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Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2005-2714
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The Journal of Clinical Endocrinology & Metabolism Vol. 91, No. 6 2244-2249
Copyright © 2006 by The Endocrine Society

Adiponectin in Umbilical Cord Blood Is Inversely Related to Low-Density Lipoprotein Cholesterol But Not Ethnicity

Narinder Bansal, Valentine Charlton-Menys, Philip Pemberton, Patrick McElduff, John Oldroyd, Avni Vyas, Abir Koudsi, Peter E. Clayton, J. Kennedy Cruickshank and Paul N. Durrington

Clinical Epidemiology and Cardiovascular Medicine Groups (N.B., J.O., A.V., A.K., J.K.C.) and Division of Cardiovascular and Endocrine Science (V.C.-M., P.N.D.), Department of Medicine, and Clinical Research Department (P.P.), University of Manchester, Manchester Royal Infirmary, Manchester M13 9WL, United Kingdom; Hunter New England Population Health (P.M.), Hunter New England Area Health Service, Newcastle NSW 2300, Australia; and Endocrine Science Research Group (P.E.C.), University of Manchester, Manchester M13 9PT, United Kingdom

Address all correspondence and requests for reprints to: Narinder Bansal, Clinical Epidemiology Group, University of Manchester Medical School, Stopford Building, Oxford Road, Manchester M13 9PT. E-mail: n.bansal{at}postgrad.manchester.ac.uk.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Context: Adiponectin is a recognized protective risk marker for cardiovascular disease in adults and is associated with an optimal lipid profile. The role of adiponectin at birth is not well understood, and its relationship with the neonatal lipid profile is unknown. Because ethnic disparities in cardiovascular risk have been attributed to low adiponectin and its associated low high-density lipoprotein cholesterol (HDL-C), investigation at birth may help determine the etiology of these risk patterns.

Objective: Our objective was to investigate the relationship between neonatal adiponectin and lipid profile at birth in two ethnic groups in cord blood.

Design, Setting, and Participants: Seventy-four healthy mothers and their newborns of South Asian and White European origin were studied in this cross-sectional study at St. Mary’s Hospital, Manchester, United Kingdom.

Main Outcome Measures: Serum adiponectin, total cholesterol, HDL-C, low-density lipoprotein cholesterol (LDL-C), and triglyceride levels were measured in umbilical venous blood at birth and in maternal blood collected at 28 wk gestation.

Results: Cord adiponectin was significantly inversely associated with cord LDL-C (r = –0.32; P = 0.005) but not HDL-C. In a multiple regression analysis, cord LDL-C remained the most significant association of cord adiponectin (ß = –0.13; P < 0.001). We did not find any significant ethnic differences in cord adiponectin or lipids with the exception of triglycerides, which were significantly lower in South Asian newborns (P < 0.05).

Conclusion: This is the first report of an inverse relationship between cord adiponectin and LDL-C at birth. In contrast to adult studies, we found no significant association between adiponectin and HDL-C in cord blood. Our results and the strong independent association between adiponectin and HDL-C observed in adult studies suggest a role for adiponectin in lipid metabolism. Ethnic differences in adiponectin may arise after birth.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
ADIPONECTIN IS THE most abundant protein secreted by the adipocyte and, in contrast to other adipokines, is down-regulated in obesity in adults (1) and children (2), particularly in relation to visceral adiposity (3, 4, 5), and is increased by weight reduction (6, 7). Atheroprotective properties of adiponectin are widely reported, particularly its insulin-sensitizing (8, 9) and antiinflammatory properties (10, 11). High plasma levels of adiponectin are associated with lower incidence of type 2 diabetes (6, 12) and coronary heart disease (13). The adipokine is strongly positively associated with high-density lipoprotein cholesterol (HDL-C) (14, 15, 16) and negatively with triglycerides (17). Recent findings suggest that adiponectin predicts HDL-C partly independently of visceral adiposity (17), intraabdominal fat (5), body mass index (BMI) (18), and insulin sensitivity in adults (16, 19). The association between adiponectin and HDL-C is of interest because low HDL has been associated with increased coronary heart disease risk independent of high low-density lipoprotein cholesterol (LDL-C) and triglycerides (20). This may be particularly so in Indo-Asians in whom low levels of adiponectin and HDL-C and the high levels of central obesity have been linked (15).

Adiponectin circulates in higher concentrations in the fetus, as judged from cord blood levels, than in the adult (21) and does not seem to be related to maternal levels (22). There is a 20-fold increase in adiponectin between 24 wk gestation and term (23), which then decreases with increasing age and weight during childhood (24, 25). Cord blood cholesterol concentrations are considerably lower than in adults (26, 27), and the relative proportion present in HDL as opposed to LDL is much higher (28). The lipid profile in cord blood is influenced by several prenatal factors (29). Maternal factors such as diet and cholesterol phenotype (30, 31) during pregnancy have been associated with cord lipids. Also, factors contributing to fetal stress such as mode of delivery have been associated with alterations in lipids at birth (32). In contrast to the clear association with body weight in adults, there is no inverse relationship between birth size and adiponectin in neonates, probably because of the lack of visceral fat in the newborn. Some, but not all, studies have even suggested a positive relationship between adiponectin and adiposity in the neonate (21, 22, 33, 34). In addition, little is known about the relationship between adiponectin and the lipid profile in the newborn.

The purpose of the present study was to investigate the relationship between serum adiponectin and total cholesterol (TC), LDL-C, HDL-C, and triglycerides in umbilical cord blood and relationships to infant anthropometry and maternal factors. Because the increased prevalence of cardiovascular disease in adults of South Asian origin has been attributed partly to low levels of adiponectin either as the consequence or cause of high prevalence of central obesity and low HDL-C in this ethnic group, we compared adiponectin and HDL-C in British-born South Asian babies with those of White European origin to determine whether this ethnically distinct risk profile was present at birth.


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

Adiponectin and cholesterol levels were measured in umbilical venous blood (obtained from a clamped segment of the cord after birth and before delivery of the placenta) in 74 healthy newborns (30 males and 44 females) of South Asian and White European origin between 35 and 42 wk of gestation, together with fasting maternal blood collected at 28 wk gestation in St. Mary’s Hospital, Manchester, UK. Carefully standardized measures of maternal anthropometry and clinical characteristics were taken at the time of blood sampling as well as of infant anthropometry including subscapular, triceps, and suprailiac skin-fold measurements by a trained research midwife at birth. All mothers had healthy pregnancies without maternal complications (pregnancies with complications such as preeclampsia and gestational diabetes mellitus were excluded from the cohort) or fetal distress. Newborns were delivered by spontaneous vaginal delivery in 60 cases, five were induced, and nine were delivered by cesarean section. The study was approved by the Central Manchester Ethics Committee, and all women provided written informed consent before enrollment.

Maternal and newborn anthropometry

An infant electronic scale was used to obtain birth weight (grams). Birth length (centimeters) was obtained using a standardized infant plastic length board. Suprailiac, subscapular, and triceps skin-fold measurements were obtained using Harpenden skin-fold calipers (BATY International, Burgess Hill, West Sussex, UK) and recorded to the nearest 0.1 mm. Maternal weight (kilograms) was obtained using calibrated scales and height (centimeters) using a fixed stadiometer. All anthropometric measurements were carried out by a trained research midwife, and the mean of two measures was used in the analysis.

Adiponectin assay

Adiponectin was measured using the DuoSet ELISA development system (R&D Systems, Minneapolis, MN). The lower limit of detection was 0.001 mg/liter, and the intra- and interassay coefficients of variation were 6.8 and 10.2%, respectively.

Cholesterol assay

Maternal plasma and cord serum total cholesterol and triglycerides were measured by the cholesterol esterase/cholesterol oxidase/4-aminoantipyreneperoxidase (enzymic CHOD/PAP) and lipoprotein lipase/glycerokinase/glycerol-3-phosphate oxidase/peroxidase (enzymic GPO/PAP) methods, respectively, on a Cobas Mira S analyzer (ABX Diagnostics, Shefford, UK), and all reagents were obtained from the same source. HDL-C was measured using a second-generation homogenous method using polyethylene glycol (PEG)-modified enzymes (PEG-cholesterol esterase and PEG-cholesterol oxidase) by the enzymic CHOD/PAP method (Roche Diagnostics, Lewes, UK). LDL-C was calculated using the Friedewald formula. The reliability of this method has been previously demonstrated in cord blood (35). Calculated LDL-C of less than 3.867 mg/dl (0.1 mmol/liter) was set the detection limit for cholesterol of 3.867 mg/dl (0.1 mmol/liter).

Statistical methods

Stata version 8 (Stata Corp., College Station, TX) was used for statistical analysis. The Kruskal-Wallis and Mann-Whitney U test was used to test for statistically significant differences between ethnic groups and gender, respectively. Spearman’s rho (rs) was used to calculate correlation coefficient to measure the association between continuous variables and linear regression analysis to examine maternal predictors of, and infant factors associated with, cord adiponectin.


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

Maternal characteristics are presented in Table 1Go. Prepregnancy weight, height at 28 wk gestation, TC, and LDL-C were significantly lower in women of South Asian origin (14 Pakistani, three Bangladeshi, and three Indian) compared with White European women (P = 0.01, P = 0.002, P = 0.01, and P = 0.027, respectively) but not maternal adiponectin (P = 0.17). Newborn characteristics are shown in Table 2Go. There were no significant differences in the mean levels of adiponectin or lipoproteins between South Asian and White European newborns with the exception of triglycerides, which were significantly lower in South Asian newborns (P < 0.05). No significant differences were observed in adiponectin or other measured variables between males and females with the exception of birth length, which was higher in males (P < 0.05).


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  		TABLE 1. Maternal clinical and metabolic characteristics at 28 wk gestation

 

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  		TABLE 2. Newborn clinical and metabolic characteristics at birth

 
Cord adiponectin and anthropometry

Cord adiponectin was not significantly associated with birth weight (r = 0.20; P = 0.09), length (r = 0.16; P = 0.19), skin-fold thickness measures of triceps, subscapular, and flank (r = 0.11, 0.13, and 0.10 respectively; all P > 0.20), or gestational age (r = 0.14; P = 0.24).

Cord adiponectin and maternal factors

Cord adiponectin was not significantly associated with maternal level of adiponectin (r = 0.20; P = 0.25), BMI (r = –0.11; P = 0.38), or maternal lipids except for maternal TC (r = 0.23; P = 0.04).

Cord adiponectin and infant lipids

In a univariate analysis, cord TC [ß = –0.06; P = 0.01; 95% confidence interval (CI), –0.12 to –0.01], LDL-C (ß = –0.10; P = 0.001; 95% CI, –0.16 to –0.04), and TC:HDL-C (ß = –1.13; P = 0.025; 95% CI, –2.11 to –0.14) was inversely associated with cord adiponectin but was not significant with HDL-C (ß = 0.04; P = 0.51). The strength of the inverse relationship with LDL-C is shown in Fig. 1Go.


Figure 1
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  		FIG. 1. Inverse relationship between cord adiponectin and LDL-C. r = –0.32; P = 0.005.

 
In a multiple linear regression analysis (Table 3Go) that included ethnicity, maternal age, BMI, and lipids together with mode of delivery, newborn anthropometry, lipids, and gestational age, cord LDL-C (ß = –0.12; P = 0.005) was the only significant predictor of cord adiponectin. In a backward stepwise regression (Table 3Go), cord LDL-C remained the most significant predictor of cord adiponectin (ß = –0.13; P < 0.001), followed by maternal TC (ß = 0.02; P = 0.019) and cord HDL-C (ß = 0.10; P = 0.05). Newborn anthropometry was not significantly associated with cord adiponectin as individual variables or as measures of ponderal index, sum of skin-folds or central vs. peripheral body fat distribution. In the final regression model, newborn anthropometric measures were entered as individual variables.


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  		TABLE 3. Multiple linear regression analysis of predictors of cord adiponectin

 
Maternal adiponectin, maternal lipids, and BMI

In a univariate analysis, maternal triglycerides (ß = –0.01; P = 0.001; 95% CI, –0.02 to –0.004) and BMI (ß = –0.10; P = 0.001; 95% CI, –0.17 to –0.04) were inversely and maternal HDL-C positively (ß = 0.03; P = 0.003; 95% CI, 0.01–0.05) associated with maternal adiponectin. Maternal LDL-C (ß = 0.007; P = 0.114; 95% CI, –0.002 to 0.02) and maternal age (ß = 0.03; P = 0.440; 95% CI, –0.04 to 0.09) were not significantly associated with maternal adiponectin. Maternal triglycerides (ß = –0.008; P = 0.01; 95% CI, –0.01 to –0.002) and HDL-C (ß = 0.02; P = 0.03; 95% CI, 0.002–0.04) remained significantly associated with maternal adiponectin after adjustment for maternal BMI, age, and ethnicity.


   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
Our study shows that cord adiponectin is inversely associated with cord LDL independently of maternal factors and newborn growth measures. Our findings do not support the hypothesis that ethnic differences in HDL and adiponectin observed in adults are present at birth at least when both are living in the same environment.

We found lower levels of maternal adiponectin in mothers of South Asian origin compared with those of White European origin, and this is in agreement with previous findings of hypoadiponectinemia during pregnancy in South Asian women (36) and coronary heart disease patients (37) when compared with their White European counterparts. However, in our study, this difference was not statistically significant. In other studies, the persistence of lower adiponectin levels in South Asian adults after adjustment for classical risk factors such as BMI, pregnancy weight gain, fasting insulin, and glucose tolerance suggest that these metabolic factors alone do not explain the ethnic disparities in adiponectin (36). Body fat distribution, particularly central obesity and the high prevalence of this in the South Asian population appears to be more of an attributable risk factor for hypoadiponectinemia as well as low HDL-C (15). We did not find any significant ethnic differences between newborn body fat distribution or HDL-C in our study and therefore suggest that differences in HDL-C, central obesity, and thus adiponectin between adults of European and South Asian origin may be a result of later environmental exposures.

Adiponectin was not significantly related to infant anthropometry (birth weight, ponderal index, or peripheral and central skin-fold thickness) in our study, and this finding is in agreement with other similar studies (21, 34) but not all (22, 33, 38). Several factors may explain the lack of consistency in this finding. In particular, most studies failed to adjust for gestational age and thus observe the independent effects of birth weight, especially because a different range of gestational ages and birth weights were observed by each study. Findings from previous studies suggest that adiponectin is not strongly related to birth weight in healthy term, appropriate-for-gestational-age infants compared with those born preterm, small, or large for gestational age (21). Our study population consisted of healthy neonates; all were born at term and appropriate for gestational age, with the exception of two born at 35 wk and four born small for gestational age, respectively (term and birth weight ≤ 2500 g). Birth weight was not associated with neonate adiponectin in the univariate analysis or in the final multiple regression model (after adjustment for gestational age and birth weight), and thus we can confirm the lack of association between birth weight and adiponectin in healthy term neonates. Because the inverse association between adiponectin and obesity in children is dependent on visceral fat accumulation (2), it is probably the near absence of this in newborns that explains the lack of association between newborn birth weight and adiponectin.

Cord adiponectin was considerably higher than maternal levels, and our findings are consistent with those from similar studies. These higher levels and recent findings from the literature suggest that cord adiponectin does not originate from placental (34) or maternal tissues (22, 39) and so must have a fetal origin. In adults, adiponectin decreases with increasing visceral adiposity, and it had been hypothesized that it is a lack of negative feedback on adiponectin production in visceral-thin neonates that contributes to the hyperadiponectinemia seen in cord blood (39). Furthermore, it has been hypothesized that the presence of brown adipose tissue in the human neonate may be the source of abundant levels of adiponectin at birth (39). Experimental findings from rodent studies reveal a high expression of adiponectin in brown adipose tissue with fetal serum adiponectin levels peaking at birth (40).

We found adiponectin was inversely associated with LDL-C at birth. Okada et al. (41) have recently reported a similar negative relationship between LDL-C and adiponectin in 11- to 12-yr-old girls, suggesting that low levels of adiponectin may present an atherogenic risk profile early in life. However, little is known about the mechanisms underlying the inverse association between adiponectin and LDL-C. Results from human studies suggest a role for adiponectin in the regulation of intracellular triglyceride content in the liver (42), and findings in mouse models demonstrate that increased endogenous adiponectin may stimulate lipoprotein lipase and improve triglyceride clearance (43). Findings from a recent study in men also support the role of adiponectin in lipoprotein metabolism. Low plasma adiponectin was found to be predictive of increased plasma very-low-density lipoprotein apo B concentration attributed to impaired catabolism of very-low-density lipoprotein apo B. This effect was found to be independent of insulin resistance and size of adipocyte compartments (44).

It is evident that HDL-C and triglycerides are strongly associated with adiponectin levels in the adult (36). We did not observe any significant relationship between cord triglycerides and adiponectin, and HDL-C was only borderline significant in the backward stepwise regression. The poor relationship with the latter lipids and adiponectin may be because of the low levels of visceral adiposity in our newborns, given that the association between triglycerides and HDL-C with adiponectin has been shown to strengthen with increasing adiposity in adolescents (45).

This study is limited by its small sample size, and thus we may have missed associations and ethnic differences because of a lack of statistical power. To conclude, we have demonstrated, to our knowledge for the first time, a strong inverse relationship between cord adiponectin and LDL-C at birth. Both our results and the strong independent association between adiponectin and HDL-C observed in adult studies suggest a role for adiponectin in lipid metabolism (46, 47), although the mechanisms for this are yet unclear. Additional studies are needed to examine the relationship between LDL-C and adiponectin in the newborn, moreover, to explore the change in this relationship with age and the attainment of visceral adiposity in childhood and early adult life.


   Footnotes
 
First Published Online March 21, 2006

Abbreviations: BMI, Body mass index; CI, confidence interval; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; TC, total cholesterol.

Received December 15, 2005.

Accepted March 13, 2006.


   References
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 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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