Clin Endocrinol (Oxf). 2011 Feb 1. doi: 10.1111/j.1365-2265.2011.03997.x. [Epub ahead of print]
ANDROGENS MODULATE OSTEOCALCIN RELEASE BY HUMAN VISCERAL ADIPOSE TISSUE.
Foresta C, Strapazzon G, De Toni L, Gianesello L, Bruttocao A, Scarda A, Plebani M, Garolla A.
SourceDepartment of Histology, Microbiology and Medical Biotechnologies, Section of Clinical Pathology and Centre for Male Gamete Cryopreservation, University of Padova, Italy Endocrine-Metabolic Laboratory (A.S.), Internal Medicine 3, University of Padova, Italy Department of Laboratory Medicine (M.P.), University Hospital of Padova, Italy EURAC Institute of Mountain Emergency Medicine (G.S.), Bozen/Bolzano, Italy Clinical Surgery II (A.B), Department of Oncological and Surgical Sciences, University Hospital of Padova, Italy.
Abstract
Objective: Androgens inhibit adipogenic differentiation through an androgen receptor (AR)-mediated pathway, increase lipolysis and reduce lipid accumulation in adipocytes. Undercarboxylated osteocalcin (ucOCN) regulates insulin and adiponectin secretion and is released by adipose tissue (AT). Our objective was to investigate, ex vivo and in vivo, the role of androgens on osteocalcin (OCN) modulation in human AT. Design, Patients, Setting: Omental AT (OAT) for in vitro study and blood samples from 91 male patients of Padova University Hospital were used. Measurements: OAT was treated with dihydrotestosterone (DHT) in presence and in absence of flutamide. cOCN and ucOCN release by AT in a simple growth medium was evaluated by ELISA. OCN, both undercarboxylated (ucOCN) and carboxylated (cOCN) form, were measured in serum by ELISA. Results: After 24h DHT stimulation, the release of both cOCN and ucOCN by OAT was statistically increased (P<0.05). Co-incubation with flutamide blunted OCN production. Overweight and obese patients had lower total and free testosterone (T), associated with lower ucOCN and ucOCN/OCN ratio. Free T was negatively correlated to BMI (ρ=-0.706, P<0.05) and positively correlated to ucOCN/OCN ratio (ρ =0.223, P<0.05). Conclusions: Our data suggest that androgens modulate OCN release by OAT in vitro. In addition to the anti-adipogenic role of androgens, they support a novel mechanism by which androgens could exert a protective effect in energy metabolism. This hypothesis appears even more significant considering that sexual hormones levels are greatly altered in obesity and that AT is both highly involved in their clearance and able to produce OCN.
Copyright © 2011 Blackwell Publishing Ltd.
ANDROGENS MODULATE OSTEOCALCIN RELEASE BY HUMAN VISCERAL ADIPOSE TISSUE.
Foresta C, Strapazzon G, De Toni L, Gianesello L, Bruttocao A, Scarda A, Plebani M, Garolla A.
SourceDepartment of Histology, Microbiology and Medical Biotechnologies, Section of Clinical Pathology and Centre for Male Gamete Cryopreservation, University of Padova, Italy Endocrine-Metabolic Laboratory (A.S.), Internal Medicine 3, University of Padova, Italy Department of Laboratory Medicine (M.P.), University Hospital of Padova, Italy EURAC Institute of Mountain Emergency Medicine (G.S.), Bozen/Bolzano, Italy Clinical Surgery II (A.B), Department of Oncological and Surgical Sciences, University Hospital of Padova, Italy.
Abstract
Objective: Androgens inhibit adipogenic differentiation through an androgen receptor (AR)-mediated pathway, increase lipolysis and reduce lipid accumulation in adipocytes. Undercarboxylated osteocalcin (ucOCN) regulates insulin and adiponectin secretion and is released by adipose tissue (AT). Our objective was to investigate, ex vivo and in vivo, the role of androgens on osteocalcin (OCN) modulation in human AT. Design, Patients, Setting: Omental AT (OAT) for in vitro study and blood samples from 91 male patients of Padova University Hospital were used. Measurements: OAT was treated with dihydrotestosterone (DHT) in presence and in absence of flutamide. cOCN and ucOCN release by AT in a simple growth medium was evaluated by ELISA. OCN, both undercarboxylated (ucOCN) and carboxylated (cOCN) form, were measured in serum by ELISA. Results: After 24h DHT stimulation, the release of both cOCN and ucOCN by OAT was statistically increased (P<0.05). Co-incubation with flutamide blunted OCN production. Overweight and obese patients had lower total and free testosterone (T), associated with lower ucOCN and ucOCN/OCN ratio. Free T was negatively correlated to BMI (ρ=-0.706, P<0.05) and positively correlated to ucOCN/OCN ratio (ρ =0.223, P<0.05). Conclusions: Our data suggest that androgens modulate OCN release by OAT in vitro. In addition to the anti-adipogenic role of androgens, they support a novel mechanism by which androgens could exert a protective effect in energy metabolism. This hypothesis appears even more significant considering that sexual hormones levels are greatly altered in obesity and that AT is both highly involved in their clearance and able to produce OCN.
Copyright © 2011 Blackwell Publishing Ltd.
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