ESPE2024 Poster Category 3 Fat, Metabolism and Obesity (35 abstracts)
1Department of Human Pathology of Adulthood and Childhood, University of Messina, Messina, Italy. 2Department of Clinical and Experimental Medicine, University Hospital of Messina, Messina, Italy
Background: Recent studies suggest that osteocalcin (OC) promotes glucose and lipid metabolism via ACAM, integrin αVβ3, GLUT1 and GLUT8 expression, directly affecting adipocytes. OC represents a link between bone and glucose metabolism; it stimulates insulin and stimulates pancreatic β-cells proliferation through Gprc6a receptor. Low levels of OC were observed in adult patients with Type 2 DM suggesting an association with glucose intolerance and insulin resistance. The aim of our study was to evaluate the relationship between bone remodeling biomarkers, including OC, and glucose metabolism in pediatric patients with essential obesity.
Methods: The study included 33 obese patients, 13 males and 20 females, with mean age of 10,37 ± 2,9 yrs and body mass index (BMI) ≥ 95th percentile. Auxological (bone age, weight, height, BMI) and biochemical (glycemia, insulinemia, HOMA-IR index, total cholesterol, HDL, LDL, triglycerides, transaminases, GOT and GPT, uric acid, TSH, FT3 and FT4, somatomedin C, calcium, phosphorus, alkaline phosphatase, vitamin D3, parathormone, C-terminal telopeptide of collagen type 1 and osteocalcin) parameters were assessed.
Results: 22 out of 33 children presented insulin resistance (HOMA-IR index > 2.5) and a pathological insulinemic curve, while maintaining normal glucose tolerance and not satisfying the diagnostic criteria for type 2 DM. At baseline, mean blood glucose was 88.09 ± 10.83 mg/dl and mean insulinemia was 24.91 ± 12.98 mg/dl. Serum OC levels were higher in obese children with insulin resistance (112.08 ± 56.05 ng/mL); a positive correlation between OC and insulinemia (P = 0.02) and between OC and HOMA-IR index (P = 0.01) was observed.
Conclusion: In contrast to other studies in which low levels of OC are reported in children with obesity, our data show higher levels of OC in patients with obesity and hyperinsulinism, possibly due to a compensatory mechanism finalized to improve insulin secretion and sensitivity. Therefore, it is likely that impaired glucose tolerance is associated with reduced OC levels, given the relationship between bone and pancreatic β-cells. A bidirectional interference between bone and pancreatic β-cells may be proposed because OC stimulate insulin production, but insulin can also rise OC secretion by stimulating insulin receptors in osteoblasts.