Journal of Clinical and Diagnostic Research, ISSN - 0973 - 709X

Users Online : 18612

Experimental Research
Table of Contents - Year : 2016 | Month : April | Volume : 10 | Issue : 4 | Page : CF06 - CF11

Implication of Renal Aquaporin-3 in Fructose-Induced Metabolic Syndrome and Melatonin Protection CF06-CF11

Suzy Fayez Ewida, Dalia Rifaat Al-Sharaky

Dr. Suzy Fayez Ewida,
Faculty of Medicine, Department of Physiology, Faulty of Medicine, Gamal Abd El-Naser ST., Shebin El-Kom, Menofia Egypt.

Introduction: Metabolic Syndrome (MetS) can be induced by ingestion of large amounts of fructose as a consequence of oxidative stress and dyslipidemia.

Aim: We investigated the possible protective effects of melatonin administration on MetS induced in fructose-fed rats with special focus on the role of renal aquaporin-3 (AQP-3).

Materials and Methods: Thirty rats were randomly divided into three groups; control, fructose, and fructose plus melatonin. MetS was induced by fructose rich diet and melatonin was injected at a dose of 5 mg/kg dissolved in 1% ethanol in normal saline. After the end of the 6-week experimental period, body weight and fat accretion were assessed. Invasive blood pressure and vascular reactivity were evaluated. Serum lipid profile, glucose, insulin levels, insulin resistance, malondialdehyde (MDA) and uric acid were measured, also underwent renal AQP-3 immunohistochemistry.

Results: Fructose consumption significantly increased fat accretion, systolic blood pressure, serum lipids, insulin levels and insulin resistance, confirming successful establishment of the MetS model. Also serum MDA, uric acid and renal AQP-3 expression increased compared to the control group. Melatonin supplementation significantly decreased the previously measured parameters compared to fructose group.

Conclusion: Increased AQP-3 expression may be implicated in fructose induced MetS. Melatonin protective effect against metabolic consensus and vascular affection may be linked to its antioxidant and lipid lowering effect with reduced renal AQP-3 expression.