by 27 publications

References 17 publications

Increased plasma leptin in gestational diabetes

Increased plasma leptin in gestational diabetes

Maternal leptin receptor gene variant Gln223Arg is not associated with variation in birth weight or maternal body mass index in UK and South Asian populations

Maternal serum leptin concentration during the second trimester of pregnancy: association with fetal chromosomal abnormalities

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