Key result
Amlodipine prevents fructose-induced renal fibrosis markers and sorbitol accumulation in rats.
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Besides generating renal damage, hypertension plays an important role in the progression of diabetic nephropathy. The fructose-fed rat is a well-established model both of high blood pressure and renal impairment, which is similar to diabetic nephropathy. To clarify the relationship between hypertension, glucose metabolism, and kidney remodeling, we investigated the renal level of Glut 1 and Glut 5, their relation to fibrosis and the effects of an antihypertensive drug on renal damage. Twenty-four male WK rats were divided into three groups: 8 animals received a fructose-enriched diet, 8 a control diet, and 8 animals a high-fructose diet plus amlodipine (5 mg/Kg). After six weeks of treatment, we observed a significant increase in Glut 5, fibronectin, and sorbitol in fructose-fed rats compared with control and amlodipine-treated animals; there was a positive correlation between Glut 5 and fibronectin levels (r = 0.63). Glut 1 levels were similar in all three groups, whereas collagen IV was higher in fructose-fed rats; amlodipine prevented the increase of collagen IV and sorbitol. Collagen I was statistically higher in the fructose group than in the other two groups. Therefore, prolonged fructose feeding results in renal fibrosis via polyol pathway overactivity that can be prevented by means of an antihypertensive drug.
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Bernobich et al. (2004) studied Hypertension and fructose-induced renal damage (diabetic nephropathy model) (n=24). Amlodipine vs. Fructose-enriched diet alone and control diet was evaluated on Renal levels of Glut 1, Glut 5, sorbitol, and fibrosis markers (fibronectin, collagen I, collagen IV) (r = 0.63 (correlation between Glut 5 and fibronectin)). Amlodipine (5 mg/Kg) prevented fructose-induced increases in renal Glut 5, fibronectin, sorbitol, and collagen I/IV in rats, with Glut 5 correlating with fibronectin (r=0.63).
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