ECE2017 Eposter Presentations: Calcium and Bone Bone & Osteoporosis (37 abstracts)
Pomeranian Medical University, Szczecin, Poland.
Disorders of bone mineralization observed in women with ovarian insufficiency are unlikely a simple function of decreased concentration of oestrogens. Published evidence suggests that adipose tissue is a central component within the complex system of metabolic and hormonal interactions responsible for adequate mineralization of the bone. However, to the best of our knowledge, the composite effects of specific substances synthesized within adipose tissue from various anatomical compartments, ovarian hormones and insulin on bone turnover, have not been a subject of a complex analysis in women with menstrual disorders. Therefore, the aim of this retrospective study was to verify if volume and distribution of adipose tissue may predict bone loss in this group. The study included 293 Caucasian women (mean age 26.7±4.4 years) with at least 6-month history of secondary amenorrhea. Based on T-score values for bone mineral density (BMD) in lumbar spine, the study subjects were divided into two groups, with T-scores below −0.5 and at least 0.5. Univariate logistic regression analysis showed that lower bone mineral density (as shown by T-score below −0.5) was associated with larger volumes of gynoid (odds ratio, OR=7.45), android (OR=3.03) and visceral adipose tissue (OR=1.55), as well as with higher values of body mass index (BMI, OR=1.17), fasting concentration of insulin (OR=1.08) and body weight (OR=1.06). However, none of these variables turned out to be an independent predictor of BMD deficiency on multivariate analysis. These findings imply that excessive volume of adipose tissue, irrespective of distribution thereof, is a strong determinant of reduced BMD in women with ovarian insufficiency. The lack of region-specific effects of adipose tissue volume on BMD is probably associated with the influence of ovarian insufficiency on systemic metabolism and endocrine processes, in particular with the development of insulin resistance.