Insulin and metformin may prevent renal injury in young type 2 diabetic Goto–Kakizaki rats
| Autor: | T. Louro, Raquel Seiça, Elsa Nunes, Paulo Matafome, Fernanda Xavier da Cunha |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
Blood Glucose
Male medicine.medical_specialty medicine.medical_treatment Type 2 diabetes Diabetes Mellitus Experimental Nephropathy Diabetic nephropathy Insulin resistance Diabetes mellitus Internal medicine medicine Animals Hypoglycemic Agents Insulin Diabetic Nephropathies Pharmacology Kidney business.industry Body Weight medicine.disease Metformin Rats Oxidative Stress medicine.anatomical_structure Endocrinology Diabetes Mellitus Type 2 Gliclazide Diet Atherogenic Insulin Resistance business medicine.drug |
| Zdroj: | European Journal of Pharmacology. 653:89-94 |
| ISSN: | 0014-2999 |
| DOI: | 10.1016/j.ejphar.2010.11.029 |
| Popis: | Type 2 diabetes is increasing at epidemic proportions throughout the world, and diabetic nephropathy is the principal cause of end stage renal failure. Approximately 40% of patients with type 2 diabetes may progress to nephropathy and a good metabolic control can prevent the development of diabetic renal injury. The aim of our study was to evaluate, in young type 2 diabetic Goto-Kakizaki (GK) rats fed with atherogenic diet, the effects of the anti-diabetic compounds insulin, metformin and gliclazide on renal damage. GK rats fed with atherogenic diet showed increased body weight and fasting blood glucose, total cholesterol, triglycerides, C-reactive protein and protein carbonyl levels and lower HDL-cholesterol concentration; renal markers of inflammation and fibrosis were also elevated. All the anti-diabetic agents ameliorated fasting glycaemia and insulin resistance but only insulin and metformin were able to improve glycoxidation, fibrosis and inflammation kidney parameters. Our data suggest that insulin and metformin treatments, improving glicoxidative, inflammatory and fibrotic renal damage markers, play a key role in the prevention of diabetic nephropathy. |
| Databáze: | OpenAIRE |
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