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The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 10 3230-3233
Copyright © 1997 by The Endocrine Society

Original Studies

Robust Leptin Secretory Responses to Dexamethasone in Obese Subjects1

Samuel Dagogo-Jack, Gregg Selke, Angela K. Melson and John W. Newcomer

Division of Endocrinology, Diabetes, and Metabolism (S.D.-J.) and Department of Psychiatry (G.S., A.K.M., J.W.N.), Washington University School of Medicine, St. Louis, Missouri 63110

Address all correspondence and requests for reprints to: Samuel Dagogo-Jack, M.D., Division of Endocrinology, Diabetes, and Metabolism, Washington University School of Medicine, Box 8127, 660 South Euclid Avenue, St. Louis, Missouri 63110. E-mail: sdagogo{at}imgate.wustl.edu


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Although leptin reverses obesity in rodents, its function and regulation in humans are unknown. Glucocorticoids have been reported to stimulate leptin production in both rodents and humans, but data assessing the effect of obesity on dynamic leptin secretory responses are unavailable. We, therefore, studied 52 lean and obese subjects [20 men and 32 women; aged 19–84 yr; body mass index (BMI) range, 16–47 kg/m2] randomized to treatment with dexamethasone (total dose, 10 mg/4 days) or placebo. Compared with placebo, dexamethasone increased (P = 0.0001) plasma leptin levels by 64–111% above baseline values within 2–4 days. The increases occurred in all ages, showed no sexual dimorphism, and were particularly robust in obese subjects. After dexamethasone treatment, significant interactions were observed between the change in plasma leptin and BMI (P = 0.0001), baseline plasma leptin (P = 0.0006) and plasma dexamethasone levels (P = 0.04), but not age (P = 0.28); an apparent interaction with plasma insulin no longer was significant after controlling for BMI. These results confirm dexamethasone-induced hyperleptinemia in humans and further demonstrate that the response is not defective in obesity.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
THE HYPOTHALAMIC -pituitary-adrenal axis has long been implicated in the regulation of appetite and body weight (1), and leptin has recently been characterized as a weight-regulating hormone (2, 3, 4). In rodents, leptin expression appears to be under hormonal control (5, 6, 7, 8), but the regulation (9, 10, 11, 12) and metabolism (13) of leptin in humans are poorly understood.

There have been conflicting reports of glucocorticoid effects on leptin expression in rodents (6, 7, 14) and humans (15, 16). As leptin has anorexogenic and insulin-sensitizing properties (3, 4), we hypothesized that hyperleptinemia could be a counterregulatory response to glucocorticoid-induced hyperphagia. Theoretically, obese and lean persons could differ in their responses to a leptin secretagogue under such a mechanism. However, data evaluating dynamic leptin secretion in relation to gender and obesity are unavailable. The present randomized, placebo-controlled study of the effect of dexamethasone on leptin secretion was conducted in part to provide such data.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Human subjects and study protocol

Healthy subjects (20 men and 32 women; aged 19–84 yr), whose characteristics are shown in Table 1Go, were studied before and during dexamethasone or placebo treatment. The subjects were taking no psychotropic medications or drugs known to alter carbohydrate metabolism. Obesity was defined as a body mass index (BMI) greater than 27.3 for men and greater than 27.8 for women (17). Subjects were randomized double blind to oral treatment with dexamethasone or placebo (3 active and 2 placebo) for 4 days. Dexamethasone was given in doses of 1 mg at 2300 h on day 1, and 2, 3, and 4 mg at 2300 h on days 2, 3, and 4, respectively. Blood samples (~3 h postprandial) were collected at 1600 h on days 1, 3, and 5. All subjects gave written informed consent for participation in clinical research and were advised to maintain their usual diet and physical activity throughout the period of study. The protocols were approved by the Washington University human studies committee.


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  		Table 1. Clinical and biochemical characteristics of subjects

 
Assays

Plasma leptin was measured with a RIA (Linco Research, St. Louis, MO); the limits of detection and linearity were 0.5 and 100 ng/mL in plasma, and the intra- and interassay coefficients of variation were less than 7% (18). Leptin values above 100 ng/mL were reassayed on dilution. Plasma glucose was measured with a glucose oxidase method (Beckman, Fullerton, CA), and plasma insulin (19), cortisol (20), and dexamethasone (Corning Nichols, San Juan Capistrano, CA) levels were measured with specific RIAs.

Statistical analysis

All results are expressed as the mean ± SE. Baseline variables were analyzed by unpaired t tests or {chi}2 tests, as appropriate, using the Macintosh StatView program (Abacus Concepts, Berkeley, CA). Spearman’s correlations were used to compare baseline plasma leptin and defined variables. Serial data obtained during treatment were analyzed by separate mixed design ANOVAs, and the effects of covariates on serial leptin levels were assessed by analyses of covariance (ANCOVAs) using the Macintosh SuperANOVA program.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Baseline plasma leptin levels were higher (P < 0.0001) in women than in men (21.6 ± 3.2 vs. 5.5 ± 0.52 ng/mL) of similar age (43.8 ± 3.8 vs. 40.6 ± 5.4 yr) and BMI (24.7 ± 0.7 vs. 23.7 ± 0.8 kg/m2) and were significantly correlated with BMI (r = 0.52; P = 0.005), but not with age or baseline plasma cortisol, insulin, or insulin/glucose ratios. As expected, dexamethasone treatment suppressed cortisol production and increased plasma insulin levels and insulin/glucose ratios, but glucose levels were unchanged (Fig. 1Go). Dexamethasone treatment increased mean plasma leptin levels from 16.3 ± 2.6 ng/mL at baseline to 28.5 ± 5.0 ng/mL (P < 0.0001) on study day 3 and to 27.6 ± 4.4 ng/mL (P < 0.0001) on study day 5; mean leptin levels were unchanged during placebo treatment. A significant interaction was detected between treatment condition and change in plasma leptin level (F = 11.25; P = 0.0001), change in plasma insulin (F = 4.23; P = 0.02), and change in the insulin/glucose ratio (F = 4.03; P = 0.024), but not change in plasma glucose level (F = 1.29; P = 0.28).



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  		Figure 1. Effects of dexamethasone (solid circles; n = 31) or placebo (open circles; n = 21) treatment on mean (±SE) plasma cortisol (A), glucose (B), and insulin (C) levels and insulin/glucose ratios (D) in 52 healthy subjects. Differences between baseline values in the two treatment groups were not significant. Asterisks indicate statistically significant interactions between treatment condition and changes in plasma measures: *, P = 0.024; **, P = 0.02; ***, P = 0.0001.

 
Plasma leptin responses to dexamethasone were similar in both sexes (Fig. 2Go) and were maintained across a wide age range (19–84 yr), without a significant correlation (r = 0.063; P = 0.73) or interaction (F = 1.32; P = 0.27) between age and change in plasma leptin. To determine whether obese and lean subjects differ in their responses to a leptin secretagogue, we entered BMI as a covariate into an ANCOVA testing the effect of treatment condition on the change in leptin levels. This model revealed a highly significant effect of BMI on the change in plasma leptin levels (F = 11.44; P = 0.0001). Serial leptin levels among subjects (20 lean and 11 obese) in the dexamethasone group were 11.3 ± 1.8 (baseline), 20.1 ± 3.7 (day 3), and 19.4 ± 3.2 (day 5) ng/mL for lean subjects vs. 24.3 ± 5.4 (baseline), 47.7 ± 11.3 (day 3), and 42.0 ± 10.0 (day 5) ng/mL for obese subjects. The percent increases above baseline (lean vs. obese) were 78% vs. 96% on day 3 and 71% vs. 73% on day 5. Baseline plasma leptin levels (independent of BMI) also strongly predicted the magnitude of the response to dexamethasone (F = 8.73; P = 0.0006).



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  		Figure 2. Effect of dexamethasone (hatched bars) or placebo (open bars) treatment on plasma leptin concentrations in 32 healthy women (A) and 20 healthy men (B). Nineteen women received dexamethasone, and 13 received placebo, compared with 12 men taking dexamethasone and 8 taking placebo. Baseline plasma leptin levels were 4-fold higher in women than in men; however, baseline leptin levels in dexamethasone and placebo groups were similar within each gender. *, P = 0.0001.

 
The increases in plasma leptin levels were related to plasma dexamethasone levels. A significant interaction was detected between mean plasma dexamethasone levels across days 3 and 5 (n = 24; seven subjects had incomplete data) and the change in plasma leptin levels (F = 3.62; P = 0.04). Next, we assessed the contribution of hyperinsulinemia (10) per se to the observed treatment effect. When changes in plasma insulin level or insulin/glucose ratios were used as single covariates in an ANCOVA testing the effect of treatment condition on the change in plasma leptin level, we detected a modest effect of insulin levels (F = 3.62, P = 0.03) and insulin/glucose ratios (F = 3.11; P = 0.05) to predict changes in plasma leptin, without a decrease in the strength of the relationship between treatment condition and leptin levels. When BMI was added to the model as a second covariate, the apparent contribution of insulin was no longer significant (F = 2.58; P = 0.08). Thus, steroid-induced hyperinsulinemia did not account for a significant amount of the variance in plasma leptin levels. Figure 3Go shows the relationships among change in plasma leptin level, BMI, plasma dexamethasone level, and change in plasma insulin levels.



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  		Figure 3. Scatter plots of change in plasma leptin vs. BMI (A), mean plasma dexamethasone level (B), and change in plasma insulin level (C). The change in plasma leptin or plasma insulin was the difference between the mean of day 3 and 5 levels and the level at baseline. Mean plasma dexamethasone refers to the mean of day 3 and 5 levels; seven subjects with incomplete data were excluded from the analysis. The change in plasma leptin level interacted significantly with BMI (P = 0.0001) and plasma dexamethasone (P = 0.04); an apparent interaction with insulin levels was not significant after controlling for BMI. The correlations between change in plasma leptin level and BMI, dexamethasone level, and change in insulin were 0.69 (P = 0.0003), 0.43 (P = 0.04), and 0.07 (P = 0.74), respectively.

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
The present study demonstrates acute dexamethasone stimulation of circulating leptin levels in lean as well as obese men and women across a wide age spectrum. These results together with recent concordant reports (15, 21, 22, 23) suggest that glucocorticoids regulate leptin in humans. However, there may be species as well as structure-activity differences; dexamethasone was shown to decrease leptin gene expression in mouse adipocytes (14), and methylprednisolone reportedly had no effect on leptin secretion in 10 lean subjects (16).

Steroid-induced insulin resistance and hyperinsulinemia (10) did not account for the increases in plasma leptin observed in the present study or in a previous report (15). It has been speculated that hypersecretion of leptin in the presence of obesity indicates leptin resistance (24), analogous to the hyperinsulinemia of insulin resistance and early type 2 diabetes mellitus. However, the hyperinsulinemia in type 2 diabetes is associated with a subnormal insulin response to glucose stimulation (25), whereas our results indicate that obese subjects have an intact (and often robust) leptin response to a secretagogue. The latter finding predicts that exogenous leptin may not be dramatically effective as an antiobesity therapy, as obese subjects seem to have an adequate leptin secretory reserve. However, because there were few subjects with BMI greater than 35 kg/m2 in our study population, these results cannot be generalized to persons with morbid obesity.

We suggest that increased leptin secretion might be a counterregulatory attempt to limit glucocorticoid-induced hyperphagia and weight gain (26). Although such a mechanism may be overcome by severe hypercortisolemia (27), it is possible that augmentation of circulating leptin may provide a link between less severe hypercortisolemia in such diverse states as depression, dementia, severe illness, and chronic stress and the well known anorexia and weight loss in these conditions. This would be in contrast to the low leptin levels found in women with a primary eating disorder (28). The mechanism(s) of glucocorticoid stimulation of plasma leptin in humans remain to be clarified. Possible mechanisms include a direct effect on adipocytes (7, 23, 29) and central effects, probably mediated by neuropeptide Y (30, 31). In conclusion, we here confirm the acute leptin secretory response to dexamethasone as a general phenomenon in humans and show that this response is not defective in obese subjects.


   Acknowledgments
 
We thank Joy Brothers, Carolyn Fritschle, Zina Lubovitch, and Michael Morris for technical assistance.


   Footnotes
 
1 This work was supported by grants from the American Diabetes Association (to S.D.-J.), the NIMH (MH-01045, to J.W.N.), and USPHS Grants MO1-RR-00036 and P60-DK-20579. Back

Received May 30, 1997.

Revised June 27, 1997.

Accepted July 1, 1997.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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J. W. Newcomer, G. Selke, A. K. Melson, J. Gross, G. P. Vogler, and S. Dagogo-Jack
Dose-Dependent Cortisol-Induced Increases in Plasma Leptin Concentration in Healthy Humans
Arch Gen Psychiatry, November 1, 1998; 55(11): 995 - 1000.
[Abstract] [Full Text] [PDF]

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 J. Clin. Endocrinol. Metab.Home page
G. Van den Berghe, P. Wouters, L. Carlsson, R. C. Baxter, R. Bouillon, and C. Y. Bowers
Leptin Levels in Protracted Critical Illness: Effects of Growth Hormone-Secretagogues and Thyrotropin-Releasing Hormone
J. Clin. Endocrinol. Metab., September 1, 1998; 83(9): 3062 - 3070.
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 Am. J. Physiol. Endocrinol. Metab.Home page
C. D. Russell, R. N. Petersen, S. P. Rao, M. R. Ricci, A. Prasad, Y. Zhang, R. E. Brolin, and S. K. Fried
Leptin expression in adipose tissue from obese humans: depot-specific regulation by insulin and dexamethasone
Am J Physiol Endocrinol Metab, September 1, 1998; 275(3): E507 - E515.
[Abstract] [Full Text] [PDF]

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 J. Clin. Endocrinol. Metab.Home page
X. Casabiell, V. Piñeiro, R. Peino, M. Lage, J. Camiña, R. Gallego, L. G. Vallejo, C. Dieguez, and F. F. Casanueva
Gender Differences in Both Spontaneous and Stimulated Leptin Secretion by Human Omental Adipose Tissue in Vitro: Dexamethasone and Estradiol Stimulate Leptin Release in Women, But Not in Men
J. Clin. Endocrinol. Metab., June 1, 1998; 83(6): 2149 - 2155.
[Abstract] [Full Text]

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 J. Clin. Endocrinol. Metab.Home page
D. Torpy, S. Bornstein, G Cizza, and G. Chrousos
The Effects of Glucocorticoids on Leptin Levels in Humans May Be Restricted to Acute Pharmacologic Dosinga
J. Clin. Endocrinol. Metab., May 1, 1998; 83(5): 1821 - 1822.
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