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Am J Physiol Endocrinol Metab (January 28, 2003). doi:10.1152/ajpendo.00262.2002
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Submitted on June 13, 2002
Accepted on January 13, 2003

Greater replication and differentiation of preadipocytes in inherited corticosteroid binding globulin deficiency

Julie M. Joyner1, Louise J. Hutley2, Anthony W. Bachmann3, David J. Torpy3, and Johannes B. Prins2*

1 Department of Medicine, Redland Hospital, Cleveland, Queensland, Australia; Department of Medicine, University of Queensland, Woolloongabba, Queensland, Australia
2 Department of Medicine, University of Queensland, Woolloongabba, Queensland, Australia; Department of Diabetes and Endocrinology, Princess Alexandra Hospital, Woolloongabba, Queensland, Australia
3 Department of Medicine, University of Queensland, Woolloongabba, Queensland, Australia; Greenslopes Private Hospital, Greenslopes, Queensland, Australia

* To whom correspondence should be addressed. E-mail: jprins{at}medicine.pa.uq.edu.au.

Glucocorticoids are pivotal for adipose tissue development. Rodent studies suggest corticosteroid-binding globulin (CBG) modulates glucocorticoid action in adipose tissue. In humans, both genetic CBG deficiency and suppressed CBG concentrations in hyperinsulinemic states, are associated with obesity. We hypothesised that CBG deficiency in humans modulates the response of human preadipocytes to glucocorticoids, predisposing to obesity. We compared subcultured preadipocytes from an individual with the first ever described complete deficiency of CBG due to a homozygous null mutation, with normal preadipocytes. CBG-negative preadipocytes proliferated more rapidly and showed greater PPAR-{gamma}-mediated differentiation than normal preadipocytes. CBG was not expressed in normal human preadipocytes. Glucocorticoid receptor number and binding characteristics, and 11{beta}-hydroxysteroid dehydrogenase activity were similar for CBG-negative and normal preadipocytes. We propose that the increased proliferation and enhanced differentiation of CBG-negative preadipocytes may promote adipose tissue deposition and explain the obesity seen in individuals with genetic CBG deficiency. Furthermore these observations may be relevant to obesity occurring with suppressed CBG concentrations associated with hyperinsulinemia.




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