Introduction
Osteoporosis is one of the commonest metabolic bone diseases, and its prevalence is expected to rise as the population grows older. Although osteoporosis is less prevelant in men than in women, the morbidity and mortality due to male osteoporosis is higher (1,2). The major causes of osteoporosis in men are hypogonadism, hypercortisolism and excessive alcohol intake. Other abnormalities such as hyperthyroidism and malignancy are less commonly responsible for osteoporosis. All above mentioned disorders account for osteoporosis in approximately 60% of men (3,4). The remaining subset of men with idiopathic osteoporosis has been poorly characterized. With no readily identifiable causes of reduced bone density in men with idiopathic osteoporosis, it is attractive to consider the possibility that this disorder is the result of fundamental abnormalities of bone cell function or of the hormonal or paracrine pathways that regulate the bone cell metabolism (5,6). Growth hormone (GH) and its major mediator insulin like growth factor 1 (IGF-1) are thought to be important both in attainning peak bone mass and maintaining adult bone mass (7,8). The synthesis of circulating IGF-1 occurs principally in the liver; osteoblasts also contribute to IGF-1 production (9). Invitro and invivo studies have shown IGF-1 to enhance type 1 collagen production and bone matrix apposition rates and decrease degradation of bone collagen (10,11). A major portion of IGF-1 is bound to IGFBP-3 which is a quantitatively predominant IGFBP in the circulation. Serum IGFBP-3 level is thought to be positively regulated by GH and / or IGF-1 (12,13). It has been suggested that IGFBP-3 might augment the effect of IGF-1 on the bone (14).Recent studies have focused on the role of GH and IGF-1 in the regulation of bone metabolism in men. In elderly men, bone mineral density (BMD) is not correlated with IGF-1 concentrations. In contrast, studies including younger men suggested a weak possitive correlation between serum IGF-1 and BMD at some skeletal sites (15-20). However, these studies are not easily comparable because they were performed in mixed cohorts composed of men and women or in small samples of different age groups and based on different statistical approaches. There have also been reports indicating an association between low IGFBP-3 and BMD in both men and postmenopausal women. Others have shown only a weak association between IGFBP-3 and BMD in men and no association in women (18). Therefore, we attempted to evaluate the effects of serum IGF-1 and IGFBP-3 levels on BMD at various skeletal sites in Turkish adult men. In addition, we investigated the relationship between IGF-1, IGFBP-3 and bone turnover markers.
Statistical Analyses
Descriptive characteristics of the study population were expressed in numbers and percentages (Table 1). Mean and standard deviations of baseline measurements were used to determine. These statistics are given in Table 2 and 3. Multivariate analyses were used to explain the relation between dependent variables (serum IGF-1, IGFBP-3 and BMD) and independent variables (age, BMI, daily calcium intake, smoking, alcohol intake, chronic diseases, medications, history of fracture, back pain and exercise habits). Partial correlation analyses were made to adjust for age and BMI and Pearson correlation analysis to determine the relationship between IGF-1, IGFBP-3, BMD and bone turnover markers. The results of these analyses are given in Tables 4. In addition, the subjects were assigned into two new groups: those with ‘low BMI’ and those with ‘normal BMI’. Independent samples t test was used to compare these groups in terms of serum IGF-1 and IGFBP-3 (Figures 1 - 2). The scatter plot and regression fit line plotted were used to show the relationship between age and serum IGF-1 and IGFBP-3 in each subgroupAll statistical analysis were performed with SPSS software, version 12. P< 0.05 was considered significant.
