This Article Abstract Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Nagy, T. R. Articles by Goran, M. I. Search for Related Content PubMed PubMed Citation Articles by Nagy, T. R. Articles by Goran, M. I.

Effects of Gender, Ethnicity, Body Composition, and Fat Distribution on Serum Leptin Concentrations in Children¹

Energy Metabolism Research Unit, Departments of Nutrition Sciences (T.R.N., B.A.G., C.A.T., C.D., M.I.G.) and Health Services Administration (R.M.S), School of Health-Related Professions, University of Alabama at Birmingham, Birmingham, Alabama 35294

Address all correspondence and requests for reprints to: Tim R. Nagy, Ph.D., Department of Nutrition Sciences, Energy Metabolism Research Unit, University of Alabama at Birmingham, Birmingham, Alabama 35294-3360. E-mail: tnagy{at}uab.edu

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
The Ob protein leptin has been shown to be closely correlated with measures of body fat in humans and animals. Studies have suggested that there are both gender and ethnic differences in serum leptin concentrations, even after controlling for total and relative body fat and body mass index. We hypothesized that gender and ethnic differences in serum leptin concentrations are due to differences in both body composition and body fat distribution. We measured fasting serum leptin concentration, body composition (fat mass and fat-free mass by dual energy x-ray absorptiometry), and body fat distribution (intraabdominal and sc abdominal adipose tissue by computed tomography) in 74 prepubertal boys and girls (43 African-Americans and 31 Caucasians). Our results showed that gender differences in serum leptin concentrations could not be fully explained by differences in body mass index, total fat mass, or relative body composition. However, when serum leptin concentrations were adjusted for differences in relative body composition (fat mass and fat-free mass) and body fat distribution (sc and intraabdominal adipose tissue), gender no longer had an independent effect on the serum leptin concentration. Serum leptin concentrations were not influenced by ethnicity. Thus, when comparing group differences in serum leptin concentrations, it is necessary to adequately control for group differences in body composition and fat distribution.

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
THE ob gene product, leptin, is a hormone secreted by adipose tissue (1). The circulating concentration of leptin is closely and positively correlated with body fat in humans (1, 2) and mice (2, 3). Using in vivo arteriovenous balance techniques, Klein et al. (4) have shown that leptin production by sc adipose tissue is positively related to the percent body fat. However, at any given level of percent body fat, there is a fairly large variation in the circulating concentration of leptin (1, 2). The cause of this variation is unknown.

One potential source of variation in serum leptin concentration is gender. Sexual dimorphism in serum leptin concentrations have been reported (5, 6, 7, 8). The gender difference remains significant after adjusting for body mass index (BMI), total fat mass, and percent body fat. Rosenbaum et al. (6) found differences in leptin concentrations (adjusted for total fat mass) between men and postmenopausal women, suggesting that the gender difference is not due solely to differences in sex hormones.

A second potential source of variation in serum leptin concentrations is body fat distribution, as the level of ob messenger ribonucleic acid expression has been shown to vary with anatomical site (9, 10, 11). Thus, gender and ethnic differences in fat distribution could potentially lead to variations in the concentration of serum leptin, independent of total or relative fat mass. Previous studies have produced mixed results concerning the effect of fat distribution on serum leptin concentrations (5, 7, 12). In Western Samoan women, waist circumference, but not waist to hip ratio, was related to the serum leptin concentration after controlling for BMI (5). In contrast, Rosenbaum et al. (6) and Hickey et al. (7) failed to find an effect of waist to hip ratio or waist circumference on the serum leptin concentration, independent of fat mass. However, it is important to point out that the use of these anthropometric estimates of fat distribution may not adequately assess true differences in fat distribution (13, 14, 15) and, therefore, may have limited usefulness.

The purpose of this study was to determine the effects of body fat and body fat distribution on gender and ethnic differences in circulating leptin concentrations in prepubertal, African-American, and Caucasian children. Our study differs from previous ones in that we have accurate measures of body composition (dual energy x-ray absorptiometry) and fat distribution [computed tomography (CT)]. Our results suggest that the sexual dimorphism in serum leptin concentrations may be explained by gender differences in body composition and fat distribution. We found no significant effects of ethnicity on the serum leptin concentration.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Subjects

We studied 43 prepubertal African-American (23 girls and 20 boys) and 31 Caucasian (8 girls and 23 boys) children. Children were recruited by newspaper and radio advertisements and by word of mouth. Subjects were screened by a medical history evaluation and were ineligible if they were taking medications known to affect body composition or physical activity (e.g. prednisone, ritalin, or GH), if they were diagnosed with syndromes known to affect body composition and/or fat distribution (e.g. Cushing’s syndrome, Down’s syndrome, type I diabetes, or hypothyroidism), or they had experienced any major illness since birth. Pubertal status (Tanner stage) was determined by physician evaluation of both breast and pubic hair in females (16) and genitalia in males (17). This study was approved by the institutional review board at the University of Alabama at Birmingham. The parents of all participants provided informed consent before testing commenced.

Protocol

Children were admitted to the General Clinical Research Center in the late afternoon for an overnight visit. Upon arrival, anthropometric measurements were obtained, and dinner was served at approximately 1700 h. An evening snack was allowed as long as it was consumed before 2000 h. After 2000 h, only water and noncaloric, noncaffeinated beverages were allowed until after the morning testing. Between 1850–1950 h, a single slice CT scan was taken at the level of the umbilicus. The following morning, blood was collected for hormone analyses. Two weeks later, the children arrived at the Energy Metabolism Research Unit at 0700 h in the fasted state, and body composition was determined by dual energy x-ray absorptiometry (DXA).

Fat distribution and body composition

Subcutaneous abdominal adipose tissue (SAAT) and intraabdominal adipose tissue (IAAT) were measured by CT scanning with a HiLight/Advantage Scanner (General Electric, Milwaukee, WI) as previously described (15). A single slice scan (5 mm) of the abdomen was performed at the level of the umbilicus and analyzed for cross-sectional area of adipose using the density contour program. CT data are presented as the cross-sectional area of tissue (square centimeters) with the Hounsfield units for adipose tissue as -190 to -30. We have shown the test-retest reliability for IAAT to be 1.7% (18). All scans were analyzed by the same investigator (T.R.N.). The total body radiation dose to each subject was approximately 0.26 rad. This total body radiation dose is less than that received from a standard chest x-ray.

Body composition [fat mass and fat-free mass (FFM)] was measured by DXA using a Lunar DPX-L densitometer (Lunar Radiation Corp., Madison, WI). We have previously validated the use of DXA against carcass analysis in a pig model that encompassed the pediatric weight range (19). Subjects were scanned in light clothing while lying flat on their backs with arms at their sides. DXA scans were performed and analyzed with pediatric software version 1.5e.

Serum leptin concentrations

Serum leptin was determined using serum from the fasted children with a RIA kit (Linco Research, St. Charles, MO). All serum samples (100 µL) were analyzed in duplicate in a single assay. The intraassay coefficient of variation was 4.2% at 64% bound (2.61 ng/mL) and 3.5% at 28% bound (14.9 ng/mL).

Statistical methods

Because the data for some variables were not normally distributed, they were log₁₀ transformed to increase the normality of their distribution. In these cases, the values shown are the back-transformed means (geometric mean). Differences in subject characteristics were determined by two-way ANOVA, with gender and ethnicity as class variables (the interaction of gender and ethnicity was included in the ANOVA). Simple correlations (Pearson product moment) were assessed for serum leptin concentration and measures of fat. To determine the independent effects of variables on the serum leptin concentration, multiple linear regression analyses were performed (general linear models procedure). All statistics were performed using SAS for Windows (version 6.10, SAS Institute, Cary, NC). Data were considered significant if P < 0.05.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Descriptive statistics are shown in Table 1. There were no significant effects of gender or ethnicity on age, weight, BMI, or absolute values for total fat, SAAT, or IAAT. Percent body fat, serum leptin, and FFM were all significantly affected by gender; girls had greater body fat and leptin concentrations and lesser FFM than boys.

View larger version (27K): [in this window] [in a new window]   Figure 1. Serum leptin concentration (nanograms per mL) by gender in 74 children. Data were analyzed by ANOVA (unadjusted) or by analysis of covariance (ANCOVA) with the listed variables as covariates. Both gender and ethnicity were included as class variables in the models. Data shown are back-transformed least square means for the effect of gender. The serum leptin concentration, total fat, FFM, SAAT, and IAAT were transformed (log10) before analysis. *, P < 0.05, **, P < 0.01; ***, P < 0.001.

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

Our data agree with those reported by others, in that the sexual dimorphism in serum leptin concentrations persists after controlling for BMI, fat mass, or relative fat mass (5, 6, 7, 8, 12, 20, 21). However, when body fat distribution (SAAT and IAAT) was added to the model (in addition to body composition), gender no longer was significantly related to the serum leptin concentration. Our data suggest that the sexual dimorphism in serum leptin concentrations may be due to both relative body composition and fat distribution. To our knowledge, no other study investigating the sexual dimorphism in serum leptin concentrations has controlled for both relative body composition and fat distribution using DXA and CT.

A previous study in children (20) found a significant effect of gender on the serum leptin concentration after controlling for BMI and SAAT. Our results concur; when we controled for differences in BMI and SAAT, gender remained significant (P < 0.01; data not shown). However, BMI may not be a good measure of body composition. For instance, at any given BMI, women tend to have more body fat then men (22). Moreover, when we control for BMI in our data set, girls have significantly greater percent relative body fat than boys (P < 0.001; data not shown).

Because of the inherent problems with using ratios (percent fat) to normalize data (23, 24), we chose to enter both fat mass and FFM into our regression models to control for differences in body composition. When entered together, both fat mass and FFM were independent predictors, albeit in different directions, of the serum leptin concentration. As has been shown, the serum leptin concentration is positively associated with fat mass. However, when FFM is entered into the model with fat mass, FFM is negatively related to serum leptin concentrations. These results suggest that at a given fat mass, a person with a greater FFM would have a lower serum leptin concentration than a person with a lesser FFM, if all else is equal. This finding implies that FFM or some factor related to FFM or relative body composition plays a role in the regulation of leptin production.

We found that fat distribution was a contributor to the variations in serum leptin concentrations independent of body composition. Thus, at any given body composition, individuals with relatively greater fat mass partitioned to the sc areas would be expected to have greater serum leptin concentrations. As premenopausal women, relative to men, tend to partition fat to the sc spaces (25), they would be expected to have greater serum leptin concentrations then men at any given body composition. This relationship may explain the persistence of the sexual dimorphism in serum leptin concentrations after controlling for body composition and the lack of a gender effect when both body composition and fat distribution are considered.

Similarly, gender differences in serum leptin may also be explained by the sexual dimorphism in IAAT. Men tend to deposit relatively more fat in the intraabdominal space than do women (25), and leptin production from IAAT does not appear to be related to body fatness in an independent manner. Our study shows that although IAAT was positively correlated with the serum leptin concentration, the relationship was not independent of total fat mass (P = 0.89; data not show) or of body composition and SAAT, a result similar to that reported by Dua et al. (26). In addition, Montague et al. (11) showed that leptin messenger ribonucleic acid expression from intraabdominal adipocytes does not correlate with BMI in either men or women. Thus, fat distribution appears to have a profound effect on the serum leptin concentration; if all else is equal, individuals with fat distributed in the intraabdominal area (male distribution?) would be expected to have lower serum leptin levels than individuals with fat distributed to the sc area (female distribution?).

We found no effect of ethnicity (African-American vs. Caucasian) on the serum leptin concentration. Two previous studies likewise failed to find ethnic differences in serum leptin concentrations once body fat was taken into account. Hassink et al. (21) found no difference in serum leptin concentrations when comparing Caucasian to African-American and Hispanic children (the latter two groups were collapsed into one group due to sample size) after controlling for BMI and tricep skinfold. Similarly, Dagoga-Jack et al. (27) found no difference in leptin levels between Caucasian and African-American adults after controlling for BMI.

In contrast to the above reports and the present study, Nicklas et al. (28) reported differences in serum leptin concentrations between African-American and Caucasian obese postmenopausal women. The lower leptin concentrations in African-American women persisted after controlling for total fat mass. Although the two groups of women did not differ with respect to fat mass, the African-American women did have significantly more lean tissue mass. Based on our multiple regression model (fat mass was a positive, whereas FFM was a negative, predictor of the leptin concentration), the African-American women in their study would be predicted to have lower serum leptin concentrations than the Caucasians. Therefore, the ethnic difference in serum leptin concentration in the study by Nicklas et al. (28) may be explained by differences in body composition.

In conclusion, our data show that serum leptin concentrations in children are highly correlated with measures of body fat, and that gender differences in serum leptin concentrations may be due to differences in body composition and body fat distribution. Future studies examining the role of gender in serum leptin concentrations should consider both relative body composition (fat vs. FFM) and fat distribution (intraabdominal vs. sc). Additionally, the inclusion of both fat and FFM in our regression models showed that FFM had a negative effect on the serum leptin concentration, suggesting that FFM or something closely correlated with FFM may have a negative feedback effect on serum leptin concentrations. Our data also showed that the effect of body fat distribution on the serum leptin concentration is independent of body composition. Lastly, we found no evidence for an effect of ethnicity on the serum leptin concentration in our sample of children.

	Acknowledgments

 
We thank the children and their parents for participating in this study, Tena Hilario for subject recruitment and testing, and the members of the Energy Metabolism Research Unit for helpful comments.

	Footnotes

 
¹ This work was supported by grants from the USDA (95–37200-1643), the NICHHD (R29-HD-3268, RO1-HD/HL-33064, and F32-HD-08025), and the GCRC (M01-RR-00032).

Received February 10, 1997.

Revised March 21, 1997.

Accepted March 31, 1997.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 

1. Considine RV, Sinha MK, Heiman ML, et al. 1996 Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med. 334:292–295.[Abstract/Free Full Text]
2. Maffei M, Halaas J, Ravussin E, et al. 1995 Leptin levels in human and rodent: Measurements of plasma leptin and ob RNA in obese and weight-reduced subjects. Nat Med. 1:1155–1161.[CrossRef][Medline]
3. Frederich RC, Hamann A, Anderson S, Lollmann B, Lowell BB, Flier JS. 1995 Leptin levels reflect body lipid content in mice: evidence for diet-induced resistance to leptin action. Nat Med. 1:1311–1314.[CrossRef][Medline]
4. Klein S, Coppack SW, Mohamed-Ali V, Landt M. 1996 Adipose tissue leptin production and plasma leptin kinetics in humans. Diabetes. 45:984–987.[Abstract]
5. Zimmet P, Hodge A, Nicolson M, et al. 1996 Serum leptin concentration, obesity, and insulin resistance in Western Samoans: a cross sectional study. Br Med J. 313:965–969.[Abstract/Free Full Text]
6. Rosenbaum M, Nicholson M, Hirsch J, et al. 1996 Effects of gender, body composition, and menopause on plasma concentrations of leptin. J Clin Endocrinol Metab. 81:3424–3427.[Abstract]
7. Hickey MS, Isreal RG, Gardiner SN, et al. 1996 Gender differences in serum leptin levels in humans. Biochem Mol Med. 59:1–6.[CrossRef][Medline]
8. Havel PJ, Kasim-Karakas S, Dubuc GR, Mueller W, Phinney SD. 1996 Gender differences in plasma leptin concentrations. Nat Med. 2:949–950.[Medline]
9. Masuzaki H, Ogawa Y, Isse N, et al. 1995 Human obese gene expression: adipocyte-specific expression and regional differences in the adipose tissue. Diabetes. 44:855–858.[Abstract]
10. Ogawa Y, Masuzaki H, Isse N, et al. 1995 Molecular cloning of rat obese cDNA and augmented gene expression in genetically obese Zucker fatty (fa/fa) rats. J Clin Invest. 96:1647–1652.
11. Montague CGT, Prins JB, Sanders L, Digby JE, O’Rahilly S. 1997 Depot- and sex-specific differences in human leptin mRNA expression: implications for the control of regional fat distribution. Diabetes. 46:342–347.[Abstract]
12. Ostlund Jr RE, Yang JW, Klein S, Gingerich R. 1996 Relation between plasma leptin concentration and body fat, gender, diet, age, and metabolic covariates. J Clin Endocrinol Metab. 81:3909–3913.[Abstract/Free Full Text]
13. van der Kooy K, Leenen R, Seidell JC, Deurenberg P, Droop A, Bakker CJG. 1993 Waist-hip ratio is a poor predictor of changes in visceral fat. Am J Clin Nutr. 57:327–333.[Abstract/Free Full Text]
14. Després JP, Prud’Homme D, Pouliot MC, Tremblay A, Bouchard C. 1991 Estimation of deep abdominal adipose-tissue accumulation from simple anthropometric measurements in men. Am J Clin Nutr. 54:471–477.[Abstract/Free Full Text]
15. Treuth MS, Hunter GR, Kekes-Szabo T. 1995 Estimating intraabdominal adipose tissue in women by dual-energy x-ray absorptiometry. Am J Clin Nutr. 62:527–532.[Abstract/Free Full Text]
16. Marshall WA, Tanner JM. 1969 Variations in pattern of pubertal changes in girls. Arch Dis Child. 44:291–303.
17. Marshall WA, Tanner JM. 1970 Variations in the pattern of pubertal changes in boys. Arch Dis Child. 45:13–23.
18. Goran MI, Kaskoun M, Shuman WP. 1995 Intra-abdominal adipose tissue in young children. Int J Obesity. 19:279–283.
19. Pintuaro SJ, Nagy TR, Duthie CM, Goran MI. 1996 Cross-calibration of fat and lean measurements by dual-energy x-ray absorptiometry to pig carcass analysis in the pediatric body weight range. Am J Clin Nutr. 63:293–298.[Abstract/Free Full Text]
20. Caprio S, Tamborlane WV, Silver D, et al. 1996 Hyperleptinemia: an early sign of juvenile obesity. Relations to body fat depots and insulin concentrations. Am J Physiol 271:E626–E630.
21. Hassink SG, Sheslow DV, de Lancey E, Opentanova I, Considine RV, Caro JF. 1996 Serum leptin in children with obesity: relatioship to gender and development. Pediatrics. 98:201–203.[Abstract/Free Full Text]
22. Pouliot M, Despres J, Lemieux S, et al. 1994 Waist circumference and abdominal sagittal diameter: best simple anthropometric indexes of abdominal visceral adipose tissue accumulation and related cardiovascular risk in men and women. Am J Cardiol. 73:460–468.[CrossRef][Medline]
23. Allison DB, Paultre F, Goran MI, Poehlman ET, Heymsfield SB. 1995 Statistical considerations regarding the use of ratios to adjust data. Int J Obesity. 19:644–652.[Medline]
24. Goran MI, Allison DB, Poehlman ET. 1995 Issues relating to normalization of body fat content. Int J Obesity. 19:638–643.[Medline]
25. Seidell JC, Oosterlee A, Deurenberg P, Hautvast JG, Ruijs JH. 1988 Abdominal fat depots measured with computed tomography: effects of degree of obesity, sex, and age. Eur J Clin Nutr. 42:805–815.[Medline]
26. Dua A, Hennes MI, Hoffmann RG, et al. 1996 Leptin: a significant indicator of total body fat but not of visceral fat and insulin insensitivity in African-American women. Diabetes. 45:1635–1637.[Abstract]
27. Dagogo-Jack S, Fanelli C, Paramore D, Brothers J, Landt M. 1996 Plasma leptin and insulin relationships in obese and nonobese humans. Diabetes. 45:695–698.[Abstract]
28. Nicklas BJ, Toth MJ, Goldberg AP, Poehlman ET. 1997 Racial differences in plasma leptin concentrations in obese postmenopausal women. J Clin Endocrinol Metab. 82:315–317.[Abstract/Free Full Text]

This article has been cited by other articles:

				S. Zhang, X. Liu, W. J. Brickman, K. K. Christoffel, D. Zimmerman, H.-J. Tsai, G. Wang, B. Wang, Z. Li, G. Tang, et al. Association of Plasma Leptin Concentrations with Adiposity Measurements in Rural Chinese Adolescents J. Clin. Endocrinol. Metab., September 1, 2009; 94(9): 3497 - 3504. [Abstract] [Full Text] [PDF]

				A. A Venner, P. K Doyle-Baker, M. E Lyon, and T. S Fung A meta-analysis of leptin reference ranges in the healthy paediatric prepubertal population Ann Clin Biochem, January 1, 2009; 46(1): 65 - 72. [Abstract] [Full Text] [PDF]

				S. Kayemba-Kay's, M. P P Geary, J. Pringle, C. H Rodeck, J. C P Kingdom, and P. C Hindmarsh Gender, smoking during pregnancy and gestational age influence cord leptin concentrations in newborn infants Eur. J. Endocrinol., September 1, 2008; 159(3): 217 - 224. [Abstract] [Full Text] [PDF]

				J. M. Hibbert, L. L. Hsu, S. J. Bhathena, I. Irune, B. Sarfo, M. S. Creary, B. E. Gee, A. I. Mohamed, I. D. Buchanan, A. Al-Mahmoud, et al. Proinflammatory Cytokines and the Hypermetabolism of Children with Sickle Cell Disease Experimental Biology and Medicine, January 1, 2005; 230(1): 68 - 74. [Abstract] [Full Text] [PDF]

				J. Munoz and B. A. Gower Relationship between Serum Leptin Concentration and Low-Density Muscle in Postmenopausal Women J. Clin. Endocrinol. Metab., March 1, 2003; 88(3): 1157 - 1161. [Abstract] [Full Text] [PDF]

				K. Arfai, P. D. Pitukcheewanont, M. I. Goran, C. J. Tavare, L. Heller, and V. Gilsanz Bone, Muscle, and Fat: Sex-related Differences in Prepubertal Children Radiology, August 1, 2002; 224(2): 338 - 344. [Abstract] [Full Text] [PDF]

				P. Marzullo, C. Buckway, K. L. Pratt, A. Colao, J. Guevara-Aguirre, and R. G. Rosenfeld Leptin Concentrations in GH Deficiency: The Effect of GH Insensitivity J. Clin. Endocrinol. Metab., February 1, 2002; 87(2): 540 - 545. [Abstract] [Full Text] [PDF]

				M. I. Goran and B. A. Gower Longitudinal Study on Pubertal Insulin Resistance Diabetes, November 1, 2001; 50(11): 2444 - 2450. [Abstract] [Full Text] [PDF]

				J. S. Harrell, P. Bomar, R. McMurray, C. Bradley, and S. Deng Leptin and Obesity in Mother-Child Pairs Biol Res Nurs, October 1, 2001; 3(2): 55 - 64. [Abstract] [PDF]

				K G Tantisira and S T Weiss Complex interactions in complex traits: obesity and asthma Thorax, September 1, 2001; 56(90002): ii64 - 74. [Full Text] [PDF]

				L. Ghizzoni, G. Mastorakos, M. Ziveri, M. Furlini, A. Solazzi, A. Vottero, and S. Bernasconi Interactions of Leptin and Thyrotropin 24-Hour Secretory Profiles in Short Normal Children J. Clin. Endocrinol. Metab., May 1, 2001; 86(5): 2065 - 2072. [Abstract] [Full Text]

				M. I Goran Metabolic precursors and effects of obesity in children: a decade of progress, 1990-1999 Am. J. Clinical Nutrition, February 1, 2001; 73(2): 158 - 171. [Abstract] [Full Text] [PDF]

				B. Lonnerdal and P. J Havel Serum leptin concentrations in infants: effects of diet, sex, and adiposity Am. J. Clinical Nutrition, August 1, 2000; 72(2): 484 - 489. [Abstract] [Full Text] [PDF]

				M. B. HORLICK, M. ROSENBAUM, M. NICOLSON, L. S. LEVINE, B. FEDUN, J. WANG, R. N. PIERSON Jr., and R. L. LEIBEL Effect of Puberty on the Relationship between Circulating Leptin and Body Composition J. Clin. Endocrinol. Metab., July 1, 2000; 85(7): 2509 - 2518. [Abstract] [Full Text]

				B. A. Gower, T. R. Nagy, M. I. Goran, A. Smith, and E. Kent Leptin in Postmenopausal Women: Influence of Hormone Therapy, Insulin, and Fat Distribution J. Clin. Endocrinol. Metab., May 1, 2000; 85(5): 1770 - 1775. [Abstract] [Full Text]

				H. Fors, H. Matsuoka, I. Bosaeus, S. Rosberg, K. A. Wikland, and R. Bjarnason Serum Leptin Levels Correlate with Growth Hormone Secretion and Body Fat in Children J. Clin. Endocrinol. Metab., October 1, 1999; 84(10): 3586 - 3590. [Abstract] [Full Text] [PDF]

				M. Rosenbaum and R. L. Leibel Role of Gonadal Steroids in the Sexual Dimorphisms in Body Composition and Circulating Concentrations of Leptin J. Clin. Endocrinol. Metab., June 1, 1999; 84(6): 1784 - 1789. [Full Text]

				M. Miyakawa, T. Tsushima, H. Murakami, O. Isozaki, H. Demura, and T. Tanaka Effect of Growth Hormone (GH) on Serum Concentrations of Leptin: Study in Patients with Acromegaly and GH Deficiency J. Clin. Endocrinol. Metab., October 1, 1998; 83(10): 3476 - 3479. [Abstract] [Full Text]

				W. W. Wong, M. Nicolson, J. E. Stuff, N. F. Butte, K. J. Ellis, A. C. Hergenroeder, R. B. Hill, and E. O. Smith Serum Leptin Concentrations in Caucasian and African-American Girls J. Clin. Endocrinol. Metab., October 1, 1998; 83(10): 3574 - 3577. [Abstract] [Full Text]

				J. N. Roemmich, P. A. Clark, S. S. Berr, V. Mai, C. S. Mantzoros, J. S. Flier, A. Weltman, and A. D. Rogol Gender differences in leptin levels during puberty are related to the subcutaneous fat depot and sex steroids Am J Physiol Endocrinol Metab, September 1, 1998; 275(3): E543 - E551. [Abstract] [Full Text] [PDF]

				M. R. Palmert, S. Radovick, and P. A. Boepple Leptin Levels in Children with Central Precocious Puberty J. Clin. Endocrinol. Metab., July 1, 1998; 83(7): 2260 - 2265. [Abstract] [Full Text]

				M. A. Llopis, M. L. Granada, G. Cuatrecasas, X. Formiguera, L. Sánchez-Planell, A. SanmartÍ, A. Alastrué, M. Rull, A. Corominas, and M. Foz Growth Hormone-Binding Protein Directly Depends on Serum Leptin Levels in Adults with Different Nutritional Status J. Clin. Endocrinol. Metab., June 1, 1998; 83(6): 2006 - 2011. [Abstract] [Full Text]

				M. R. Palmert, S. Radovick, and P. A. Boepple The Impact of Reversible Gonadal Sex Steroid Suppression on Serum Leptin Concentrations in Children with Central Precocious Puberty J. Clin. Endocrinol. Metab., April 1, 1998; 83(4): 1091 - 1096. [Abstract] [Full Text]

				T. R. Nagy, B. A. Gower, R. M. Shewchuk, and M. I. Goran Serum Leptin and Energy Expenditure in Children J. Clin. Endocrinol. Metab., December 1, 1997; 82(12): 4149 - 4153. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Nagy, T. R. Articles by Goran, M. I. Search for Related Content PubMed PubMed Citation Articles by Nagy, T. R. Articles by Goran, M. I.