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Correspondence to:
Peter Arner
Decreased lipolytic effect of catecholamines in adipose tissue has repeatedly been demonstrated in obesity and may be a cause of excess accumulation of body fat. However, the mechanisms behind this lipolysis defect are unclear. The role of hormone-sensitive lipase was examined using abdominal subcutaneous adipocytes from 34 obese drug-free and otherwise healthy males or females and 14 non-obese control subjects. The enzyme catalyzes the rate-limiting step of the lipolysis pathway. The maximum lipolytic capacity of fat cells was significantly decreased in obesity when measured using either a non-selective beta-adrenergic receptor agonist (isoprenaline) or a phosphodiesterase resistant cyclic AMP analogue (dibutyryl cyclic AMP). Likewise, enzyme activity, protein expression, and mRNA of hormone-sensitive lipase were significantly decreased in adipocytes of obese subjects. The findings were not influenced by age or gender.
The data suggest that a decreased expression of hormone-sensitive lipase in subcutaneous fat cells, which in turn causes decreased enzyme function and impaired lipolytic capacity of adipocytes, is present in obesity. Impaired expression of the hormone-sensitive lipase gene might at least in part explain the enzyme defect.—Large, V., S. Reynisdottir, D. Langin, K. Fredby, M. Klannemark, C. Holm, and P. Arner. Decreased expression and function of adipocyte hormone-sensitive lipase in subcutaneous fat cells of obese subjects. J. Lipid Res. 1999. 40: 2059;–2065.
Supplementary key words:
mRNA, enzymes, lipolysis, catecholamines, obesity, lipase, adipose tissue, hormone sensitive lipase
Copyright © 1999 by Lipid Research, Inc.
Original Article
Decreased expression and function of adipocyte hormone-sensitive lipase in subcutaneous fat cells of obese subjects
Valerie Largea,
Signy Reynisdottira,
Dominique Langinb,
Katrin Fredbya,
Mia Klannemarkd,
Cecilia Holmc, and
Peter Arnera
a Department of Medicine, Karolinska Institute, Huddinge University Hospital , Stockholm, Sweden
b INSERM U137, Institut Louis Bugnard, CHU Rangueil, Toulouse, France
c Department of Cell and Molecular Biology, Lund University, Lund, Sweden
d Department of Endocrinology, Malmö University Hospital, Lund University, Malmö, Sweden
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