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Updated: May 13, 2026
Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
The effect of insulin treatment on Rac1 expression in diabetic kidney
Mukaddes Gumustekin1, Serap Cilaker Micili, Mualla Aylin Arici
1Department of Pharmacology, School of Medicine, Dokuz Eylul University, Izmir, Turkey. gumustek@deu.edu.tr
Abstract:
This study was designed to evaluate the renoprotective effect of insulin on diabetic nephropathy through Rac1 inhibition. Twenty Wistar rats were divided into three groups: control (C), diabetic (D), and insulin-treated diabetic (D + I). Diabetes was induced by a single streptozotocin (STZ) injection (45 mg/kg i.p.) in adult male rats. Diabetic animals were treated subcutaneously with insulin (6 U/kg), or saline once a day for 8 weeks. Age-matched control rats received only saline. The kidney tissue samples were analyzed by immunohistochemical staining for Rac1 and cleaved caspase-3 expressions and using the TUNEL method for determining apoptotic cells. Diabetes increased the number of TUNEL (+) cells and cleaved caspase-3 and Rac1 expression levels in kidney. Administration of insulin for 8 weeks reduced Rac1 expression and ameliorated histopathological changes in kidney of STZ-induced diabetes model. These results may suggest that the renoprotective effect of insulin at least partly results from inhibition of Rac1 overexpression.
Insights
Insulin protects kidneys in diabetic nephropathy by inhibiting Rac1 overexpression. This study in rats demonstrates insulin
Area of Science:
- Nephrology
- Endocrinology
- Molecular Biology
Background:
- Diabetic nephropathy is a major complication of diabetes mellitus.
- Rac1 signaling pathway plays a role in the development of kidney damage.
Purpose of the Study:
- To investigate the renoprotective effect of insulin in a rat model of diabetic nephropathy.
- To explore the role of Rac1 inhibition in insulin's protective mechanism.
Main Methods:
- Diabetes was induced in Wistar rats using streptozotocin (STZ).
- Diabetic rats were treated with insulin or saline for 8 weeks.
- Kidney tissues were analyzed for Rac1, cleaved caspase-3, and apoptosis using immunohistochemistry and TUNEL assay.
Main Results:
- Diabetes significantly increased kidney cell apoptosis, cleaved caspase-3, and Rac1 expression.
- Insulin treatment reduced Rac1 expression and ameliorated kidney damage in diabetic rats.
- Insulin administration decreased the number of apoptotic cells in the kidney.
Conclusions:
- Insulin exhibits a renoprotective effect in STZ-induced diabetic nephropathy.
- Inhibition of Rac1 overexpression may be a key mechanism underlying insulin's renoprotective action.
- These findings suggest a therapeutic target for managing diabetic kidney disease.
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