TY - JOUR
T1 - Leptin responses to overfeeding
T2 - Relationship with body fat and nonexercise activity thermogenesis
AU - Levine, James A.
AU - Eberhardt, Norman L.
AU - Jensen, Michael D.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1999
Y1 - 1999
N2 - Administration of leptin to rodents results in weight loss through decreased food intake and increased energy expenditure that occurs in part through increased spontaneous activity. In humans, low levels of spontaneous physical activity and below normal plasma leptin concentrations predict subsequent excess weight gain. We recently found that failure to increase nonexercise activity thermogenesis (NEAT) with overfeeding results in greater fat gain in humans, and subsequently evaluated whether changes in leptin are related to NEAT activation. We measured plasma leptin concentrations and adipose tissue leptin messenger ribonucleic acid together with the components of energy expenditure in 16 nonobese humans before and after overfeeding to assess the relationship between leptin responses to overfeeding and the changes in NEAT. Adipocyte leptin expression was up-regulated with overfeeding, and leptin concentrations increased. Leptin concentrations correlated with body fat before and after overfeeding. Changes in leptin with overfeeding were strongly related to changes in body fat, but not to changes in NEAT. Changes in NEAT correlated inversely with fat gain. It is, therefore, unlikely that leptin mediates activation of NEAT with overfeeding in nonobese humans; rather, leptin directly reflects body fat mass and fat mass gain.
AB - Administration of leptin to rodents results in weight loss through decreased food intake and increased energy expenditure that occurs in part through increased spontaneous activity. In humans, low levels of spontaneous physical activity and below normal plasma leptin concentrations predict subsequent excess weight gain. We recently found that failure to increase nonexercise activity thermogenesis (NEAT) with overfeeding results in greater fat gain in humans, and subsequently evaluated whether changes in leptin are related to NEAT activation. We measured plasma leptin concentrations and adipose tissue leptin messenger ribonucleic acid together with the components of energy expenditure in 16 nonobese humans before and after overfeeding to assess the relationship between leptin responses to overfeeding and the changes in NEAT. Adipocyte leptin expression was up-regulated with overfeeding, and leptin concentrations increased. Leptin concentrations correlated with body fat before and after overfeeding. Changes in leptin with overfeeding were strongly related to changes in body fat, but not to changes in NEAT. Changes in NEAT correlated inversely with fat gain. It is, therefore, unlikely that leptin mediates activation of NEAT with overfeeding in nonobese humans; rather, leptin directly reflects body fat mass and fat mass gain.
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U2 - 10.1210/jc.84.8.2751
DO - 10.1210/jc.84.8.2751
M3 - Article
C2 - 10443673
AN - SCOPUS:0033306878
SN - 0021-972X
VL - 84
SP - 2751
EP - 2754
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 8
ER -