IRS1/PDX1 mRNA expression profiles in Co-Occurring Diabetes and Thyroid Dysfunction: A Diagnostic and Predictive Approach
Diabetes Mellitus and thyroid dysfunction are among the most common endocrine conditions, frequently coexisting due to shared mechanisms such as insulin resistance and beta-cell impairment. Conventional biomarkers such as thyroid stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4) often fall short in diagnosing co-occurring disorders due to overlapping symptoms. This study aims to investigate the expression of insulin Receptor Substrate 1 (IRS1) and pancreatic and duodenal Homeobox 1 (PDX1) mRNA for type 2 diabetes and hyperthyroidism. IRS1 and prognostic potential of PDX1 mRNA expression were analyzed in serum samples from 46 patients (15 with type 2 diabetes and 16 with hyperthyroidism) and 15 normal control using qRT-PCR and expression was normalized to GAPDH. Statistical analysis was performed using SPSS software and data was expressed as median ± IQR and correlation between age and relative expression was graphed. Results revealed a significant up-regulation of IRS1 and down-regulation of PDX1 in diabetic samples, likely due to treatment response, while both were downregulated in hyperthyroid samples, likely due to TSH’s inhibitory effect on IRS1 and thyroid hormone impact of beta-cell growth. Therefore, this study underlines the potential of IRS1 and PDX1 as biomarkers for predicting disorder outcome. Larger-scale research is recommended to validate these findings and confirm their diagnostic and prognostic utility.
Authors
- MOHAMED ZID
- Gehan Safwat (ORCID: https://orcid.org/0000-0002-1671-5778)
- Gehad Tarek
- Marwan R. Karamelah
- Mohamed A. Rawash
Institutions
- October University of Modern Sciences and Arts (EG)
Publication Details
- Journal
- International Journal for Biotech Research and Innovations
- Published
- 2025-12-31
- DOI
- https://doi.org/10.21608/ijbraj.2025.418988.1010
- Primary Topic
- Thyroid Disorders and Treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.00