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Reproductive Endocrinology |
United States Department of Agriculture/Agricultural Research Service Children’s Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine (N.F.B., J.M.H.), Houston, Texas 77030; and Amgen Incorporated (M.A.N.), Thousand Oaks, California 91320
Address all correspondence and requests for reprints to: Nancy F. Butte, Children’s Nutrition Research Center, Baylor College of Medicine, 1100 Bates Street, Houston, Texas 77030.
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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Introduction |
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Infertility and menstrual dysfunction are associated with human obesity; abdominal android fat distribution is associated with menstrual irregularities and infertility (2). Basal gonadotropin levels and the response of LH to gonadotropin-releasing hormone are related to weight and basal metabolism (2). However, these effects cannot be attributed to a lack of leptin, because obese individuals have elevated, albeit variable, levels of serum leptin (3, 4, 5, 6). Conversely, it is possible that reduced sensitivity to the effects of leptin may lead to obesity and a compensatory increase in serum leptin levels. Weight reduction lowers plasma leptin, androgens, and LH, and improves ovulation in infertile obese women but not in ob/ob mice. There is accumulating evidence that body fat plays a role in sex-steroid metabolism. Fat contains aromatase that converts androgens, particularly androstenedione, to estrone, which may induce an elevated LH/FSH ratio, and thereby stimulate ovarian androgen synthesis (7). Although it is becoming increasingly evident that expression of the ob gene is modulated by a variety of factors, including hormone levels, nutrient intake, and metabolic state (8), factors affecting ob gene expression during reproduction and its potential effect on human reproduction are yet unexplored.
The aim of this study was to characterize serum leptin in pregnant and lactating women, and to investigate factors influencing the expression of leptin in reproductive women. Putative relationships between serum leptin and body fat, rates of energy expenditure, milk production, and other hormones were tested. Herewith, we present unexpected changes in serum leptin levels between pregnancy and the postpartum period, and evidence that factors other than FM alone modulate serum leptin in reproductive women.
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Materials and Methods |
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Sixty-five healthy, nonsmoking women were studied longitudinally. Mean (± SD) age, parity, and gravidity were 29.0 ± 4.2 yr, 0.6 ± 0.8, and 2.1 ± 1.3, respectively. Serum leptin, body composition, and energy expenditure were measured at 36 weeks of gestation and at 3 and 6 months postpartum; milk production was evaluated in women (n = 39) choosing to breastfeed. Prepregnancy weight averaged 61.3 ± 8.8 kg. Gestational weight gain was equal to 15.9 ± 5.2 kg. Women gave birth to healthy, term infants weighing 3.46 ± 0.45 kg. This study was approved by the Baylor Affiliates Review Boards for Human Subject Research, and informed written consent was obtained from each subject.
Body composition
Body weight and height were measured using an electronic balance (Healthometer, Bridgeview, IL) and stadiometer (Holtain Limited, Crymych, U.K.), respectively. Body volume was measured with an underwater weighing system (Precision Biomedical Systems, State College, PA), corrected for residual lung volume by a simplified nitrogen washout method (9). Total body water was determined by deuterium dilution (40 mg 2H2O/kg) using gas-isotope-ratio mass spectrometry (Delta-E, Finnigan MAT, San Jose, CA). Dual-energy x-ray absorptiometry (QDR2000, Hologic, Madison, WI) (software version 5.56) was used to measure total body bone mineral content at 15 days postpartum (used for pregnancy) and at 3 and 6 months postpartum. The Fuller (10) four-component model was used to compute fat-free mass (FFM) and FM from weight, total body water, body volume, and bone mineral content.
Serum chemistry
After a 12-h overnight fast, a blood sample was drawn at approximately 0800 h. Serum was separated and stored at -70 C. Serum leptin levels were measured in a solid-phase sandwich enzyme immunoassay, utilizing an affinity-purified polyvalent antibody immobilized in microtiter wells. The antibody was raised against recombinant human leptin and was affinity purified over a human leptin column. Bound leptin was detected with affinity-purified antibody conjugated to horseradish peroxidase and quantitated with a chromogenic substrate (TMB/peroxide). Leptin concentrations were calculated from standard curves generated for each assay using recombinant human leptin. The minimal leptin detection limit was 70 pg/mL. The intra- and interassay coefficients of variation were 3% and 8%, respectively. The slope of the dose-response curve was 0.80, and the mid range of the assay was 588 pg/mL. A solid-phase 125I RIA (Diagnostic Products Corp., Los Angeles, CA) was used to measure serum insulin (intra- and interassay coefficients of variation = 5% and 7%, respectively) and serum PRL (intra- and interassay coefficients of variation = 6% and 7%, respectively).
Milk production
Milk production was determined from a 24-h complete milk expression while the mother was in the calorimeter and separated from her infant. The milk contents of each breast were completely expressed using an electric breast pump (Egnell, Cary, IL) and weighed on an electronic scale.
Energy expenditure
Oxygen consumption and carbon dioxide were measured continuously in a room-sized calorimeter for 24 h. The performance of the respiration calorimeters is described elsewhere (11). Subjects adhered to a specific eating, exercise (two 15-min treadmill walks at 2 mph), and sleeping schedule while in the calorimeter. Basal metabolic rate was measured for 40 min while the subject lay quietly on awakening after a 12-h fast. Sleeping metabolic rate (SMR) was the average expenditure during night sleep.
Statistic analyses
Minitab Statistical Software program (release 10.5X, Minitab,
1995, State College, PA) was used for data reduction and statistical
analysis which entailed Student’s t test and multiple
linear regression. ANOVA with repeated measures (BMDP2V Statistical
Software, 1993) was used to test for time effects. Statistical
significance was set at P 
0.05.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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). In 92% of the
women studied, leptin declined from pregnancy to 3 months
postpartum.
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). Leptin was positively correlated with FM (r =
0.63, 0.60, 0.54; P = 0.001) and percentage body fat
(r = 0.64, 0.58, 0.52; P = 0.001) but not with FFM
(kilograms or percent weight). Serum leptin levels at 36 weeks of
gestation were positively correlated with leptin levels at 3 months
(r = 0.72; P = 0.001), as were levels between 3
months and 6 months (r = 0.88; P = 0.001).
Adjusted for fat mass, the partial correlations between leptin levels
were r = 0.50 (P = 0.001) between 36 weeks and 3
months and r = 0.82 (p-0.001) between 3 months and 6 months.
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). At 3 and 6 months, the linear
regressions of leptin on FM were nearly superimposable (Table 2).
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Leptin was positively correlated with fasting serum insulin during
pregnancy (9.3 ± 3.9 µIU/mL) and at 3 months (7.6 ± 3.3
µIU/mL) and 6 months (8.6 ± 3.9 µIU/mL) postpartum (r =
0.35, 0.41, 0.56; P = 0.001). However, controlled for
body FM or percentage body fat, no independent effect of insulin on
leptin was detected. The change in leptin observed between pregnancy
and 3 months postpartum (-11.9 ± 12.5 ng/mL) was negatively
associated with gestational weight gain (r = -0.45;
P = 0.001) and positively associated with corresponding
changes in weight (r = 0.43; P = 0.001), FM
(r = 0.44; P = 0.001) and serum insulin (r =
0.25; P = 0.05) (Fig. 3). The change in
leptin between 3 and 6 months postpartum (0.01 ± 5.7 ng/mL) was
positively correlated with the corresponding change in weight (r =
0.40; P = 0.001) and FM (r = 0.24;
P = 0.05) (Fig. 4). Changes in leptin were not related
to changes in FFM at either interval.
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Leptin was not significantly different between lactating (L, n = 39) and nonlactating (NL, n = 26) women at 3 months (L 16.5 ± 15.7 vs. NL 20.2 ± 14.5 ng/mL) and 6 months postpartum (L 13.1 ± 10.6 vs. NL 20.1 ± 15.2 ng/mL) with or without adjustment for FM. Fasting serum PRL concentrations of the lactating women averaged 84.7 ± 53.5 and 37.5 ± 22.3 ng/mL at 3 and 6 months postpartum, respectively. Negative correlations between serum leptin and PRL were observed at 3 (r = -0.30; P = 0.06) and 6 months postpartum (r = -0.45; P = 0.01). The amount of human milk expressed over a 24-h period was 813 ± 226 and 725 ± 268 g/day at 3 and 6 months postpartum, respectively. There was a tendency for the 24-h milk expression to be negatively correlated with leptin at 3 (r = -0.45; P = 0.004) and 6 months postpartum (r = -0.29; P = 0.11). However, this relationship could be explained by the negative association between leptin and PRL. In a multiple regression analysis of 24-h milk production on PRL and leptin, leptin was not significant.
Fasting serum leptin was positively correlated with 24-h energy
expenditure, BMR and SMR at 36 weeks of pregnancy and at 3 and 6 months
postpartum (r = 0.28–0.36; P 0.03). However,
adjusted for weight or FFM and FM, rates of energy expenditure were not
significantly correlated with leptin. Changes in energy expenditure
were not correlated with corresponding changes in leptin, once they
were controlled for changes in weight or FM, except for the change in
SMR between 3 and 6 months (r2adj = 10.5%;
P = 0.005).
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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In agreement with other reports (3, 5), we found that leptin was correlated positively with weight, BMI, FM, and percentage FM. Changes in leptin also correlated with changes in weight and FM. Women who gained more weight during pregnancy had higher leptin levels. Similarly, women who gained or failed to lose weight postpartum had higher leptin levels. Postpartum weight retention (up to 18 kg) was positively associated with leptin levels. These findings support the lipostatic role of leptin as an afferent signal in a feedback loop regulating FM, a signal that may be defective in obese individuals. High levels of serum leptin and ob messenger RNA in obese vs. lean individuals are likely a consequence of reduced leptin sensitivity rather than inadequate leptin (3, 4, 5, 6, 12). Leptin sensitivity may also influence the hypothalamic-pituitary-gonadal axis, and thereby play a role in fertility and menstrual function; further research is needed in this area.
Pregnancy is characterized by insulin resistance with advancing gestation. Obesity in humans is also characterized by hyperinsulinemia. The close association between hyperinsulinemia and hyperleptinemia suggests that ob gene expression may be mediated by insulin (13, 14). Both insulin and leptin are suppressed during fasting and increase with refeeding. However, the relationship between insulin and leptin appears to be more complex. Insulin treatment only partially restored ob gene expression in the streptozotocin-diabetic rat (15). In Zucker diabetic fatty rats and db/db mice, administration of the antidiabetic agent, thiazolidinedione, not only improved insulin sensitivity and glucose homeostasis, but also down-regulated ob gene expression (8). We found a positive correlation between fasting serum insulin and leptin, but not an independent effect of insulin on leptin after controlling for FM. Considine et al. (5) reported similar results in adult men and women; no independent effects of BMI, age, gender, race, or fasting serum insulin and glucose on leptin were found after controlling for percentage body fat. Leptin does not appear to be responsive to acute metabolic changes, at least in humans. The 24-h diurnal pattern for leptin did not parallel changes in insulin (4). The leptin pattern resembled that seen for PRL and thyrotropin, showing levels that were highest at 2400 h and early morning, and lowest at 1200 h. However, Kolaczynski et al. (16) demonstrated a long-term stimulatory effect of insulin on leptin production in vivo and in vitro in humans.
Evidence is accumulating that the hypothalamus is the main site for leptin action (17). Leptin receptor (OB-R) has been identified not only in the mouse choroid plexus, but also in the arcuate nucleus of the hypothalamus, suggesting that leptin may be involved in signal transduction within the hypothalamus (18, 19, 20). A long isoform of the wild-type leptin receptor is preferentially expressed in the hypothalamus and can activate signal transducers and activators of transcription, which may mediate the antiobesity effects of leptin (21). Leptin not only decreased food intake, but also normalized elevated levels of appetite-stimulating hypothalamic peptide neuropeptide Y (arcuate nucleus) in genetically obese mice and rats. Receptor OB-R also is expressed in the lung, kidney (18), and ovary (1), implicating leptin involvement in other pathways. Experiments with ob/ob mice have documented leptin’s role in suppressing appetite, as well as accelerating metabolism and selectively suppressing fat synthesis (13), and most recently elucidated a fascinating role in reproduction (1).
Recombinant human leptin corrected sterility in the ob/ob female mouse (1). Daily injections of leptin brought ovulation, pregnancy, and parturition to fruition. Previous studies demonstrated that reproductive function was restored with hypothalamic extracts, pituitary extracts, gonadotrophic hormones, progesterone, and relaxin, but not by weight reduction (1).
During pregnancy, factors in addition to FM must regulate the expression of ob gene. In our study, the relation (i.e. slope) between leptin and FM did not differ between pregnancy and the postpartum intervals; however, the line shifted upward during pregnancy. Between pregnancy and 3 months postpartum, a mean 6% reduction in FM was associated with a mean 61% decrease in leptin. The decline in leptin was explained partially by the decrease in insulin, but much of the variation (80%) has yet to be explained. Reproductive hormones likely are involved. Increased basal and glucose-stimulated levels of plasma insulin with advancing gestation parallel progressive increases in plasma progesterone, estrogen, and human placental lactogen, which may affect the expression of ob gene.
As expected, energy expenditure increased during pregnancy because of additional maternal and fetal tissues, and decreased postpartum in accordance with weight losses. The positive correlations observed between leptin and the rates of energy expenditure and their changes were accounted for by body mass, or FFM and FM, with one exception: the change in leptin was positively associated with the change in SMR between 3 and 6 months postpartum.
During pregnancy, the secretory apparatus of the mammary gland undergoes considerable development through the interaction of many hormones. Insulin, cortisol, and thyroid hormones are required, but estrogen, progesterone, PRL, and placental mammotropic hormones are the major promoters (22). After delivery, the fall in estrogen and progesterone enables PRL to initiate lactation. Secretion of PRL involves the balance of PRL-stimulating and -inhibitory factors, which are integrated at the level of the hypothalamus. PRL release from the anterior pituitary is under the tonic inhibitory control of dopamine and various PRL-releasing factors (PRFs) (23). Putative PRFs include TRH and vasoactive intestinal peptide (24). PRL secretion is also modulated by neurotransmitter influences impinging on the hypothalamus. The suckling reflex stimulates PRFs and inhibits PRL-inhibitory factors. In our lactating women, an inverse relation was observed between leptin and PRL. No direct effect of leptin was observed on milk production independent of PRL.
The profound effects of leptin on reproductive function in the ob/ob mouse have reaffirmed that adipose tissue is not simply an inert energy depot, but an active player influencing the hypothalamic-pituitary-gonadal axis. The identification of ob receptors in the hypothalamus raises the possible role of leptin in the regulation of hypothalamic gonadotropins and PRL-releasing and -inhibitory factors in reproductive women.
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Acknowledgments |
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Received August 20, 1996.
Revised October 15, 1996.
Accepted October 21, 1996.
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References |
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leptin (ng/mL) = -9.2 +
1.7 