Abstract

Abstract Objectives Adenomyosis is a benign uterine disease that occurs with the invasion of the endometrial gland and stoma into the myometrium. The etiology and molecular pathology of adenomyosis are not yet fully understood. Tissue samples of patients diagnosed with adenomyosis and healthy endometrial tissues were investigated for the lipogenesis and cholesterol synthesis pathways. It was aimed to determine the difference between adenomyosis and healthy endometrial tissues in terms of lipid metabolism and to investigate the mechanism of adenomyosis in this context. Methods Formalin-fixed paraffin-embedded archival tissues were used in the current retrospective study. A total of 76 patient samples and 3 groups were used. Group 1: adenomyotic tissue (n=28), Group 2: eutopic endometrial tissue (n=30), and Control Group (n=18). In these groups, Sterol regulatory element binding protein 1 (SREBP1) molecule, fatty acid synthase (FASN), acetyl-CoA carboxylase (ACACA), ATP-citrate lyase (ACLY), HMG-CoA reductase (HMGCR), and HMG-CoA synthase (HMGCS) markers were evaluated by using RT-PCR method. Results Statistically significant differences (p<0.05) were found between the groups regarding expression levels of HMGCR, HMGCS, ACLY, ACACA, and SREBP1. HMGCR, HMGCS, ACLY, and SREBP1 gene expression levels between Group 1 and Group 2 and HMGCS, ACACA, ACLY, and SREBP1 gene expression levels between Group 1 and Control Group were determined as statistically different. A significant difference was detected only in HMGCR gene expression levels between Group 2 and the Control Group. Conclusions These results show that genes involved in lipid metabolism may be associated with the molecular pathogenesis of adenomyosis.

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