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Changes in bone biological markers after treatment of Iranian diabetic patients with pioglitazone: No relation to polymorphism of PPAR-γ (Pro12Ala)

BACKGROUND: Thiazolidinediones (TZDs) improves insulin sensitivity by activating the peroxisome proliferator-activated receptor γ (PPAR-g). We aimed to study any association between variation in bone biochemical markers and single nucleotide polymorphism (SNP) in PPAR-γ (Pro12Ala) and investigate if...

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Detalles Bibliográficos
Autores principales: Namvaran, Fatemeh, Rahimi-Moghaddam, Parvaneh, Azarpira, Negar, Dabbaghmanesh, Mohammad Hossien, Bakhshayeshkaram, Marzieh, Namvaran, Mohamad Mahdi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3793371/
https://www.ncbi.nlm.nih.gov/pubmed/24124423
Descripción
Sumario:BACKGROUND: Thiazolidinediones (TZDs) improves insulin sensitivity by activating the peroxisome proliferator-activated receptor γ (PPAR-g). We aimed to study any association between variation in bone biochemical markers and single nucleotide polymorphism (SNP) in PPAR-γ (Pro12Ala) and investigate if these genetic variants affect bone turnover markers in Iranian diabetic population before and after treatment with pioglitazone. MATERIALS AND METHODS: A total of 101 patients (type 2 diabetic (T2D) were treated for 12 weeks with pioglitazone (15 mg/day). Bone Biological markers, osteocalcin, and C-terminal telopeptide of type 1 collagen (CTx) were measured before and after pioglitazone therapy. We genotyped 128 nondiabetic controls and 101 T2D patients as well. Pro12Ala polymorphism in PPAR-γ was done by real-time polymerase chain reaction (RT-PCR) using TaqMan assay. RESULTS: There were statistically significant differences in allele frequencies of Pro12Ala while comparing the controls with T2D subjects. Ala frequency was 7 vs 3%, P = 0.036 and genotypic frequency of Pro/Ala was 5.94 vs 14.06%, P = 0.04. After treatment, the homeostasis model of assessment of insulin resistance (HOMA-IR) as a maker of insulin resistance was significantly decreased (P < 0.001). In respect of bone turnover markers, CTx values decreased and osteocalcin significantly increased. (P < 0.001). CONCLUSION: Our findings did not reveal a significant association between this polymorphism and bone turnover markers after pioglitazone treatment. The reduced insulin resistance might be the reason that CTx values decreased and osteocalcin increased significantly after short-term pioglitazone treatment. These findings suggest the need for further studies on the possible role of insulin in regulation of bone metabolism.