Interrelationship between osteocalcin (BGP) and energetic metabolism in two strains of rats

MAROTTE C; BRYK G; ZENI CORONEL M; LUCERO DM; SCHERIER L,; DE PORTELA MARIA L; ZENI SN

Lisboa

Congreso; 40th. Annual Congress of European Calcified Tissue Society (ECTS). Lisboa; 2013

European Calcified Tissue Society

It has suggested that BGP is inversely related to body fat. BGP appears to regulate energetic metabolism through the insulin receptor signaling pathway in the osteoblast, which affects bone resorption and BGP activity. Fat tissue is an endocrine organ that secretes different hormones and growth factors; several of them affect bone remodeling and insulin secretion. The present report comparatively studied total BGP levels, glucose homeostasis and body fat mass in spontaneous obese (OB) strain and Wistar (W) rats. Both group were fed since their mother’s pregnancy until the end of the experience (50 days of age) AIN 93 diet that supplied 0.5 mg%Ca, 0.4 mg%P, 200IUvitamin D% Serum BGP, insulin and C-terminal type I collagen telopeptide (CTX) were evaluated by ELISA; glucose and triglycerides (TGL) by colorimetric enzymology and 25OHD by a competitive protein-binding method (Diasorin). HOMA-IR was calculated. At the end of experience body composition was evaluated, according AOAC methods. Results of OBN vs WN, respectively (mean ± ES): fat (g/100body weight): 13.1±2.2 vs. 10.4±0.8 (p<0.01); Liver weight (g): 12.3±0.9 vs. 8.1±1.5 (p<0.01); TGL (mg/dL): 225±37 vs. 59±16 (p<0.001); glucose (mg/dl): 152±69 vs 99±41 (p<0.01); insulin (ng/dl): 4.75±2.44 vs 0.14±0.02 (p<0.001); CTX (ng/ml): 83±8 vs 94±6 (p<0.01); BGP (ng/ml): 375±18 vs 840±106 (p<0.001); 25OHD (ng/dl): 19.0±5.4 vs.15.4±2.8 (pns).   The OB group showed a higher fat content, liver weight, glucose, TGL, insulin and 25OHD levels but lower BGP and CTX levels. Conclusion: The results confirmed that there was an inverse relationship between levels of BGP and body fat content. The concomitant reduction in bone resorption of OB rats, may suggest a decrease in the biological active BGP that could be the responsible of the observed increment in fasting glucose levels and insulin resistance. The study was partially supported by UBACyT 20020100100320 and CONICET: