Abstract
Metabolic Syndrome (MetS) can be induced by ingestion of large amounts of fructose as a consequence of oxidative stress and dyslipidemia. 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). 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. 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. 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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.