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Osteopenia is a recognised complication of diabetes mellitus which could be due to abnormal bone turnover or disturbances in the calcium/parathyroid hormone/vitamin D axis or both. Genetic factors also play an important part in determining bone mass although this has not been studied in diabetes. Recently a polymorphism of the collagen type 1 α 1 (COL1A1) gene has been shown to be associated with low bone mass in British women. To identify subjects with diabetes who may be at risk of developing osteoporosis and fractures, we analysed bone mineral density in relation to the biochemical markers of bone turnover, calcium homeostasis and the COL1A1 genotype in a group of premenopausal women with Type I (insulin-dependent) diabetes mellitus ( n = 31), Type II (non-insulin dependent) diabetes mellitus ( n = 21) and control subjects ( n = 20). Bone mineral density was lower at the femoral neck in the subjects with Type I diabetes ( p = 0.08) as were serum 25-hydroxyvitamin D compared with control subjects ( p = 0.023) and this was negatively correlated with serum collagen type 1 C-terminal propeptide ( r = –0.56, p < 0.001). Bone mineral density in Type II diabetes was not different from control subjects, after correction for body mass index. Bone resorption was, however, raised in the Type II diabetic subjects as reflected by the higher urinary deoxypyridinoline values ( p = 0.016) and lower collagen type 1 C-terminal propeptide:deoxypyridinoline ratio ( p = 0.04). In the whole group studied, subjects with the COL1A1 ’s' genotype had lower bone mineral density at the femoral neck ( p = 0.01) which was partly attributable to a lower body mass index. Following multiple regression analysis body mass index and collagen type 1 C-terminal propeptide concentrations remained determinants of bone mass at all three sites, whereas genotype appeared to be a predictor of bone mass at the femoral neck only. We conclude that measurement of these variables could prove useful in firstly identifying those diabetic women at risk of osteoporosis and secondly guiding therapeutic intervention. [Diabetologia (1998) 41: 1314–1320] [ABSTRACT FROM AUTHOR]