Abstract

BackgroundAbnormal metabolic features have been previously described in adolescent idiopathic scoliosis (AIS) patients. As an important regulator involved in energy metabolism, DPP-4 activity was reported to be remarkably decreased in osteoblasts of AIS patients. To date, there was still a lack of knowledge concerning the role of DPP-4 in the myogenesis of AIS.MethodsCirculation DPP-4 level was assessed in the serum of 80 AIS girls and 50 healthy controls by ELISA. Myoblasts were purified from muscle specimens of AIS patients and LDH controls, and then treated with metabolic effectors including glucose and insulin. CCK-8 assay was used to assess the cell viability and myotube fusion index was calculated to evaluate myogenesis ability. Gene expressions of downstream signals of DPP-4 were evaluated by RT-qPCR and Western blot respectively.ResultsAIS girls had remarkably down-expressed DPP-4 in both serum level (0.76 fold) and tissue (0.68 fold) level. Treatment with metabolic effectors led to significantly increased DPP-4 expression in the control cells, while there was no increase of DPP-4 in AIS cells. CCK-8 assay showed that the proliferation rate of control cells was significantly increased after being treated. Remarkably higher fusion index was also observed in the treated control cells. By contrast, the fusion index and cell proliferation rate were comparable between the treated and the untreated AIS cells.ConclusionsOur study suggested a potential role of DPP-4 in abnormal metabolic condition of AIS patients. Compared with control cells, AIS myoblasts presented obviously impaired sensitivity to the treatment of glucose and insulin. Aberrant DPP-4 expression could lead to impaired insulin sensitivity in myoblasts and further influence the cell viability during myogenesis. The molecular mechanism connecting DPP-4 and insulin-related signaling in AIS is worthy of further investigation.

Highlights

  • Adolescent idiopathic scoliosis (AIS) is a 3-dimensional deformity which occurs during the pubertal growth [1]

  • Since there was no significant difference of nutrition intake between adolescent idiopathic scoliosis (AIS) girls and controls, it was speculated that the abnormal energy homeostasis including appetite regulation, energy expenditure and insulin sensitivity might be impaired in AIS girls [7]

  • To further determine the role of Dipeptidyl peptidase-4 (DPP-4) in the etiology of AIS, we investigated the relationship between DPP-4 expression and insulin sensitivity in the patients

Read more

Summary

Introduction

Adolescent idiopathic scoliosis (AIS) is a 3-dimensional deformity which occurs during the pubertal growth [1]. There is no consensus on the etiology of AIS. Many factors were proposed to be involved in the development of AIS, including genetic variation, metabolism dysfunction, and abnormal neuromuscular function. It has been well documented that AIS patients tended to have different anthropometric parameters compared with age-matched controls, such as taller stature with lower body mass index (BMI) and lower bone mineral density (BMD), while the cause of these differences remains obscure [5, 6]. Abnormal metabolic features have been previously described in adolescent idiopathic scoliosis (AIS) patients. As an important regulator involved in energy metabolism, DPP-4 activity was reported to be remarkably decreased in osteoblasts of AIS patients. There was still a lack of knowledge concerning the role of DPP-4 in the myogenesis of AIS

Objectives
Methods
Results
Discussion
Conclusion

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.