Peroxisome proliferator-activated receptor-γ (PPARγ) expression in parathyroid adenomas in primary hyperparathyroidism


Akçay G., Akçay M. N., Arslan R.

11th European Congress of Endocrinology, İstanbul, Türkiye, 25 - 29 Nisan 2009, ss.80-81

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: İstanbul
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.80-81
  • Atatürk Üniversitesi Adresli: Evet

Özet

Peroxisome proliferator-activated receptor-γ (PPARγ) expression in parathyroid adenomas in primary hyperparathyroidism

Güngör Akçay1, Müfide Nuran Akçay2 & Remzi Arslan3

Background: Primary hyperparathyroidism (pHPT) is an important endocrinologic cause of metabolic bone disorder in human. The regulatory mechanism of the cells of parathyroid gland proliferation is not exactly known. Peroxisome proliferator-activated receptor-γ (PPARγ) is a member of nuclear receptor superfamily. PPARγ is expressed in adipose tissue at a high level. It plays a role on number of disorders such as adipose tissue differantiation, insulin sensivity, lipid metabolism, osteoporosis, arteriosclerosis, cancer, inflammation, antiangiogenesis, and cell differentiation.

Methods: This study was carried out to evaluate PPARγ expression with immunohistochemical staining in parathyroid adenomas in pHPT. Twenty surgically removed parathyroid adenomas diagnosed with the biochemical and imaging methods preoperatively in the patients with pHPT and 10 normal parathyroid tissue samples which were obtained from the archives of the Pathology Department were included in the study. The samples were incubated in mouse monoclonal antibody against PPAR gamma.

Results: Two (10%) of 20 adenomas with pHPT had +++, 14 (70%) had +, 4 (20%) had − (negative) staining. However, 7 (70%) of 10 normal parathyroid gland samples had +++, 1 (10%) had ++, and 2 (20%) had − (negative) staining. There was a significant difference between parathyroid adenomas and normal parathyroid tissues (P<0.001).

Conclusions: PPARγ expression was insufficient in pHPT. We concluded that PPARγ expression deficiency in parathyroid adenomas may explain the pathogenesis of the development of adenomas, insulin resistance and glucose intolerance in the patients with pHPT.