1. Department of Cell and Molecular Biology, Karolinska Institute, SE-171 77 Stockholm, Sweden
2. Institute for Theoretical Biology (ITB), Humboldt University Berlin and Charité, Invalidenstrasse 43, 10115 Berlin, Germany
3. Institute of Applied and Computational Mathematics, Foundation of Research and Technology, 71110 Heraklion Crete, Greece
4. Center for Accelerator Mass Spectrometry, Lawrence Livermore National Laboratory, 7000 East Avenue, L-397, Livermore, California 94551, USA
5. Department of Medicine, Karolinska University Hospital, SE-141 86 Stockholm, Sweden
6. Division of Surgery, Department of Clinical Science, Danderyds Hospital, Karolinska Institutet, SE-182 88 Stockholm, Sweden
7. Department of Mathematics, Stockholm University, 106 91 Stockholm, Sweden

Correspondence to: Kirsty L. Spalding¹Jonas Frisén¹Peter Arner⁵ Correspondence and requests for materials should be addressed to K.L.S. (Email: kirsty.spalding@ki.se), J.F. (Email: jonas.frisen@ki.se) or P.A. (Email: peter.arner@ki.se).

Abstract

Obesity is increasing in an epidemic manner in most countries and constitutes a public health problem by enhancing the risk for cardiovascular disease and metabolic disorders such as type 2 diabetes^{1, 2}. Owing to the increase in obesity, life expectancy may start to decrease in developed countries for the first time in recent history³. The factors determining fat mass in adult humans are not fully understood, but increased lipid storage in already developed fat cells (adipocytes) is thought to be most important^{4, 5}. Here we show that adipocyte number is a major determinant for the fat mass in adults. However, the number of fat cells stays constant in adulthood in lean and obese individuals, even after marked weight loss, indicating that the number of adipocytes is set during childhood and adolescence. To establish the dynamics within the stable population of adipocytes in adults, we have measured adipocyte turnover by analysing the integration of ¹⁴C derived from nuclear bomb tests in genomic DNA⁶. Approximately 10% of fat cells are renewed annually at all adult ages and levels of body mass index. Neither adipocyte death nor generation rate is altered in early onset obesity, suggesting a tight regulation of fat cell number in this condition during adulthood. The high turnover of adipocytes establishes a new therapeutic target for pharmacological intervention in obesity.

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