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Amendment history:
  • Correction (August 1998)

Research Article Free access | 10.1172/JCI119422

Leptin secretion from adipose tissue in women. Relationship to plasma levels and gene expression.

F Lönnqvist, L Nordfors, M Jansson, A Thörne, M Schalling, and P Arner

Department of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, S-141 86 Stockholm, Sweden.

Find articles by Lönnqvist, F. in: JCI | PubMed | Google Scholar

Department of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, S-141 86 Stockholm, Sweden.

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Department of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, S-141 86 Stockholm, Sweden.

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Department of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, S-141 86 Stockholm, Sweden.

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Department of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, S-141 86 Stockholm, Sweden.

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Department of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, S-141 86 Stockholm, Sweden.

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Published May 15, 1997 - More info

Published in Volume 99, Issue 10 on May 15, 1997
J Clin Invest. 1997;99(10):2398–2404. https://doi.org/10.1172/JCI119422.
© 1997 The American Society for Clinical Investigation
Published May 15, 1997 - Version history
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Abstract

The role of expression and secretion of the ob gene product, leptin, for the regulation of plasma leptin levels has been investigated in vitro using abdominal subcutaneous adipose tissue of 20 obese, otherwise healthy, and 11 nonobese women. Body mass index (BMI, mean+/-SEM; kg/m2) in the two groups was 41+/-2 and 23+/-1, respectively. Fat cell volume was 815+/-55 pl in the obese and 320+/-46 pl in the nonobese group. In the obese group, plasma leptin concentrations and adipose leptin mRNA (relative to gamma actin) were increased five and two times, respectively. Moreover, adipose tissue secretion rates per gram lipid weight or per fat cell number were also increased two and seven times, respectively, in the obese group. There were strong linear correlations (r = 0.6-0.8) between plasma leptin, leptin secretion, and leptin mRNA. All of these leptin measurements correlated strongly with BMI and fat cell volume (r = 0.7- 0.9). About 60% of the variation in plasma leptin could be attributed to variations in leptin secretion rate, BMI, or fat cell volume. We conclude that elevated circulating levels of leptin in obese women above all result from accelerated secretion rates of the peptide from adipose tissue because of increased ob gene expression. However, leptin mRNA, leptin secretion, and circulating leptin levels are all more closely related to the stored amount of lipids in the fat cells of adipose tissue than they are to an arbitrary division into obese versus nonobese.

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