The same measurements were performed at baseline and after four months. Height and weight were measured wearing light clothing and no shoes, and fasting blood samples were drawn. Serum calcium and creatinine, PTH, 25(OH)D, blood glucose, serum insulin and HbA1c and homeostatic model assessment for insulin resistance (HOMA-IR) were calculated as previously described [13 (link)]. BMI was calculated as weight (kg) divide by height (m) squared.
CTX-1 and P1NP were measured by electrochemiluminescence immunoassays with a Cobas e601 kit (Roche Diagnostics, NJ, USA), at the Hormone Laboratory, Oslo University Hospital, Norway. DKK1, leptin, OPG, sclerostin, TNF-α were analyzed using multianalyte profiling Milliplex MAP assay, and RANKL by a single analyte assay (Millipore Corporation, Billerica, MA, USA).
BMD was measured by DXA (GE Lunar Prodigy, Lunar Corporation, Madison, WI, USA) at the hip and lumbar spine, with total hip (mean of left and right, or one side if not both could be measured) and L1 (which had valid measurement in almost every subject) used in the analyses.
CTX-1 and P1NP were measured by electrochemiluminescence immunoassays with a Cobas e601 kit (Roche Diagnostics, NJ, USA), at the Hormone Laboratory, Oslo University Hospital, Norway. DKK1, leptin, OPG, sclerostin, TNF-α were analyzed using multianalyte profiling Milliplex MAP assay, and RANKL by a single analyte assay (Millipore Corporation, Billerica, MA, USA).
BMD was measured by DXA (GE Lunar Prodigy, Lunar Corporation, Madison, WI, USA) at the hip and lumbar spine, with total hip (mean of left and right, or one side if not both could be measured) and L1 (which had valid measurement in almost every subject) used in the analyses.