Article Publish Status: FREE
Abstract Title:

A novel osteoporosis model with ascorbic acid deficiency in Akr1A1 gene knockout mice.

Abstract Source:

Oncotarget. 2017 Jan 31 ;8(5):7357-7369. PMID: 28060768

Abstract Author(s):

Cheng-Wei Lai, Hsiao-Ling Chen, Min-Yu Tu, Wei-Yu Lin, Theresa Röhrig, Shang-Hsun Yang, Ying-Wei Lan, Kowit-Yu Chong, Chuan-Mu Chen

Article Affiliation:

Cheng-Wei Lai


The AKR1A1 protein is a member of the aldo-keto reductase superfamily that is responsible for the conversion of D-glucuronate to L-gulonate in the ascorbic acid (vitamin C) synthesis pathway. In a pCAG-eGFP transgenic mouse line that was produced by pronuclear microinjection, the integration of the transgene resulted in a 30-kb genomic DNA deletion, including the Akr1A1 gene, and thus caused the knockout (KO) of the Akr1A1 gene and targeting of the eGFP gene. The Akr1A1 KO mice (Akr1A1eGFP/eGFP) exhibited insufficient serum ascorbic acid levels, abnormal bone development and osteoporosis. Using micro-CT analysis, the results showed that the microarchitecture of the 12-week-old Akr1A1eGFP/eGFP mouse femur was shorter in length and exhibited less cortical bone thickness, enlargement of the bone marrow cavity and a complete loss of the trabecular bone in the distal femur. The femoral head and neck of the proximal femur also showed a severe loss of bone mass. Based on the decreased levels of serum osteocalcin and osteoblast activity in the Akr1A1eGFP/eGFP mice, the osteoporosis might be caused by impaired bone formation. In addition, administration of ascorbic acid to the Akr1A1eGFP/eGFP mice significantly prevented the condition of osteoporotic femurs and increased bone formation. Therefore, through ascorbic acid administration, the Akr1A1 KO mice exhibited controllable osteoporosis and may serve as a novel model for osteoporotic research.

Study Type : Transgenic Animal Study
Additional Links
Pharmacological Actions : Osteoprotective : CK(20) : AC(6)

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