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Burnett L.C.,Columbia University | Burnett L.C.,Naomi Berrie Diabetes Center | Skowronski A.A.,Columbia University | Skowronski A.A.,Naomi Berrie Diabetes Center | And 8 more authors.
International Journal of Obesity | Year: 2017

Background:The adipokine hormone, leptin, is a major component of body weight homeostasis. Numerous studies have been performed administering recombinant mouse leptin as an experimental reagent; however, the half-life of circulating leptin following exogenous administration of recombinant mouse leptin has not been carefully evaluated.Methods:Exogenous leptin was administered (3 mg leptin per kg body weight) to 10-week-old fasted non-obese male mice and plasma was serially collected at seven time points; plasma leptin concentration was measured by enzyme-linked immunosorbent assay at each time point to estimate the circulating half-life of mouse leptin.Results:Under the physiological circumstances tested, the half-life of mouse leptin was 40.2 (±2.2) min. Circulating leptin concentrations up to 1 h following exogenous leptin administration were 170-fold higher than endogenous levels at fasting.Conclusions:The half-life of mouse leptin was determined to be 40.2 min. These results should be useful in planning and interpreting experiments employing exogenous leptin. The unphysiological elevations in circulating leptin resulting from widely used dosing regimens for exogenous leptin are likely to confound inferences regarding some aspects of the hormone's clinical biology. © 2017 Macmillan Publishers Limited, part of Springer Nature. All rights reserved.


Stevens J.R.,Saint Louis University | Kearney M.L.,University of Missouri | St-Onge M.-P.,New York Obesity Research Center | St-Onge M.-P.,Columbia University | And 6 more authors.
Obesity | Year: 2016

Objective: The role of metabolic condition and diet in regulating circulating levels of adropin, a peptide hormone linked to cardiometabolic control, is not well understood. In this study, weight loss and diet effects on plasma adropin concentrations were examined. Methods: This report includes data from (1) a weight loss trial, (2) an evaluation of acute exercise effects on mixed-meal (60% kcal from carbohydrates) tolerance test responses, and (3) a meta-analysis to determine normal fasting adropin concentrations. Results: Distribution of plasma adropin concentrations exhibited positive skew and kurtosis. The effect of weight loss on plasma adropin concentrations was dependent on baseline plasma adropin concentrations, with an inverse association between baseline and a decline in concentrations after weight loss (Spearman's ρ = −0.575; P < 0.001). When ranked by baseline plasma adropin concentrations, only values in the upper quartile declined with weight loss. Plasma adropin concentrations under the main area of the bell curve correlated negatively with habitual carbohydrate intake and plasma lipids. There was a negative correlation between baseline values and a transient decline in plasma adropin during the mixed-meal tolerance test. Conclusions: Plasma adropin concentrations in humans are sensitive to dietary macronutrients, perhaps due to habitual consumption of carbohydrate-rich diets suppressing circulating levels. Very high adropin levels may indicate cardiometabolic conditions sensitive to weight loss. © 2016 The Obesity Society


PubMed | University of Missouri, New York Obesity Research Center, Saint Louis University, University of Kansas Medical Center and University of California at Davis
Type: Journal Article | Journal: Obesity (Silver Spring, Md.) | Year: 2016

The role of metabolic condition and diet in regulating circulating levels of adropin, a peptide hormone linked to cardiometabolic control, is not well understood. In this study, weight loss and diet effects on plasma adropin concentrations were examined.This report includes data from (1) a weight loss trial, (2) an evaluation of acute exercise effects on mixed-meal (60% kcal from carbohydrates) tolerance test responses, and (3) a meta-analysis to determine normal fasting adropin concentrations.Distribution of plasma adropin concentrations exhibited positive skew and kurtosis. The effect of weight loss on plasma adropin concentrations was dependent on baseline plasma adropin concentrations, with an inverse association between baseline and a decline in concentrations after weight loss (Spearmans =-0.575; P < 0.001). When ranked by baseline plasma adropin concentrations, only values in the upper quartile declined with weight loss. Plasma adropin concentrations under the main area of the bell curve correlated negatively with habitual carbohydrate intake and plasma lipids. There was a negative correlation between baseline values and a transient decline in plasma adropin during the mixed-meal tolerance test.Plasma adropin concentrations in humans are sensitive to dietary macronutrients, perhaps due to habitual consumption of carbohydrate-rich diets suppressing circulating levels. Very high adropin levels may indicate cardiometabolic conditions sensitive to weight loss.


Widen E.M.,Columbia University | Widen E.M.,New York Obesity Research Center | Whyatt R.M.,Columbia University | Hoepner L.A.,Columbia University Medical Center | And 10 more authors.
American Journal of Clinical Nutrition | Year: 2015

Background: Excessive gestational weight gain (GWG) is associated with postpartum weight retention (PPWR) and abdominal adiposity, but long-term effects are understudied in low-income and minority populations at high risk of obesity and associated sequelae. Objective: We examined associations between GWG and long-term PPWR and adiposity in a prospective cohort of African American and Dominican mothers in the Bronx and Northern Manhattan. Design:Women (n = 302) were enrolled during pregnancy and were followed for 7 y postpartum. Linear regression was used to relate excessive GWG [greater than 2009 Institute of Medicine (IOM) guidelines] to outcomes [percentage body fat and long-term PPWR (change in weight from prepregnancy to 7 y postpartum)], adjusting for covariates and included an interaction term between prepregnancy body mass index (BMI; in kg/m2) and GWG. Results: Mean 6 SD prepregnancy BMI and total GWG were 25.6 6 5.8 (42% of women had BMI $25) and 16.6 6 7.8 kg (64% of women had total GWG greater than IOM guidelines), respectively. Associations between GWG and long-term PPWR and the percentage body fat varied by prepregnancy BMI (P-interaction # 0.06); excessive GWG was associated with a higher percentage body fat and greater long-term PPWR in mothers with lower prepregnancy BMI. To illustrate the interaction, a predicted covariateadjusted model, which was used to derive estimates for the percentage body fat and PPWR associated with excessive GWG, was estimated for 2 prepregnancy BMI examples. For a woman with prepregnancy BMI of 22, excessive GWG was associated with 3.0% higher body fat (P , 0.001) and a 5.6-kg higher PPWR (P , 0.001); however, for a woman with a prepregnancy BMI of 30, excessive GWG was associated with 0.58% higher body fat (P = 0.55) and 2.06 kg PPWR (P = 0.24). Conclusions: Long-term adiposity and PPWR in low-income African American and Dominican mothers were predicted by interacting effects of prepregnancy BMI and excessive GWG. The provision of support for mothers to begin pregnancy at a healthy weight and to gain weight appropriately during pregnancy may have important lasting implications for weight-related health in this population. This study was registered at clinicaltrials.gov as NCT00043498. © 2015 American Society for Nutrition.

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