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Acarbose Protects Glucolipotoxicity-Induced Diabetic Nephropathy by Inhibiting Ras Expression in High-Fat Diet-Fed
Tung-Wei Hung1,2, Meng-Hsun Yu3,4, Tsung-Yuan Yang1,5
1School of Medicine, Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
Abstract:
Diabetic nephropathy (DN) exacerbates renal tissue damage and is a major cause of end-stage renal disease. Reactive oxygen species play a vital role in hyperglycemia-induced renal injury. This study examined whether the oral hypoglycemic drug acarbose (Ab) could attenuate the progression of DN in type 2 diabetes mellitus mice. In this study, 50 mg/kg body weight of Ab was administered to high-fat diet (HFD)-fed db/db mice. Their body weight was recorded every week, and the serum glucose concentration was monitored every 2 weeks. Following their euthanasia, the kidneys of mice were analyzed through hematoxylin and eosin, periodic acid Schiff, Masson's trichrome, and immunohistochemistry (IHC) staining. The results revealed that Ab stabilized the plasma glucose and indirectly improved the insulin sensitivity and renal functional biomarkers in diabetic mice. In addition, diabetes-induced glomerular hypertrophy, the saccharide accumulation, and formation of collagen fiber were reduced in diabetic mice receiving Ab. Although the dosages of Ab cannot decrease the blood sugar in db/db mice, our results indicate that Ab alleviates glucolipotoxicity-induced DN by inhibiting kidney fibrosis-related proteins through the Ras/ERK pathway.
Insights
Acarbose (Ab) treatment in diabetic mice reduced kidney damage and fibrosis, indicating potential for treating diabetic nephropathy (DN) by inhibiting fibrosis pathways, even without lowering blood sugar.
Area of Science:
- Nephrology
- Endocrinology
- Pharmacology
Background:
- Diabetic nephropathy (DN) is a severe complication of diabetes, leading to kidney damage and end-stage renal disease.
- Hyperglycemia-induced reactive oxygen species contribute significantly to renal injury in diabetes.
Purpose of the Study:
- To investigate the efficacy of acarbose (Ab) in attenuating diabetic nephropathy progression in a mouse model of type 2 diabetes.
- To explore the underlying mechanisms by which acarbose may protect against kidney damage.
Main Methods:
- Administration of acarbose (50 mg/kg) to high-fat diet-fed db/db mice.
- Weekly body weight monitoring and bi-weekly serum glucose level measurements.
- Kidney tissue analysis using H&E, PAS, Masson's trichrome staining, and immunohistochemistry (IHC).
Main Results:
- Acarbose stabilized plasma glucose and improved insulin sensitivity and renal biomarkers in diabetic mice.
- Acarbose treatment reduced diabetes-induced glomerular hypertrophy, saccharide accumulation, and collagen fiber formation.
- Acarbose inhibited kidney fibrosis-related proteins via the Ras/ERK pathway, despite not significantly lowering blood glucose in db/db mice.
Conclusions:
- Acarbose demonstrates a protective effect against diabetic nephropathy in mice.
- The renoprotective effects of acarbose are mediated by the inhibition of kidney fibrosis through the Ras/ERK pathway.
- Acarbose may be a therapeutic option for managing diabetic nephropathy, particularly by targeting fibrotic processes.
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