Osteoporosis is characterised by low bone mass accompanied by bone microarchitectural changes that increase fracture susceptibility
[18, 19]. The precise balance between bone formation and resorption is critical for the maintenance of bone mass density (BMD) and systemic mineral homoeostasis
[1, 2]. Osteoporosis is mainly caused by bone remodelling failure, which is regulated by many factors
As a novel hormone, preptin increases the bone area and mineralising surface in adult mice by stimulating osteoblast proliferation and reducing osteoblast apoptosis
. Therefore, preptin is involved in bone anabolism and contributes to bone mass preservation
. However, the function and mechanism of preptin in human osteoporosis remain unclear.
The current study found that preptin levels are correlated with BMD. The preptin level was the lowest in osteoporosis patients than in osteopaenia and normal bone mass subjects. The present study is the first to investigate preptin levels in subjects with different BMDs.
Bone formation markers were reduced in elderly male patients with osteoporosis and positively correlated with preptin levels. However, the bone resorption marker was not correlated with preptin levels. Lower circulating preptin was correlated with reduced osteogenesis, which is consistent with the characteristics of Type II (senile) osteoporosis (reduced bone formation and low bone turnover). Hence, preptin may be involved in Type II osteoporosis by affecting bone formation. Understanding these mechanisms will facilitate further research on bone remodelling and osteoporosis. Future investigations on the endogenous regulation of osteoblastogenesis will increase the current knowledge for developing potential drug targets for treating osteoporosis.
The present study has limitations that need to be considered. The cross-sectional design limits our ability to infer a causal relationship between reduced serum preptin level and low BMD. Our analyses are based on a single blood preptin measurement, which does not reflect the relationship between preptin levels and BMD over time. Measuring serial changes in blood preptin levels in preosteoporotic and osteoporotic subjects will further clarify the role of preptin in the pathogenesis of osteoporosis. Furthermore, the effects of oestrogen were not included. Hence, postmenopausal osteoporotic patients were excluded from the present study. Detecting the blood preptin levels in females and comparing them with male osteoporotic patients will help elucidate the differences in pathogenesis of osteoporosis between males and females.
Diabetes mellitus (DM) alters bone remodelling, and osteopaenia and osteoporosis are among its complications. High extracellular glucose concentrations act as an endogenous factor that increases biomineralisation degree but reduces mineral quality
. Preptin functions in the pathogenesis of Type II DM
. Thus, subjects with DM or hyperglycaemia were excluded.