Endocrine Abstracts

One of the causes of secondary osteoporosis is type 1 DM (1DM), an autoimmune disease where insulin replacement is mandatory for controlling blood sugar levels. Among the mechanisms involved in osteoporosis in 1DM is increased bone resorption, mainly osteoclasts being responsible for this process. However, osteoblasts also seem to have an active contribution by secreting products with resorptive properties, one of these being cysteine protease Cathepsin K, as mentioned by a few studies.

Aim: Our study was directed towards assessing the secretion of Cathepsin K in human primary osteoblastic cell cultures and observing how different glucose concentrations in culture media influence the levels of this enzyme.

Material and methods: Primary human osteoblastic cell cultures were obtained using bone from patients with total hip replacement interventions. After reaching subconfluence in the third passage, cells were treated with several glucose concentrations: 2.8 mmol/l (hypoglycemia), 5.6 mmol/l (normoglycemia), 11.1 mmol/l (moderate hyperglycemia) and 28 mmol/l (extreme hyperglycemia). After 24 h of incubation in these particular media, supernatants were collected and Cathepsin K was measured quantitatively (ELISA).

Results: Cathepsin K levels obtained were: 31.04±0.73SD pmol/l (moderate hyperglycemia), 31.54±2.8SD pmol/l (extreme hyperglycemia), 34.78±7.56SD pmol/l (normoglycemia) and 35.51±6.97SD pmol/l (hypoglycemia). A trend towards lower Cathepsin K levels in both hyperglycemic supernatants compared to hypoglycemic and normoglycemic conditions was observed, however, these differences were not statistically significant (hypoglycemia–moderate hyperglycemia: P=0.74; hypoglycemia–extreme hyperglycemia: P=0.8; normoglycemia–moderate hyperglycemia: P=0.83; normoglycemia–extreme hyperglycemia: P=0.88).

Conclusion: Our experiment proves the secretion of Cathepsin K by osteoblasts; it can be speculated that the lower levels in both hyperglycemic supernatants may be explained by the growth-inhibitory effect of high glucose on osteoblasts but further studies on the topic are warranted.