We examined 51 participants who were randomized to either weight stable (WS) (n
= 25; men: 12; women: 13) or weight loss (WL) (n
= 26; men: 12; women: 14) groups. There were no significant differences in demographics, initial body weight, BMI, and medical history between the WS and WL groups (). In our initial population, body weight was matched between groups, but because more women than men dropped out of the study or had insufficient plasma samples, the initial body weights were no longer matched between WL and WS groups. For the 51 randomized participants included in the adipokine analysis, their medical history showed that nearly two-thirds had high blood pressure, while 22% had palpitations, arrhythmia, or heart surgery, 22% had cancer, and 20% had diabetes. Most of the participants were female (53%) and Caucasian (88%); mean age was 69.3 ± 0.9 years (range 60 to 84 years). Initial weight and BMI for the active cohort were 101.2
kg and 35.0
. Additionally, there were no differences in physical fitness among the groups at baseline as indicated by maximal work capacity.
Baseline demographics and medical history for participants categorized as total completers, dropouts, or incomplete data, and completers by randomized group.
A major goal of this study was to develop a successful intensive weight loss intervention in older obese adults that incorporated meal replacements and exercise training. The aim of this analysis was to explore the effect of the weight loss intervention on biomarkers. Compliance with the WL intervention for the 26 participants was measured by attendance to the weekly nutrition classes (mean = 74.0%; ~20 of 26 classes attended) and exercise training classes (mean = 76.3%; ~50 out of 66 sessions attended). shows measures for groups at baseline and 6 months for body weight and composition outcomes and behaviors associated with the interventions (step counts and dietary intake). Analyses of covariance between groups on 6 month measures were adjusted for covariates of age, race, and respective baseline measure. The WL groups showed weight change of −13.0 ± 2.3% and −6.7 ± 1.6% relative to initial body weight for men and women, respectively, which is greater than the −1.0 ± 2.1% and 0.6 ± 1.6% change in the WS men and women, respectively. Additionally, women in the WL had reduced amounts of three measures of body fat at 6 months compared to the WS group. Men also had trends for reduction in BMI (P = 0.062; 95% confidence interval for mean difference is −6.02, 0.17) and body fat (P = 0.087; 95% confidence interval for mean difference is −9.91, 0.74). Also, men showed reduced levels of fat-free mass at 6 months for WL versus WS, which was not apparent in women. For the lifestyle behaviors, men in WL showed an increase in step counts, a reduction in energy intake and fat intake (% of total kcals), an increase in carbohydrate intake (% of total kcals), and a trend for increase in protein intake (P = 0.078; 95% confidence interval for mean difference is −0.40 and 6.79). Although women showed similar patterns in diet and physical activity behaviors for comparisons between WL versus WS at 6 months, these only reached statistical significance for a reduction in dietary fat and an increase in dietary carbohydrate.
Measures of body weight and body composition outcomes and diet and physical activity behaviors at baseline and 6 month followup separated by gender. Statistical analysis was performed on 6 month values.
To present useful additional detail to the above tests, we present all of the corresponding 95% confidence intervals for the mean group differences. Note that there is a significant difference (at critical P value of 0.050) when the corresponding 95% confidence interval does not overlap 0.0. Since the power of a t-test is 0.500 (i.e., 50%) when the absolute value of the true population mean value equals the half width of the 95% confidence interval, we also derive and present, in braces, the cutoff true mean differences which would have had 50% power for our study. True mean differences that are less extreme (smaller in absolute value) would have smaller power, while more extreme differences would have larger power.
Few studies have examined how adipokines can be altered by a dietary restriction and exercise training intensive weight loss program in obese older men and women. Since leptin levels are linked to fat mass and to signaling the brain to reduce food consumption, understanding how these change during weight loss can provide insight into metabolic changes associated with weight loss. Plasma levels of leptin and its soluble receptor, and adiponectin, along with calculations among these to obtain free leptin index and ratios between leptin and adiponectin, and leptin and body fat mass were quantified at baseline and follow-up visits as shown in . Again, due to expected gender differences, these are presented for men and women separately. Because these values were not normally distributed, the log of the baseline and 6 month concentrations of each adipokine were obtained and used in the analysis. Both the log and nontransformed values are presented in the table for clarity. Surprisingly, the only significant effect of the intervention on these measures and calculations was for a lower leptin
adiponectin ratio in women for WL versus WS at 6 months (P
= 0.021; 95% confidence interval for mean (WL–WS) difference: −0.54 and −0.05). However, there was a trend for leptin to be lower for WL versus WS in women (P
= 0.081; 95% confidence interval for mean difference: −0.31 and 0.02). Note that the power is 50% for the above two tests at true population mean differences of ±(0.49/2) and ±(0.33/2), respectively.
One striking difference in this table is in the levels of leptin between the men and the women. In younger individuals, the higher levels of leptin in females than males, even when matched for BMI, have been reported, so we asked if these differences are still present in older and obese individuals. To highlight this difference, the leptin levels in these groups are shown in . This data set indicates that there are 2- to 3- fold higher levels of leptin in women, than in men, in older obese adults; these gender differences are statistically significant based on an independent two-sample t-test. The trend for leptin decreasing in women is also noted on this graph.
Figure 1 Group comparisons of leptin concentrations at baseline and 6 months for women and men. ∧ Represents significant differences between WS and WL for women at the 6 months at P < 0.100. Bars present sample means augmented with their standard (more ...)
Examination of partial correlations between the 6 month adipokines' levels after adjustment for background, gender, group, and age suggests some potential causal influences between the adipokines. For men of the WS group, the partial correlation between leptin and soluble leptin receptor was r = −0.461 (P = 0.251), between leptin and adiponectin was r = 0.273 (P = 0.512), and between soluble leptin receptor and adiponectin was r = 0.557 (P = 0.152). For women of the WS group the partial correlations are for the leptin and soluble leptin receptor (r = 0.587, P = 0.126), for leptin and adiponectin (r = 0.296, P = 0.476), and for soluble leptin receptor and adiponectin (r = −0.083, P = 0.845). For men of the WL group, the partial correlations are the following: leptin and soluble leptin receptor (r = 0.155, P = 0.691), leptin and adiponectin (r = 0.333, P = 0.381), and soluble leptin receptor and adiponectin (r = −0.064, P = 0.871). For women of the WL group the partial correlations for the adipokine pairs are: leptin and soluble leptin receptor (r = 0.316, P = 0.374); leptin and adiponectin (r = −0.457, P = 0.184) and soluble leptin receptor and adiponectin (r = −0.047, P = 0.898). It is interesting that there were trends of gender and group differences in these partial correlations.
Spearman correlations were performed to look at associations between measures of body composition, fitness, physical activity, and dietary intake with the adipokines, separately by gender ( for men and for women). For both men and women, the strongest correlations were seen for leptin with percent body fat at baseline and 6 months. Furthermore, percent body fat was significantly correlated with free leptin index; also, percent body fat showed a trend towards significance with adiponectin at baseline (P
= 0.058). The only other significant findings or trends towards significant correlations for men were between carbohydrate intake and soluble leptin receptor at baseline and protein intake for free leptin index (6 months only). For women, in addition to leptin, percent body fat also showed significance or trends towards significance for soluble leptin receptor (r
= 0.347, P
= 0.076 at 6 months), free leptin index (r
= 0.369, P
= 0.058 at baseline; r
= 0.631, P
< 0.001 at 6 months), and leptin
adiponectin ratio (r
= 0.333, P
= 0.089 at baseline; r
= 0.562, P
= 0.002 at 6 months). Additionally, trunk fat, an index for visceral abdominal fat, was at 6 months correlated with leptin (r
= 0.471, P
= 0.013), soluble leptin receptor (r
= 0.368, P
= 0.059), free leptin index (r
= 0.335, P
= 0.087), and leptin
adiponectin ratio (r
= 0.454, P
= 0.017). Women also showed a number of significant (and trends for significant) correlations between adipokines and step counts and intake of total calories and macronutrients. Step counts were negatively correlated at 6 months with leptin (r
= −0.464, P
= 0.034) and free leptin index (r
= −0.408, P
= 0.067). Energy intake was associated with soluble leptin receptor at baseline (r
= 0.411, P
= 0.037). Fat intake was associated with soluble leptin receptor at 6 months (r
= 0.449, P
= 0.021). At baseline, carbohydrate intake was associated with leptin (r
= 0.498, P
= 0.010), free leptin index (r
= 0.413, P
= 0.036), and leptin
adiponectin ratio (r
= 0.428, P
= 0.029). Finally, soluble leptin receptor was negatively correlated with protein intake at both baseline (r
= −0.342, P
= 0.088) and 6 months (r
= −0.393, P
Spearman correlations at baseline and 6 months for men between adipokines and body fat %, trunk fat, step counts, dietary intake, and peak METS from GXT (baseline only). Data are presented as rho correlation coefficient (P value).
Spearman correlations at baseline and 6 months for women between adipokines and body fat %, trunk fat, step counts, dietary intake, and peak METS from GXT (baseline only). Data are presented as rho correlation coefficient (P value).
Interestingly, the gender differences in adipokines were apparent when the percentage changes from baseline to 6 months were examined. The relationship between the percent change in adipokine levels and differences in % body fat, trunk fat, and step counts is shown in . In the women, the change in leptin, the free leptin index, and the leptin
adiponectin ratio were also significantly correlated with the change in percent body fat (r
= 0.590, P
= 0.001 for leptin; r
= 0.431, P
= 0.025 for free leptin index; r
= 0.430, P
= 0.025 for leptin
adiponectin) and trunk fat (r
= 0.540, P
= 0.004 for leptin, r
= 0.386, P
= 0.047 for free leptin index; r
= 0.422, P
= 0.028 for leptin
adiponectin). In men, the only significant relationships were between changes in the free leptin index and the leptin
adiponectin ratio with the change in step counts (r
= −0.425, P
= 0.049 for free leptin index; r
= −0.530, P
= 0.011 for leptin
Spearman correlations by gender for percent change from baseline to 6 months in adipokines and body fat and step counts.