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

Abstract

Introduction: Metabolic Syndrome (MetS) can be induced by ingestion of large amounts of fructose as a con sequence of oxidative stress and dyslipidemia. aim: We investi gated 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.

Melatonin, mitochondria, and the metabolic syndrome

“…In rats fed from weaning with a high-fat diet melatonin decreased body weight gain, feed efficiency and plasma glucose, leptin and triglyceride levels [53] In middle-aged rats receiving a high caloric liquid diet, melatonin reduced weight gain and plasma insulin and leptin levels [54] In high-fat diet-fed mice, melatonin improved insulin sensitivity and glucose tolerance [55] In ovariectomized rats, melatonin was effective to reduce obesity [56][57][58] In olanzapine-treated rats, melatonin was effective to reduce obesity [59] In goldfish body weight gain and specific growth rate were reduced by melatonin treatment [60] Melatonin and its analog piromelatonin inhibited weight gain and improves insulin sensitivity in high-fat fed rats [52] In high-fat fed rats, melatonin attenuated body weight increase, the increase in plasma glucose, insulin, adiponectin, leptin, triglycerides and cholesterol levels, and counteracted disrupted 24 h patterns [61] Melatonin improves inflammation processes in liver and pancreas of senescence-accelerated prone male mice (SAMP8) [62,63] Melatonin reduced body weight gain, visceral adiposity, blood triglyceride and insulin levels and TBARS under a high calorie diet in rats. [64] In young male Zucker diabetic fatty rats melatonin treatment reduced mean weight gain without affecting food intake, decreased in a nonsignificant way blood pressure, and improved dyslipidemia [65] Melatonin improves MS induced by high fructose intake in rats without affecting food intake [66][67][68][69][70] Melatonin and its analog piromelatonin reduced blood pressure in spontaneously hypertensive rats [71] Melatonin prevents the development of the MS in male rats exposed to different light/dark regimens [72] Melatonin attenuates high fat diet-induced fatty liver disease in rats [73] Melatonin, given at the time of reperfusion, prevents ventricular arrhythmias in isolated hearts from fructose-fed rats and spontaneously hypertensive rats [74] Melatonin ameliorates low-grade inflammation and oxidative stress in young Zucker diabetic fatty rats [75] Melatonin improves hyperglycemia, hypertriglyceridemia, polyphagia, and polydipsia in streptozotocin diabetic rats [76,…”

Meta‐analysis and machine learning reveal the antiobesity effects of melatonin on obese rodents

“…To ensure the quality of the database, only articles from peer‐reviewed journals were further evaluated. After a rigorous assessment of the abstracts and full texts, a database was established for meta‐analysis and machine learning using 31 articles 7–11,20–45 . The recruited dataset comprised 286 effect sizes from the 31 studies ( k = 49 for body weight, k = 22 for liver weight, k = 17 for eWAT, k = 22 for GLU, k = 45 for TG, k = 36 for LDL, k = 39 for HDL, k = 36 for TC, and k = 20 for clock‐related genes).…”

Modulation of Aquaporins by Dietary Patterns and Plant Bioactive Compounds

“…A recent study [61] investigated the possible protective effects of melatonin administration on metabolic syndrome induced in fructose-fed rats with special attention on the possible role of renal AQP3, an aquaglyceroporin contributing to the reabsorption of glycerol in renal tubules among other functions [62]. Fructose consumption led to the establishment of the metabolic syndrome model, condition that was accompanied with elevation of serum malondialdehyde, uric acid and renal AQP3 expression compared to the control rats receiving the standard diet.…”