High fructose diet feeding accelerates diabetic nephropathy in Spontaneously Diabetic Torii (SDT) rats

• Published in: Journal of toxicological sciences Vol. 43; no. 1; pp. 45 - 58
• Main Authors: Toyoda, Kaoru, Suzuki, Yusuke, Muta, Kyotaka, Masuyama, Taku, Kakimoto, Kochi, Kobayashi, Akio, Shoda, Toshiyuki, Sugai, Shoichiro
• Format: Journal Article
• Language: English
• Published: Japan The Japanese Society of Toxicology 01-01-2018; Japan Science and Technology Agency
• Subjects: Animals; Carbohydrates; Complications; Diabetes; Diabetes mellitus; Diabetic animal model; Diabetic Nephropathies - etiology; Diabetic Nephropathies - metabolism; Diabetic Nephropathies - pathology; Diet; Dietary Carbohydrates - adverse effects; Disease Progression; End-stage renal disease; Excretion; Feeding; Fructose; Fructose - adverse effects; Glucose; Glucose - metabolism; Hyperglycemia; Kidney diseases; Kidney Tubules - metabolism; Kidney Tubules - pathology; Kidneys; Lesions; Male; Nephropathy; Nephrotoxicity; Rats, Sprague-Dawley; Sweet taste; Tubules; Uric acid; Uric Acid - metabolism; Diabetic animal model; Hyperglycemia; Uric acid; Nephrotoxicity; Fructose
• ISSN: 0388-1350; 1880-3989
• DOI: 10.2131/jts.43.45

Diabetic nephropathy (DN) is one of the complications of diabetes and is now the most common cause of end-stage renal disease. Fructose is a simple carbohydrate that is present in fruits and honey and is used as a sweetener because of its sweet taste. Fructose has been reported to have the potential to progress diabetes and DN in humans even though fructose itself does not increase postprandial plasma glucose levels. In this study, we investigated the effects of high fructose intake on the kidney of the Spontaneously Diabetic Torii (SDT) rats which have renal lesions similar to those in DN patients and compared these with the effects in normal SD rats. This study revealed that a 4-week feeding of the high fructose diet increased urinary excretion of kidney injury makers for tubular injury and accelerated mainly renal tubular and interstitial lesions in the SDT rats but not in normal rats. The progression of the nephropathy in the SDT rats was considered to be related to increased internal uric acid and blood glucose levels due to the high fructose intake. In conclusion, high fructose intake exaggerated the renal lesions in the SDT rats probably due to effects on the tubules and interstitium through metabolic implications for uric acid and glucose.