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The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 8 3847-3850
Copyright © 2004 by The Endocrine Society

Low Cord Ghrelin Levels in Term Infants Are Associated with Slow Weight Gain Over the First 3 Months of Life

R. J. A. James, R. F. Drewett and T. D. Cheetham

Department of Psychology, University of Durham (R.J.A.J., R.F.D.), Durham, United Kingdom DH1 3LE; and Department of Child Health, University of Newcastle-upon-Tyne (T.D.C.), Newcastle-upon-Tyne, United Kingdom NE1 4LP

Address all correspondence and requests for reprints to: Dr. T. D. Cheetham, Pediatric Outpatient Department, Royal Victoria Infirmary, Newcastle-upon-Tyne, United Kingdom NE1 4LP. E-mail: tim.cheetham{at}nuth.northy.nhs.uk.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Lower ghrelin levels have been related to slower growth in small for gestational age infants, and infants with higher cord leptin levels have been reported to gain weight more slowly from birth to 2 yr. This study investigated whether cord blood ghrelin and leptin levels are related to weight gain up to 12 wk of age. One hundred infants were weighed at birth and at 12 wk, and cord blood was assayed for ghrelin and leptin. The mean (±SD) birth weight was 3.458 (0.433) kg (median, 3.390; range, 2.510–4.615 kg). The mean (±SD) leptin level was 10.1 (6.7) ng/ml (median, 8.4; range, 1.6–36.7 ng/ml), and that of ghrelin was 760.9 (282.9) pg/ml (median, 770; range, 210-1670 pg/ml). Higher birth weight was associated with slower weight gain. Leptin was correlated with birth weight, but ghrelin was not, and leptin and ghrelin levels were not significantly correlated with one another. With birth weight as a control variable, ghrelin was significantly associated with slow weight gain ({chi}2 = 7.20 with 1 df; P < 0.01), although leptin was not ({chi}2 = 1.59 with 1 df; P > 0.1). In conclusion, lower cord ghrelin levels are associated with slower weight gain from birth to 3 months of age.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
RESEARCH IN BOTH rodents and humans has shown that leptin is an important regulator of appetite and energy balance (1, 2). Rare forms of childhood obesity arising from leptin gene (3, 4) and receptor (5) mutations have demonstrated the crucial importance of leptin in the regulation of appetite and weight gain. These infants were of normal birth weight, but gained weight rapidly between 2 and 4 months of age. Healthy infants with higher cord leptin levels at birth have since been shown to gain weight more slowly over the period from birth to 4 months (6). More recently, the gut peptide ghrelin has been described (7), and it has also been detected in cord blood (8). Ghrelin may be implicated in the stimulation of appetite and GH release in both rodents (9, 10) and humans (11). Human subjects administered ghrelin by iv injection reported increased ratings of hunger on a visual analog scale (11). High fasting ghrelin levels have also been reported in young adults with Prader-Willi syndrome (12, 13); therefore, altered ghrelin concentrations could be linked to the hyperphagia and rapid weight gain in childhood and adolescence that are characteristic of this syndrome. High circulating ghrelin concentrations have been described in small for gestational age (SGA) neonates (14), and SGA infants showing slower weight gain over the first year of life had lower ghrelin levels after an iv glucose load (15). These findings suggest that leptin and ghrelin may be important regulators of weight gain in early infancy, and we therefore examined the relationship between cord blood ghrelin and leptin in relation to weight gain up to 3 months of age.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Subjects

Women with singleton term pregnancies were recruited consecutively from the delivery suite of the Royal Victoria Infirmary (Newcastle-upon-Tyne, UK). The mothers recruited were in good health with no known underlying medical disorder. One hundred infants, 50 males and 50 females, with a gestational age from 37–42 wk, with no known congenital abnormalities, and with an Apgar score of 8 or above at 5 min were recruited. All infants were formula fed and were studied from birth to 3 months of age. The local ethical committee approved this study. The parents of each infant gave their written informed consent.

Procedure

Cord blood samples were taken at the time of delivery into chilled heparin-coated tubes (LIP Ltd., Shipley, UK) containing 2000 kallikrein inactivator units (0.2 ml) aprotinin (Trasylol; Bayer, Newbury, UK), were transported on ice, and centrifuged immediately. The plasma specimens were stored frozen in separate aliquots at –40 C (leptin) and –70 C (ghrelin). These were later assayed for leptin (RIA, Linco Research, Inc., St. Charles, MO), with intra- and interassay coefficients of 8.3% and 6.2%, respectively, at 4.9 ng/ml and 3.9% and 4.7% at 10.4 ng/ml, and for total ghrelin (RIA, Phoenix Pharmaceuticals, Belmont, CA), with a limit of sensitivity of 30 pg/ml and intra- and interassay coefficients of less than 5% and less than 14%, respectively. This assay uses 125I-labeled bioactive ghrelin as tracer and a rabbit polyclonal antibody against full-length octanoylated human ghrelin, and thus detects both ghrelin and des-octanoyl-ghrelin. All samples were assayed together at the end of study, so measurements of growth were recorded blind to the hormone levels. Infants were weighed naked at birth and at 12 wk on electronic weighing scales (model 727; Seca, Birmingham, UK), which were accurate to 5 g, by the same researcher.

Statistical analysis

In the analysis leptin (nanograms per milliliter) and ghrelin (picograms per milliliter) were used as their natural logarithms. The infants’ weights at both time points were used after conversion to standard scores (z-scores) using British 1995 growth reference data (16, 17). Following a previously published criterion (6), we used a difference of –0.67 in the z-scores to identify slow weight gain; this is equivalent to crossing down one intercentile space on the UK Child Growth Foundation 1996/1 growth chart. An indicator variable was used to identify the 17 infants with slow weight gain (slow gainers, coded 1), and they were then contrasted with the remaining 83 infants (controls, coded 0) using logistic regression in SPSS (version 10, SPSS, Inc., Chicago, IL). In supplementary analyses, another indicator variable was used to identify the 24 infants with fast weight gain (a difference of +0.67 or more in the z-score). Weight gain in infancy is related to birth weight (18), so we used birth weight as a covariate in the analysis. The likelihood ratio {chi}2 was used for testing statistical significance.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Summary statistics for birth weight and leptin and ghrelin levels are presented in Table 1Go. Leptin was correlated with birth weight, but ghrelin was not, and leptin and ghrelin levels were not significantly correlated with one another. In the group as a whole, there was no significant relationship between weight gain and cord blood leptin and ghrelin levels after controlling for birth weight and sex.


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  		TABLE 1. Summary statistics for birth weight, leptin, and ghrelin

 
Using the indicator variable described above, there was a positive correlation between birth weight and slow weight gain, showing that infants with a higher birth weight were more likely to show slow weight gain over the first 3 months of life (Table 2Go). Leptin levels were positively correlated with slow weight gain, and ghrelin levels were negatively correlated with slow weight gain, showing that infants with higher leptin and lower ghrelin levels were more likely to have slower weight gain over the first 3 months of life. This correlation does not take birth weight into account, so further analysis used logistic regression to control for birth weight. Entered last in the regression, with birth weight and ghrelin as control variables, leptin was not significantly associated with slow weight gain ({chi}2 = 1.59 with 1 df; P > 0.1). With birth weight and leptin concentrations as control variables, ghrelin was significantly associated with slow weight gain ({chi}2 = 7.20 with 1 df; P < 0.01). The odds ratio was 0.14 (95% confidence interval, 0.03–0.66). Figure 1Go shows the unadjusted ghrelin levels for the infants in the control group and the slow gainers. Related analyses in infants with fast weight gain did not show any significant relationships with either ghrelin or leptin after controlling for birth weight.


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  		TABLE 2. Correlation among leptin, ghrelin, and weight gain

 


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  		FIG. 1. Box plots of cord blood ghrelin levels in infants with slow weight gain and controls from birth to 12 wk. The boxes represent the interquartile range (25th to 75th percentiles), the horizontal bars are the median, and whiskers are the range.

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
Both leptin and ghrelin are thought to have significant roles in appetite and weight regulation in humans. Evidence from individuals with congenital leptin deficiency shows that low leptin levels result in hyperphagia and profound obesity in early childhood (3, 4). Conversely, infants with higher cord leptin levels at birth have a lower weight gain over the first 4 months of life, an effect still apparent at 2 yr of age (6). Both of these observations suggest a role for leptin in the regulation of body weight. In this study we found that higher cord blood leptin levels were associated with poor weight gain, but this relationship was no longer significant after adjustment for birth weight. As cord blood leptin is significantly related to birth weight, and birth weight is a significant predictor of weight gain (18), it is important to control for birth weight in weight gain analyses. It is also interesting to note that the leptin-deficient infants did not show rapid weight gain in the first weeks of life, but this became apparent between 2 and 4 months of age.

High ghrelin concentrations sustained by a continuous infusion have been associated with increased weight and adiposity in mice (19). Other researchers did not identify an effect of daily injections of ghrelin on weight gain during the first postnatal week in neonatal rats (20), and the ghrelin-null mouse model fails to support a role for ghrelin in postnatal growth (21).

We found that lower cord ghrelin levels are associated with slow weight gain over the first 12 wk of life in healthy term infants. How ghrelin might influence weight gain in early infancy in humans is unclear, but a simple explanation would be that lower ghrelin concentrations are associated with reduced appetite, resulting in lower nutritional intake. This hypothesis would be consistent with the finding that SGA infants growing relatively slowly from birth to 1 yr of age had a greater decline in ghrelin levels from fasting values after a glucose load compared with SGA infants growing more quickly (15). High circulating ghrelin concentrations have been described in SGA neonates (14) and have been associated with faster growth over the first year of life (15). We did not, however, identify a relationship between fast weight gain and cord ghrelin levels in our healthy infants.

Ghrelin does have well documented orexigenic effects in humans (11, 22), and circulating ghrelin levels are increased by fasting (23). Obese people tend to have low ghrelin concentrations (24), which are not suppressed by food intake (25), but after gastric surgery they have lower ghrelin levels and reduced appetite with associated weight loss (26). Raised fasting ghrelin levels in patients with Prader-Willi syndrome are directly related to hunger measurements on a visual analog scale (12). Although these children typically become obese in early childhood (12, 13), it is important to note that weight gain during the neonatal period and early infancy is poor.

Ghrelin increases GH release (27, 28, 29), and it is also possible that slow weight gain is linked to alterations in GH production. GH is an important determinant of growth in infancy (30), but studies in neonates and older children do not point toward a direct effect of ghrelin on postnatal GH status and growth (31, 32).

In conclusion, lower cord ghrelin levels are associated with slower weight gain from birth to 3 months of age. The fact that ghrelin levels in cord blood are related to weight gain in infancy raises the possibility that each infant could have an inherent ghrelin status that relates to subsequent feeding behavior. This concept requires further investigation, but is clearly important because of the links between weight gain in infancy and adverse outcomes, such as poor cognitive development in childhood (33, 34, 35, 36) and ischemic heart disease in adulthood (37, 38).


   Acknowledgments
 
We thank the mothers and their infants for participating in the study. We also thank J. Jones (Diagnostic Systems Laboratories, London, UK) for conducting the ghrelin assay.


   Footnotes
 
This work was supported by a postgraduate studentship from University of Durham (to R.J.A.J.).

Abbreviation: SGA, Small for gestational age.

Received December 19, 2003.

Accepted April 30, 2004.


   References
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 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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