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Racial Differences in Plasma Leptin Concentrations in Obese Postmenopausal Women¹

Department of Medicine, Division of Gerontology, University of Maryland School of Medicine, and the Geriatric Research Education and Clinical Center, Baltimore Veterans Administration Medical Center, Baltimore, Maryland 21201

Address all correspondence and requests for reprints to: Barbara J. Nicklas, Ph.D., Division of Gerontology (18), Baltimore Veterans Administration Medical Center, 10 North Greene Street, Baltimore, Maryland 21201. E-mail: bnicklas{at}umabnet.ab.umd.edu

	Abstract

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Leptin may play an important role in the regulation of body weight by influencing energy intake and expenditure. Differences in body composition, resting energy expenditure (REE), and physical activity between African-American and Caucasian women could be reflective of racial differences in plasma leptin concentrations. Thus, we examined racial differences in leptin levels and the relationships of leptin to body composition and resting metabolism in obese postmenopausal African-American (n = 28) and Caucasian (n = 29) women matched for level of body fat. African-American and Caucasian women were similar in age (64.1 ± 1.3 vs. 63.2 ± 1.0 yr), body weight (84.7 ± 3.3 vs. 80.4 ± 1.3 kg), adipose tissue mass (39.7 ± 2.8 vs. 38.0 ± 1.0 kg), waist to hip ratio (0.81 ± 0.02 vs. 0.81 ± 0.01), and maximal aerobic capacity (1.5 ± 0.05 vs. 1.6 ± 0.05 L/min). African-American women had greater lean tissue mass than Caucasian women (41.8 ± 1.1 vs. 39.3 ± 0.6 kg; P = 0.05). The leptin concentration was 20% lower in African-American than Caucasian women (36.0 ± 4.8 vs. 45.8 ± 3.5; P < 0.05), whereas REE values were similar. Leptin correlated strongly with percent body fat in African-American (r = 0.71; P < 0.0001) and Caucasian women (r = 0.61; P < 0.001) and with REE in African-American (r = 0.58; P < 0.001), but not Caucasian, women (r = 0.08). These findings suggest racial differences in plasma leptin levels and in leptin’s role in the regulation of REE, which may play a role in the greater incidence of obesity in the African-American compared to the Caucasian population.

	Introduction

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AMONG OLDER women, the incidence of obesity in African-American women is nearly twice that in Caucasian women (1). The higher rates of obesity in African-American women are not entirely due to differences in environmental factors (i.e. socioeconomic status and education) (2), suggesting that there may be inherent metabolic and/or physiological differences between the races. In this regard, data show that African-American women have lower resting energy expenditure (REE) (3, 4) and fat oxidation (3), both of which are known predictors of future weight gain (5, 6). African-American women also exhibit lower levels of physical activity than Caucasian women, even after adjustment for differences in education level, economic status, and psychosocial factors (7). These findings suggest that racial dissimilarities in body weight and energy expenditure may be due to differences in the expression of obesity-regulating genes between the races.

Leptin, the product of the recently sequenced obesity (ob) gene, is thought to play an important role in the regulation of body weight (8). Administration of recombinant leptin causes weight loss in genetically obese, diet-induced obese, and normal weight mice by decreasing food intake and increasing resting and physical energy expenditures (9, 10). In humans, both adipose tissue ob gene expression and circulating leptin concentration are highly correlated with adipose tissue mass (11, 12, 13). However, leptin’s role in the regulation of energy expenditure in humans is not yet understood. Because of the documented differences in body composition and energy metabolism between African-American and Caucasian women, we examined racial differences in leptin levels and whether the relationships of leptin to body composition and resting metabolism differed between African-American and Caucasian women.

	Subjects and Methods

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Fifty-seven obese women were recruited for participation in metabolic research studies. Women were selected on the basis of race (African-American or Caucasian), age (>50 yr), menopausal status (no menstruation for at least 2 yr), and level of obesity (>30% fat). All women were nonsmoking, sedentary (<20 min exercise, 2 days/wk), and not receiving estrogen replacement therapy. All subjects provided informed consent to participate in the study according to the guidelines of the University of Maryland institutional review board for human research.

Measurements of body composition, maximal aerobic capacity (VO₂max), resting metabolism, and leptin concentration were performed in the morning after a 12-h fast. Body mass index (BMI) was calculated as weight divided by height squared (kilograms/meters²). Waist to hip ratio was calculated as the ratio of the minimal waist circumference to the circumference at the maximal gluteal protuberance. Percent body fat, lean tissue mass, and adipose tissue mass were measured using dual energy x-ray absorptiometry (model DPX-L, Lunar Radiation Corp., Madison, WI). VO₂max was measured on a motor-driven treadmill (Quinton) during a progressive exercise test to voluntary exhaustion as previously described (14). REE was measured by indirect calorimetry using the ventilated hood technique (Deltatrac Metabolic Monitor, SensorMedics Corp., Yorba Linda, CA) as described previously (14). The respiratory quotient (RQ) was calculated as the ratio of the volume of carbon dioxide produced to the volume of oxygen consumed.

Venous blood samples for measurement of leptin concentration were drawn into chilled tubes containing 1 mg ethylenediamine tetraacetate/cc blood. Plasma was separated by centrifugation at 4 C, and samples were stored at -70 C until analysis. Leptin was measured in duplicate using RIA (Linco, St. Louis, MO). Samples from African-American and Caucasian women were run in two separate assays, and the intra- and interassay coefficients of variation were 5.2% and 3.5%, respectively.

Data were analyzed using the Macintosh Statview program (Calabasas, CA). The data were first tested for normal distribution using the Shapiro-Wilk test for normality. Leptin concentrations were not normally distributed, so a Mann-Whitney U test was used to compare leptin levels between African-American and Caucasian women. The logarithm of leptin was normally distributed and was used for regression analyses. Relationships among the logarithm of leptin concentration and body composition variables were determined by linear regression analyses with calculation of Pearson product correlation coefficients. Analysis of covariance was used to test for race differences in leptin concentrations and REE after control for body composition. All data are presented as the mean ± SE, and statistical significance was denoted by P < 0.05.

	Results

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Groups were similar in age, VO₂max, body weight, BMI, percent body fat, adipose tissue mass, and waist to hip ratio (Table 1). African-American women had greater lean tissue mass than Caucasian women (P = 0.05). Table 2 shows leptin concentrations and REE in African-American and Caucasian women. African-American women had lower (P < 0.05) leptin levels than Caucasian women. This difference persisted when leptin levels were adjusted for individual differences in adipose tissue mass using analysis of covariance. REE was not different between African-American and Caucasian women, even when adjusted for differences in lean tissue mass. RQ did not differ between groups.

View larger version (23K): [in this window] [in a new window]   Figure 1. Relationship of REE (adjusted for lean tissue mass) to plasma leptin concentration in African-American (r = 0.63; P < 0.001) and Caucasian (r = 0.12; P = NS) women.

	Discussion

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The molecular mechanism for racial differences in plasma leptin concentration could be due to differences in ob gene expression and release from adipose tissue or to differences in the clearance of circulating leptin. Moreover, because leptin is believed to act on the hypothalamus to regulate adipose tissue mass via a negative feedback loop (15), racial differences in circulating leptin may be related to a greater receptor sensitivity to leptin in African-American than in Caucasian women. Conversely, higher leptin levels in Caucasian women could reflect a compensatory increase in adipose tissue secretion of leptin due to leptin resistance at target tissues.

In humans, the role of leptin in body weight regulation is unclear. In mice, leptin influences body weight by decreasing food intake and increasing resting and physical energy expenditures (9, 10). Therefore, the lower leptin level in African-American women may be one factor contributing to lower resting and physical energy expenditures in African-American compared to Caucasian women (3, 4, 7). In contrast to previous studies, our data showed that REE was not different between African-American and Caucasian women. However, the women in this study were much older than those previously studied, suggesting that racial differences in REE may only be evident in young women. With regard to energy expenditure due to physical activity, epidemiological studies show that African-American women are less physically active than Caucasian women (7, 16, 17). Furthermore, direct measurements of total energy expenditure using doubly labeled water (unpublished results from Dr. Poehlman’s lab) show that levels of physical activity are lower in African-American compared to Caucasian women. Although not directly measured in the present study, it is possible that racial differences in energy expenditure due to physical activity may be associated with racial differences in plasma leptin concentrations.

Our data concur with that results of other studies, which show that adipose tissue mass is the best predictor of plasma leptin concentration due to the adipocyte-specific expression of the ob gene (11, 12). We did not find a racial difference in the slope of the relationship between leptin and adipose tissue mass, suggesting that the change in leptin concentration per U adipose tissue mass is similar between African-American and Caucasian women. On the contrary, a relationship between leptin concentration and REE was evident in African-American, but not Caucasian, women. Moreover, using stepwise regression, leptin was an independent predictor of REE in African-American women only. This finding suggests that REE increases linearly with plasma leptin concentration in African-American women, but in Caucasian women, REE is not related to circulating leptin levels.

In summary, these data show that obese postmenopausal African-American women have 20% lower plasma leptin levels than obese postmenopausal Caucasian women. Furthermore, the concentration of circulating leptin was an independent predictor of REE in African-American, but not Caucasian, women. Consequently, future investigations examining the role of leptin in the regulation of obesity should be race specific. Likewise, potential pharmacological treatment of obesity with leptin may have different results in African-American and Caucasian women.

	Acknowledgments

 
We thank the women who volunteered for this study as well as the staff of the Geriatrics Service at the Baltimore V.A. Medical Center. We especially appreciate the laboratory assistance from Marilyn Lumpkin and the assistance with data collection from Sarah Schneider.

	Footnotes

 
¹ This work was supported by NIA Research and Training in Gerontology and Exercise Physiology Grant T32-AG-002109 (to B.J.N. and M.J.T.), NIH Grant R01-AG-07857 (to E.T.P.), NIH Grant K04-AG-00564 (to E.T.P.), and the Department of Veterans Affairs Baltimore Geriatric Research Education and Clinical Center.

Received June 20, 1996.

Revised August 5, 1996.

Accepted September 13, 1996.

	References

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