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Original Studies |
Laboratory of Human Behavior and Metabolism, Rockefeller University (M.R., J.H., E.M., F.C., R.L.L.), New York, New York 10021; and Amgen Incorporated (M.N.), Thousand Oaks, California 91329-1789
Address all correspondence and requests for reprints to: Michael Rosenbaum, M.D., Columbia Presbyterian Hospital Medical Center, Division of Molecular Genetics, Russ Berrie Pavillion, Room 644, 1150 St. Nicholas Avenue, New York, New York 10032.
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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In earlier experiments, we showed that, in humans, maintenance of an altered body weight 10% below usual (Wt -10%) is associated with a 15% decline in 24-h EE (TEE) [mainly nonresting EE (NREE) (13, 17)] normalized to metabolic mass, i.e., a metabolic state similar to that of mice deficient in or resistant to leptin (7). Maintenance of a body weight 10% above usual is accompanied by a 16% increase in TEE [mainly NREE (13, 17)] per unit of metabolic mass. We measured plasma concentrations of leptin, components of EE, and body composition in obese (OB) and never-obese (NO) humans at usual body weight, during 10% weight gain or 10–20% weight loss, and during weight maintenance at altered body weights to determine the effects of weight change and the maintenance of changed weight on the relationship between circulating leptin and FM, and whether changes in EE associated with weight change are significantly correlated with circulating leptin.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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OB [body mass index (BMI) >28 kg/m2] and NO (BMI
<28 kg/m2) (1, 18) subjects were at their maximal lifetime
weight and had maintained this weight within a 2-kg range for at least
6 months before enrollment. All females were premenopausal. Recruitment
procedures and exclusion criteria for these studies have been
previously described (13). All studies were approved by the
Institutional Review Board of the Rockefeller University Hospital, and
written informed consent was obtained from all subjects before
enrollment. Subject characteristics are presented in Table 1
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The protocol for these studies is described in detail elsewhere (13, 17). Briefly, subjects were admitted to the Clinical Research Center at Rockefeller University, and allowed ad libitum physical activity. They were fed a liquid formula diet plus vitamin and mineral supplements. Daily formula intake was adjusted until weight stability (defined as a slope of <0.01 kg/day in a 14-day plot of weight vs. days) was achieved. We have reported previously that 24-h EE (TEE) calculated by this method is highly correlated (r2 = 0.88, P < 0.0001) with direct measurement of TEE by doubly labeled water (17). At this point, the following metabolic tests were conducted over a period of approximately 14 days (13, 17). 1) Resting EE (REE) and the thermic effect of feeding (TEF) by indirect calorimetry (19). NREE was calculated as NREE = TEE - (REE + TEF). 2) Body composition analysis by hydrodensitometry (20). 3) Measurement of the waist circumference at a point one third of the distance from the xiphoid process to the umbilicus and the hip circumference at the head of the superior margin of the pubic bone (21). 4) Postabsorptive plasma leptin concentrations were assayed by a solid-phase sandwich enzyme immunoassay using an affinity-purified polyvalent antibody immobilized in microliter wells. Bound leptin was detected with affinity purified antibody conjugated to horseradish peroxidase, and quantified with a chromogenic substrate (3,3',5,5' tetramethylbenzidine/peroxide). Leptin concentrations were calculated from standard curves generated for each assay using recombinant human leptin. Minimal detectable leptin is 20 pg/mL. All samples from any individual subject were analyzed in the same assay (9). 5) Abdominal and gluteal subcutaneous adipose tissue aspirations were performed under local anesthesia with 1% xylocaine. Adipocyte volumes (micrograms lipid/cell) were determined by the osmium fixation method. The intraassay variability of this method is <3% (22). Postabsorptive serum insulin concentrations were measured by RIA immediately before performance of these biopsies.
Following completion of studies at usual body weight (Wt initial),
subjects were either provided maximum tolerated intake of mixed solid
self-selected foods (generally 5000–8000 kcal/day) until they had
gained 10% (Wt +10%) of Wt initial or were placed on 800 kcal/day of
the liquid formula diet until they had lost 10% (Wt -10%) or 20%
(Wt -20%) of Wt initial. Some subjects were studied at multiple
weight plateaus, and eight OB women who had completed studies at Wt
initial and Wt +10% were fed 800 kcal/day of the liquid formula diet
until body weight was reduced to their usual weight (Wt initial 2). At
each new weight plateau (Wt +10%, Wt initial2, Wt -10%, or Wt
-20%) weight was again maintained as described above and, when weight
was stable for at least 14 days, the studies described above were
repeated. Plasma leptin was also measured in the postabsorptive state
at the end of each period of weight loss or gain, when the intended new
level of weight had been achieved (10% above or 10% below Wt initial)
but the subject was still gaining or losing weight. This was done to
assess possible effects on plasma leptin of dynamic weight loss or gain
vs. static weight maintenance at the same body weight.
Subject characteristics at each plateau are indicated in Table 2.
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Direct measures of body composition [fat-free mass (FFM), FM, adipocyte volume], indices of body fatness (BMI, percent body fat), or indices of anatomic distribution of body fat (waist/hip ratio) were related to measures of EE and plasma leptin by linear regression analyses. FM and plasma concentrations of leptin did not demonstrate a normal distribution of values and were, therefore, expressed as log FM and log [leptin], respectively, to normalize data and to avoid any type I statistical error that might be engendered by a bimodal distribution of values for a parameter. All significant independent variables were then examined for interactions among variables, and effects of each variable adjusted for the effects of all other independent variables by forward stepwise multiple linear regression analyses against the same dependent variables (23).
Between-group analyses (OB vs. NO, male vs. female) were made by one-way ANOVA. Between-group analyses to determine whether initial somatotype (OB, NO), gender, or weight plateau altered the relationship between plasma leptin and measures of body composition were made by analysis of covariance using the grouping variable as a covariate. Within-group analyses, i.e. the same measures at initial weight vs. altered weight plateaus, were performed using ANOVA with repeated measures (23).
Regression equations relating EE and plasma leptin to FM and/or FFM, do
not necessarily have Y-axis intercepts = 0 (Table 1
) (13, 17, 24).
Therefore, in addition to expressing EE as kcal/kg FFM, regression
equations of EE vs. FFM and FM, and plasma leptin
vs. FM at usual (Wt initial) body weight were used to
calculate residuals (actual EE minus predicted EE based on the
regression line at Wt initial) of the same subjects at other weight
plateaus. Residuals were then tested against the null hypothesis that
residual = 0. For all statistical analyses, statistical
significance was defined as P
< 0.05.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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As reported previously (13), there were significant increases at
Wt + 10% in TEE (16.5 ± 1.8%, P < 0.001) and
NREE (36.8 ± 5.9, P < 0.001) adjusted for FFM
and in TEF expressed as a percentage of ingested calories (3.0 ±
1.6% at Wt initial vs. 5.1 ± 2.0% at Wt +10%,
P < 0.01) were significantly increased at Wt +10%. At
Wt -10% and Wt -20%, TEE (-16.2 ± 1.4% at Wt -10%;
-28.5 ± 3.8% at Wt -; both P < 0.001), REE
(-10.8 ± 2.3% at Wt -10%; -20.7 ± 5.4% at Wt -20%;
both P < 0.001), and NREE (-29.4 ± 6.2% at Wt
-10%; -35.8 ± 8.7% at Wt -20%; both P <
0.001) adjusted for FFM were significantly decreased. Weight gain and
loss were associated with respective significant increases and
decreases in both FFM and FM. No significant effects of gender, initial
somatotype, or weight gain followed by return to initial weight (Wt
initial 2) on any of these variables were noted (Table 1).
Body composition and biochemical correlates of plasma concentrations of leptin
Plasma leptin concentration was significantly correlated with FM
in all subjects at all weight plateaus (P < 0.0001,
Fig. 1). Plasma leptin
concentrations were significantly higher in females than in males,
corrected for FM, at all weight plateaus (P < 0.0001)
(9). No significant correlations were noted between plasma leptin and
age, FFM, or any index of body fatness (percent body fat, BMI, or
initial somatotype) once adjusted for the effects of FM in males or
females. In multiple stepwise regression analyses of males and females
in which FM, FFM, and gender were included as independent variables,
only gender and FM were significant covariates of plasma leptin
concentrations. In stepwise multiple regression analyses, both FM and
postabsorptive plasma concentrations of insulin (Table 3) were significantly correlated with
plasma leptin in males at Wt initial (Plasma [leptin] = 0.75(FM)] +
0.16(postabsorptive [insulin] - 9.7; Radj. = 0.99,
p-FM < 0.0001, p-insulin < 0.05) and Wt +10% (Plasma
[leptin] = 0.74(FM)] + 0.28(postabsorptive [insulin] - 17.2;
Radj. = 0.95, p-FM < 0.0001, p-insulin <
0.0005). No significant correlations between plasma leptin and
postabsorptive insulin concentrations were found in females at any
weight plateau. Neither abdominal nor gluteal fat cell size, nor any
measures of body fat distribution (waist or hip circumference,
waist/hip ratio; abdominal or gluteal fat cell size, or
abdominal/gluteal fat cell size ratio) were significantly correlated
with plasma leptin once corrected for the effects of FM.
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Maintenance of a reduced body weight was associated with a
significant reduction in plasma leptin concentration/FM only in females
(Fig. 1 and Table 1). Similarly, females studied at reduced body weight
had significantly lower plasma concentrations of leptin than body
composition-matched females studied at Wt initial (Table 2 and Fig. 2). This effect was not because of the
non-zero Y-axis intercept of the regression line relating FM to leptin,
because residual values of leptin in weight-reduced females (calculated
as actual minus predicted values based on the regression of plasma
leptin on FM at Wt initial) were significantly less than zero. Residual
values of plasma leptin at Wt -20% in females were significantly
lower than values for female subjects at Wt -10%.
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and
Table 1). Similarly, males studied at elevated body weight had
significantly higher plasma concentrations of leptin than body
composition-matched males studied at Wt initial (Table 2 and Fig. 2).
Because postabsorptive insulin concentration was a significant
covariate of plasma leptin in males at Wt initial and at Wt +10%, and
weight maintenance at Wt +10% was associated with a significant
increase in postabsorptive plasma concentration of insulin in males,
but not females (see above), we corrected the calculation of weight
plateau effects on plasma leptin concentrations for the effects of
insulin by ANCOVA. Plasma leptin/FM was not significantly increased
over Wt initial in males at Wt +10% once corrected for the effects of
the increased postabsorptive serum insulin concentrations.
The process of dynamic weight loss, but not gain, was associated
with a significant change (decrease) in plasma leptin/FM compared with
the same subjects during maintenance at the same weight (Table 4). This effect was evident in all
subjects. However, correlation coefficients between plasma leptin and
FM were not significantly different between subjects studied during
dynamic weight change and during weight maintenance at the same weight,
i.e. circulating leptin concentration was still
significantly correlated with FM during dynamic weight change. Eight
females were studied at the end of dynamic weight loss from Wt +10%
back to Wt initial, and during maintenance at usual body weight (Wt
initial 2). Postabsorptive plasma concentrations of insulin during
weight loss (16.8 ± 3.8 µU/mL) were significantly lower than
postabsorptive plasma insulin concentrations obtained during weight
maintenance at Wt initial 2 (22.9 ± 3.8 µU/mL,
P < 0.01). Plasma leptin during weight loss remained
significantly lower (P < 0.005) than plasma leptin at
Wt initial2 even when corrected for postabsorptive plasma insulin
concentrations. No significant differences between plasma leptin at Wt
initial and Wt initial 2 were noted, again providing evidence that
there is no carry over effect of the reduction in plasma leptin during
weight loss from Wt +10% to Wt initial 2 on plasma leptin during
weight maintenance.
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Plasma concentrations of leptin and FM were significantly
correlated with REE and TEE at all weight plateaus. Despite the visual
similarity between regressions relating EE to FM and leptin (Fig. 3) following multiple stepwise linear
regression analysis to adjust for the significant colinearity of FFM,
FM, and plasma leptin, only FFM and FM remained significantly
correlated with REE (Table 5). No
significant correlations were noted between changes in plasma leptin,
plasma leptin/FM, or residual values of plasma leptin and changes in
any measure of EE (whether expressed as changes in kilocalories per
kilogram FFM or as residual values) between weight plateaus in any
group. Therefore, though plasma leptin/FM did decline significantly in
females following weight loss, and did increase significantly in males
following weight gain, the degree to which these increases occurred did
not correlate with the degree to which EE was decreased or increased
following weight loss or weight gain, respectively.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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In weight-stable OB and NO humans, the circulating concentration of leptin is determined primarily by gender and by FM (9). The observation that plasma leptin was significantly decreased during dynamic weight loss compared with levels in the same subjects at the same weight during static weight maintenance indicates that plasma leptin concentration is influenced by intercurrent metabolic factors in addition to FM, in agreement with other studies in humans (25) and in rodents (26, 27). Insulin has been shown to increase leptin gene expression in adipose tissue (28, 29), and inclusion of insulin as a covariate in the analysis of the effects of weight gain on plasma leptin removes the significant differences in plasma leptin concentration in males who have gained weight (compared with FM-matched males at Wt initial). In contrast, plasma leptin concentration is not significantly different between females at Wt +10% and FM-matched females at Wt initial, despite the fact that postabsorptive insulin is significantly higher in the women at Wt +10%. However, plasma leptin concentrations in females were significantly decreased during weight loss (relative to concentrations during maintenance of the same body weight) and during weight maintenance of a reduced body weight (relative to Wt initial), even when the regression of plasma leptin vs. FM was statistically corrected for changes in postabsorptive plasma insulin concentrations.
Intracerebroventricular or intraperitoneal leptin administration to Lepob mice or intraperitoneal administration of leptin to non-OB animals at very high doses reduces food intake and increases EE, resulting in reduced body fat (6, 7, 8, 30). Intraperitoneal administration of leptin to mice during starvation rectifies many of the neuroendocrine changes that occur as a result of food deprivation (31), but does not significantly alter the rate of weight loss. We examined the correlations of changes in plasma leptin with changes in EE that occur following weight gain or loss. The lack of correlations between weight loss- or gain-associated changes in plasma leptin and EE that occur as a result of altered body weight, and the observation that there is a sexual dimorphism in the weight gain- or loss-associated increases or decreases in the plasma concentrations of leptin adjusted for body composition but there are no gender differences in the changes in EE following weight gain or loss (13, 17), suggest that leptin is not providing the primary signal mediating these changes in energy homeostasis in human beings. The striking correlation of leptin with FM in weight-stable OB and lean subjects, the reduction of leptin/FM with hypocaloric intake, and the absence of any correlation of leptin with EE in the weight-stable state are consistent with the hypothesis that leptin may have a primary physiological role as an emergency signal for depletion of energy stores rather than as a regulator (suppressor) of body fat, per se. Accordingly, depletion of adipose tissue mass, or reduction in energy intake, reduces leptin, evoking compensatory changes in hunger (increased), EE (decreased), and reproductive function (reduced fertility) (32). Once circulating brain leptin exceeds a threshold, the behavioral/metabolic stigmata of fasting are relieved. This model predicts that exogenous leptin might have some clinical utility in facilitating compliance with a hypocaloric diet and in maintenance of a reduced body weight. Genetic/developmental factors may influence the leptin-mediated stimulus strength (and hence degree of adiposity) required to turn off a metabolic and behavioral sense of deprivation mediated by ambient leptin concen-trations.
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Acknowledgments |
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Footnotes |
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Received May 16, 1997.
Accepted August 4, 1997.
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References |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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, continuous
line) compared with males (
, broken line)
during weight maintenance at Wt initial. B, Leptin concentrations
corrected for FM were significantly reduced in females during weight
maintenance at Wt -10% (
, log [leptin] = 1.23(log FM) -0.40),
Wt -20% (
, log [leptin] = 1.50(log FM) -0.99), but not
significantly changed at Wt +10% (
, log [leptin] = 0.72(log FM)
+0.62) compared with regression line for females depicted in Fig. 2A
, log [leptin] =
1.40(log FM) -0.99) but not significantly changed at Wt -10% (•,
log [leptin] = 1.04(log FM) +1.40) compared with regression line for
males depicted in Fig. 2A
;