Influence of calcium intake on bone mineral density and incidence of fractures in treatment-naive women from Lodz urban area - a part of EPOLOS study

Introduction. Inadequate calcium intake is a recognized osteoporosis risk factor. The aim of the study was to estimate calcium intake in women in the Łódż population, the influence of calcium intake on bone mineral density (BMD) and fracture incidence, as well as the relationship between calcium intake and age. Material and methods. This cross-sectional investigation is a part of the EPOLOS study (a multicentre, population-based study on osteoporosis risk factors in Poland). In this study, 277 women from the Lodz urban area were involved [aged 20–80 years, not treated for osteoporosis before]. BMD was measured by dual-energy X-ray absorptiometry (DXA) in the lumbar spine and femoral neck. Fractures were self-reported and calcium intake was calculated according to data gathered in a questionnaire. Results. An average daily calcium intake was 797±432 mg. 65.7% of the examined women took less calcium than 1,000 mg/daily. Daily calcium intake decreased with age – from 903 mg between 20–30 years of age, to 624 mg between the ages of 70–80. In women aged 50 and older, the prevalence of low BMD at the lumbar spine (T-score <–1.0) was 31.9%. Patients reported 75 low-trauma fractures. There was a weak negative correlation between age and calcium intake, and no correlation between BMD and calcium intake. Women with fractures were significantly older than women without fractures, had significantly lower BMD, and similar levels of calcium intake. Conclusions. 1) Calcium intake below the recommended dietary intake was found in the majority of examined women. 2) No correlation between calcium intake and BMD, and between calcium intake and fracture incidence may suggest the involvement of factors other than calcium intake in pathogenesis of osteoporosis development. 3) Calcium intake gradually diminished with the age of the women

Copeptin under glucagon stimulation

Stimulation of growth hormone (GH) and adrenocorticotropic hormone (ACTH) secretion by glucagon is a standard procedure to assess pituitary dysfunction but the pathomechanism of glucagon action remains unclear. As arginine vasopressin (AVP) may act on the release of both, GH and ACTH, we tested here the role of AVP in GST by measuring a stable precursor fragment, copeptin, which is stoichiometrically secreted with AVP in a 1:1 ratio. ACTH, cortisol, GH, and copeptin were measured at 0, 60, 90, 120, 150, and 180 min during GST in 79 subjects: healthy controls (Group 1, n = 32), subjects with pituitary disease, but with adequate cortisol and GH responses during GST (Group 2, n = 29), and those with overt hypopituitarism (Group 3, n = 18). Copeptin concentrations significantly increased over baseline 150 and 180 min following glucagon stimulation in controls and patients with intact pituitary function but not in hypopituitarism. Copeptin concentrations were stimulated over time and the maximal increment correlated with ACTH, while correlations between copeptin and GH were weaker. Interestingly, copeptin as well as GH secretion was significantly attenuated when comparing subjects within the highest to those in the lowest BMI quartile (p < 0.05). Copeptin is significantly released following glucagon stimulation. As this release is BMI-dependent, the time-dependent relation between copeptin and GH may be obscured, whereas the close relation to ACTH suggests that AVP/copeptin release might be linked to the activation of the adrenal axis. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s12020-015-0783-7) contains supplementary material, which is available to authorized users