Foresta Carlo, Strapazzon Giacomo, De Toni Luca, Gianesello Lisa, Bruttocao Andrea, Scarda Alessandro, Plebani Mario, Garolla Andrea
Department of Histology, Microbiology and Medical Biotechnologies, Section of Clinical Pathology and Centre for Male Gamete CryopreservationEndocrine-Metabolic Laboratory (A.S.), Internal Medicine 3, University of PadovaEURAC Institute of Mountain Emergency Medicine (G.S.), Bozen/BolzanoDepartment of Oncological and Surgical Sciences, Clinical Surgery II (A.B), University Hospital of PadovaDepartment of Laboratory Medicine (M.P.), University Hospital of Padova, Padova, Italy.
Clin Endocrinol (Oxf). 2011 Jul;75(1):64-9. doi: 10.1111/j.1365-2265.2011.03997.x.
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.
Omental AT 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) forms, was measured in serum by ELISA.
After 24-h 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).
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.
雄激素通过雄激素受体（AR）介导的途径抑制脂肪生成分化，增加脂肪分解并减少脂肪细胞中的脂质积累。羧化不足的骨钙素（ucOCN）调节胰岛素和脂联素分泌，并由脂肪组织（AT）释放。我们的目的是在体外和体内研究雄激素对人脂肪组织中骨钙素（OCN）调节的作用。设计、患者、场所：使用来自帕多瓦大学医院的91名男性患者的网膜脂肪组织（OAT）进行体外研究和血液样本。
在存在和不存在氟他胺的情况下，用二氢睾酮（DHT）处理网膜脂肪组织。通过酶联免疫吸附测定（ELISA）评估在简单生长培养基中脂肪组织释放的羧化骨钙素（cOCN）和羧化不足骨钙素（ucOCN）。通过ELISA在血清中测量羧化不足（ucOCN）和羧化（cOCN）形式的骨钙素（OCN）。
在24小时DHT刺激后，网膜脂肪组织释放的cOCN和ucOCN在统计学上均增加（P <0.05）。与氟他胺共同孵育可减弱骨钙素的产生。超重和肥胖患者的总睾酮和游离睾酮（T）较低，与较低的ucOCN和ucOCN/OCN比值相关。游离睾酮与体重指数呈负相关（ρ=-0.706，P <0.05），与ucOCN/OCN比值呈正相关（ρ=0.223，P <0.05）。
我们的数据表明，雄激素在体外调节网膜脂肪组织释放骨钙素。除了雄激素的抗脂肪生成作用外，它们还支持一种新的机制，雄激素可通过该机制在能量代谢中发挥保护作用。考虑到肥胖中性激素水平发生了很大变化，并且脂肪组织既高度参与其清除又能够产生骨钙素，这一假设显得更为重要。
