AIMS: To investigate relationships between bone mineral density (BMD), insulin secretion and insulin sensitivity, controlling for body composition, in view of data suggesting that hyperglycaemia [corrected] leads to decreased osteoblast proliferation and a negative calcium balance and that insulin stimulates osteoblast differentiation and collagen synthesis, with no clear evidence if this response in impaired in insulin resistance. METHODS: Femur and whole body (WB) BMD was measured in 55 male patients with ischaemic heart disease and 40 healthy men, using a Hologic QDR-2000 densitometer. Insulin sensitivity (Si) was estimated as the rate of glucose disappearance divided by the area under the insulin curve during an intravenous glucose tolerance test. RESULTS: Insulin and C-peptide levels were not correlated with BMD, but Si was a significant predictor of femur (log, r = 0.35) and WB BMD (log r = 0.29, both P<0.01), even after controlling for weight and age. Fat mass (FM) was a predictor of BMD (femur: r = 0.33 P<0.01, WB: r = 0.43 P<0.001). In the femur the association with FM disappeared when log(Si) was entered in the regression. Lean body mass (LBM) contributed significantly to BMD (r = 0.50 and r = 0.66, both P<0.001). CONCLUSIONS: These results are compatible with a direct influence of lean body mass on bone, while the impact of fat mass may consist of insulin resistance with increased insulin exposure of bone. It is hypothesized that patients with insulin resistance in the metabolic pathway do not exhibit resistance to the skeletal actions of insulin.
AIMS: To investigate relationships between bone mineral density (BMD), insulin secretion and insulin sensitivity, controlling for body composition, in view of data suggesting that hyperglycaemia [corrected] leads to decreased osteoblast proliferation and a negative calcium balance and that insulin stimulates osteoblast differentiation and collagen synthesis, with no clear evidence if this response in impaired in insulin resistance. METHODS: Femur and whole body (WB) BMD was measured in 55 male patients with ischaemic heart disease and 40 healthy men, using a Hologic QDR-2000 densitometer. Insulin sensitivity (Si) was estimated as the rate of glucose disappearance divided by the area under the insulin curve during an intravenous glucose tolerance test. RESULTS:Insulin and C-peptide levels were not correlated with BMD, but Si was a significant predictor of femur (log, r = 0.35) and WB BMD (log r = 0.29, both P<0.01), even after controlling for weight and age. Fat mass (FM) was a predictor of BMD (femur: r = 0.33 P<0.01, WB: r = 0.43 P<0.001). In the femur the association with FM disappeared when log(Si) was entered in the regression. Lean body mass (LBM) contributed significantly to BMD (r = 0.50 and r = 0.66, both P<0.001). CONCLUSIONS: These results are compatible with a direct influence of lean body mass on bone, while the impact of fat mass may consist of insulin resistance with increased insulin exposure of bone. It is hypothesized that patients with insulin resistance in the metabolic pathway do not exhibit resistance to the skeletal actions of insulin.
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Authors: Barbara A Gower; Norman K Pollock; Krista Casazza; Thomas L Clemens; Laura Lee Goree; Wesley M Granger Journal: J Clin Endocrinol Metab Date: 2013-04-24 Impact factor: 5.958