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ORIGINAL ARTICLE
Year : 2022  |  Volume : 25  |  Issue : 9  |  Page : 1452-1456

Alteration of inflammation marker levels with alfa keto analogs in diabetic rats


1 Haydarpaşa Numune Training and Research Hospital Division of Nephrology, University of Health Sciences Turkey, Uskudar, Istanbul, Turkey
2 Biochemistry Department, Nephrology Division, Bezmi-alem University, Fatih, Istanbul, Turkey
3 Internal Medicine Department, Nephrology Division, Bezmi-alem University, Fatih, Istanbul, Turkey

Correspondence Address:
Dr. Y D Bildaci
Department of Nephrology, Haydarpaşa Numune Training and Research Hospital, Tıbbiye Caddesi, No: 23 Selimiye Üsküdar 34668, Istanbul
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/njcp.njcp_1868_21

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Background: Diabetes mellitus is the most well-known and common cause of end-stage renal disease. Excessive inflammatory processes were hypothesized to be one of the reasons for progression to end-stage disease. Even though progression to end stage disease tried to be prevented with some dietary measures such as lowering nitrogen in diet, none of the methods tried were successful enough. Aims: In our study, we aimed to determine the effects of alfa keto analog use in altering levels of inflammatory markers when added to dietary program in a diabetic rat model. Patients and Methods: The study was performed on 22 male Sprague Dawley rats with streptozocine induced diabetic nephropathy. Both groups were fed with low protein diet except for study group with added alfa keto analogs. Biochemical values and inflammatory markers were studied with ELISA assay. Results: Significant difference in serum albumin was found between study group and control group following administration of alfa keto analogs (p <.001). Also mentioned dietary modification made a significant difference in suppression of inflammatory reactions for interleukin (IL)-1, IL-6, IL-10, IL-18 and tumor necrosis factor-α. Conclusion: Adding keto amino acids to diets that are already low on protein, can slow progression to end-stage renal disease by reducing inflammation and protein loss in an animal model.


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