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. 2015 Jun 26;7(7):5156-76.
doi: 10.3390/nu7075156.

Impact of Weight Loss on Plasma Leptin and Adiponectin in Overweight-to-Obese Post Menopausal Breast Cancer Survivors

Henry J Thompson  1 , Scot M Sedlacek  2   3 , Pamela Wolfe  4 , Devchand Paul  5 , Susan G Lakoski  6 , Mary C Playdon  7   8 , John N McGinley  9 , Shawna B Matthews  10
Affiliations

Impact of Weight Loss on Plasma Leptin and Adiponectin in Overweight-to-Obese Post Menopausal Breast Cancer Survivors

Henry J Thompson et al. Nutrients. .

Abstract

Women who are obese at the time of breast cancer diagnosis have higher overall mortality than normal weight women and some evidence implicates adiponectin and leptin as contributing to prognostic disadvantage. While intentional weight loss is thought to improve prognosis, its impact on these adipokines is unclear. This study compared the pattern of change in plasma leptin and adiponectin in overweight-to-obese post-menopausal breast cancer survivors during weight loss. Given the controversies about what dietary pattern is most appropriate for breast cancer control and regulation of adipokine metabolism, the effect of a low fat versus a low carbohydrate pattern was evaluated using a non-randomized, controlled study design. Anthropometric data and fasted plasma were obtained monthly during the six-month weight loss intervention. While leptin was associated with fat mass, adiponectin was not, and the lack of correlation between leptin and adiponectin concentrations throughout weight loss implies independent mechanisms of regulation. The temporal pattern of change in leptin but not adiponectin was affected by magnitude of weight loss. Dietary pattern was without effect on either adipokine. Mechanisms not directly related to dietary pattern, weight loss, or fat mass appear to play dominant roles in the regulation of circulating levels of these adipokines.

Keywords: adiponectin; body composition; breast cancer survivors; dietary pattern; leptin; weight loss.

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Figures

Figure 1
Figure 1
Regression Analyses of Baseline data: (a) Regression of plasma adiponectin on fat mass (kg) with 95% confidence intervals; r2 = 0.008, p = 0.210. (b) Regression of plasma leptin on fat mass (kg) with 95% confidence intervals; r2 = 0.41, p < 0.001. (c) Regression of plasma adiponectin on plasma leptin with 95% confidence intervals; r2 = 0.025, p = 0.028.
Figure 2
Figure 2
Plasma adipokine concentrations duration weight loss. Groups are non intervention control, CTRL; low fat dietary pattern weight loss intervention arm, LF; and low carbohydrate dietary pattern weight loss intervention arm, LC. Values are means ± SD. (a) Plasma adiponectin (μg/mL) as a function of months on weight loss intervention. The decrease in plasma adiponectin observed after the first month of weight loss (6%, p < 0.001 relative to baseline) was observed in both intervention arms. Thereafter, plasma adiponectin increased (p = 0.004), but was not different from the control in either intervention group by end of study. Although adiponectin levels were greater in the low fat group, the rate of increase in adiponectin from intervention months 1 to 6 in the two diet groups were approximately the same (p = 0.85); the increase in the last month of the intervention was somewhat greater in the low fat group than the low carbohydrate group (p = 0.03). (b) Plasma leptin (ng/mL) as a function of months on weight loss intervention. There was a large decrease in leptin over the first month of weight loss (81% of the six-month decrease) with relatively small decreases thereafter. This pattern of change in leptin was observed in both intervention arms and the decrease in leptin was unaffected by dietary pattern.
Figure 3
Figure 3
Body fat mass and plasma adipokines by weight loss tertile. The subset of individuals who lost at least 5% of initial body weight (92% of all individuals who completed the study) were divided into tertiles of weight loss, which corresponded to >5%, tertile 1; >10%, tertile 2; and >15%, tertile 3 of initial body weight. (a) Fat mass in kg over successive months of the weight loss intervention. (b) Body fat expressed as a (%) over successive months of the weight loss intervention. (c) Adiponectin (μg/mL) over successive months of the weight loss intervention. (d) Leptin (ng/mL) over successive months of the weight loss intervention. Values are means ± SEM. With weight loss >10%, leptin decreased progressively over time, and the decrease was significant with weight loss >15% (p = 0.007); whereas, there was no significant effect of weight loss magnitude on circulating levels of adiponectin.
Figure 4
Figure 4
Distribution of plasma adipokines at baseline and end of study. (a) Scatterplot showing the mean and range for plasma adiponectin and leptin at baseline. The plasma concentration of adiponectin that is observed in normal weight individuals is 7–5 µg/mL. Greater than 50% of participants in CHOICE were within this range at baseline. A concentration of 5 to 10 ng leptin per mL is typically observed in normal weight individuals. In this study, the mean leptin concentration at baseline was 36.0 ± 18.5 ng/mL. (b) Scatterplot showing the mean and range for plasma adiponectin and leptin at end of study. The plasma concentration of adiponectin that is observed in normal weight individuals is 7–15 µg/mL and 47% remained within this range by end of study and those percentages were not significantly affected by weight loss tertile or dietary pattern. Plasma leptin decreased to 15.8 ± 10.8 ng/mL by end of study; however, only in the highest tertile of weight loss did plasma levels reach the normal range of plasma concentrations (baseline 40.6 ±19.6 down to 10.0 ± 5.7 ng/mL). (c) Scatterplot showing the mean and range for the change (end of study-baseline) in plasma adiponectin (μg/mL) and leptin (ng/mL) at end of study relative to baseline. The distribution of change in plasma adiponectin indicates that 32% of the individuals in the intervention arms experienced a six-month decrease in adiponectin; whereas, the remainder increased somewhat. The distribution of change in plasma leptin indicates that 92% of participants in the weight loss intervention experienced a decrease in plasma leptin.
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References

    1. Ewertz M., Jensen M.B., Gunnarsdottir K.A., Hojris I., Jakobsen E.H., Nielsen D., Stenbygaard L.E., Tange U.B., Cold S. Effect of obesity on prognosis after early-stage breast cancer. J. Clin. Oncol. 2011;29:25–31. - PubMed
    1. Demark-Wahnefried W., Platz E.A., Ligibel J.A., Blair C.K., Courneya K.S., Meyerhardt J.A., Ganz P.A., Rock C.L., Schmitz K.H., Wadden T., et al. The role of obesity in cancer survival and recurrence. Cancer Epidemiol. Biomarkers Prev. 2012;21:1244–1259. - PMC - PubMed
    1. Protani M., Coory M., Martin J.H. Effect of obesity on survival of women with breast cancer: Systematic review and meta-analysis. Breast Cancer Res. Treat. 2010;123:627–635. - PubMed
    1. Al-Delaimy W.K., Flatt S.W., Natarajan L., Laughlin G.A., Rock C.L., Gold E.B., Caan B.J., Parker B.A., Pierce J.P. IGF1 and risk of additional breast cancer in the WHEL study. Endocr. Relat. Cancer. 2011;18:235–244. - PubMed
    1. Oh S.W., Park C.Y., Lee E.S., Yoon Y.S., Lee E.S., Park S.S., Kim Y., Sung N.J., Yun Y.H., Lee K.S., et al. Adipokines, insulin resistance, metabolic syndrome, and breast cancer recurrence: A cohort study. Breast Cancer Res. 2011;13:R34. - PMC - PubMed

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