Obesity and type 2 diabetes (T2D) are linked to metabolic dysregulation and chronic inflammation. Adipose tissue and skeletal muscles are key endocrine organs. Dysregulation in adipomyokines secreted by these organs could play a role in obesity-induced complications. Obesity, T2D and bone metabolism are interrelated. Our objective was to study the expression of two adipomyokines-Irisin and Meteorin-like protein (METRNL) in obesity and T2D and understand their association with various bone markers. Overall, 228 individuals were enrolled in this study, including 124 nondiabetic and 104 T2D . Plasma level of MTRNL and irisin were assessed by ELISA. Plasma level of METRNL and irisin were significantly higher in T2D (1263.5 ± 24.9 pg/ml and 623.0± 21.8 pg/ml respectively) compared to nondiabetic individuals (1198.5 ± 24.2 pg/ml for METRNL and 508.2 ± 15.3 pg/ml for irisin) p-Value < 0.05. METRNL and irisin were significantly higher in obese (1267.9 ± 24.8 pg/ml and 593.4 ± 18.1 pg/ml respectively) compared to non-obese individuals (1186.3 ± 24.2 pg/ml and 519.9 ± 19.1 respectively) p-Value < 0.05. Plasma level of bone markers Osteoactivin, Syndecan, OPG and SPARC were significantly higher in obese and T2D individuals compared to non-obese and nondiabetic individuals (P-values ≤0.01). Correlation analysis on nondiabetic population showed significant positive correlation between METRNL and irisin. Irisin showed a strong positive association with Osteoactivin, Syndecan, OPG, and SPARC. A strong positive association was observed between METRNL and Osteoactivin. The interplay between these bone markers is linked to bone remodeling. The strong positive association between the adipomyokines and bone markers suggests that, a dysregulation in the functional interaction between them may play a possible role in the development of bone related complications associated with obesity and T2D. We are currently conducting further experiments to understand mechanistically the significance of their interplay.
M. Abu-farha: None. P.T. Cherian: None. I. Al khairi: None. M. Jamal: None. S. Al-Sabah: None. H. Ali: None. C. Dsouza: None. F.K. AlOtaibi: None. W. Al-Ali: None. G.M. Al-Khaledi: None. J. Abubaker: None. F. Al-Mulla: None.
Dasman Diabetes Institute