Abstract
Nutrients influence bone turnover. Carboxylated osteocalcin (Gla-OC) participates in bone formation whereas its undercarboxylated form (Glu-OC) acts as a hormone in glucose metabolism. The aim of the study was to determine the responses of Gla-OC, Glu-OC, and total-OC (calculated as the sum of Gla-OC and Glu-OC) to a high fat mixed meal tolerance test (HFMTT) in non-obese (body mass index (BMI) < 30 kg/m2, n = 24) and obese subjects (30 < BMI < 40 kg/m2, n = 70) (both sexes, aged 25–65 years). Serum Gla-OC and Glu-OC were measured at baseline as well as at 2 and 6 h during a HFMTT by enzyme-linked immunosorbent assay (ELISA). Baseline Gla-OC, Glu-OC, and total-OC levels were lower in obese individuals compared to non-obese participants (p = 0.037, p = 0.016 and p = 0.005, respectively). The decrease in Gla-OC and total-OC, but not in Glu-OC, concentrations during the HFMTT was suppressed in obese, but not in non-obese controls (p < 0.05, p < 0.01, p = 0.08, respectively). Subjects with the highest homeostatic model assessment for insulin resistance (HOMA-IR) index values had a less pronounced decrease in total-OC compared to patients with values of HOMA-IR index in the 1st quartile (p < 0.05). Net incremental area under Gla-OC inversely correlated with adiponectin (rho = −0.35, p = 0.001). Increase in insulin sensitivity and adiponectin level in obese subjects could beneficially influence postprandial bone turnover expressed by osteocalcin concentration.
Highlights
Recent clinical and epidemiologic studies have shown that obesity did not protect against osteoporosis and even could be a risk factor for fragility fractures
Fasting blood glucose levels were similar in the studied groups of subjects, serum concentration of fasting insulin and insulin resistance index, homeostatic model assessment for insulin resistance (HOMA-IR), were significantly higher (p < 0.001, p < 0.001, respectively) in obese participants compared with non-obese controls
We focused on the effect of more physiological intake of nutrients during a high fat mixed meal on the blood levels of the carboxylated and undercarboxylated form of osteocalcin in non-obese healthy individuals as well as in insulin resistant obese volunteers
Summary
Recent clinical and epidemiologic studies have shown that obesity did not protect against osteoporosis and even could be a risk factor for fragility fractures. It was reported that in obesity, the cross-talk between adipose tissue and bone could be affected by disturbances in secretion of several adipokines and bone-derived molecules regulating bone turnover and adipogenesis as well as body weight and glucose metabolism [1,2,3,4]. Osteocalcin (OC) is a secretory product of osteoblasts, which participates in bone remodeling, and in regulating energy metabolism [5,6,7,8,9]. OC undergoes vitamin-K-dependent carboxylation (Gla-OC) and interacts with hydroxyapatite crystals of the bone matrix [5,6,7]. 15% of Gla-OC is not absorbed in bones during bone formation and could be detected in the circulation. A portion of osteocalcin in blood remains undercarboxylated (Glu-OC)
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