Allopurinol Ameliorates High Fructose Diet-Induced Metabolic Syndrome via up-regulation of Adiponectin Receptors and Heme oxygenase-1 Expressions in Rats
G. Mostafa-Hedeab1,2, Mary Shahataa1, E. Fouaad Ali3, Dina Sabry4, EL-Shaymaa EL-Nahass5, Manal Hassan6 and Fatma Mahmoud3

1Pharmacology Department faculty of medicine, Beni Suef University, Egypt.

2Pharmacology Department faculty of medicine, Al jouf University, Saudi Arabia.

3Pharmacology Department faculty of medicine, Cairo University, Egypt.

4Biochemistry and molecular biology Department faculty of medicine, Cairo University, Egypt.

5Pathology Department faculty of veterinary medicine, Beni Suef University, Egypt.

6Biochemistry and molecular biology Department faculty of medicine, Beni Suef University, Egypt.

Corresponding Author E-mail: gomaa_hedeab@yahoo.com

Abstract: Objective: to explore allopurinol action on the metabolic syndrome (MS) components induced by high fructose diet (HFD).  Material & methods: Twenty-one rats were classified randomly into 2 groups; group A (7 rats; normal control) and group B (14 rats; received a high fructose diet (HFD). Meanwhile, group B is further classified into 2 subgroups: B1 received no treatment and B2 in which rats received allopurinol (4mg/kg/d for 4 weeks). Results: Allopurinol significantly decreased body weight (BW), normalized kidneys and heart weight, blood pressure (BP) and insulin level with normalized both of fasting glucose level and insulin resistance (IR). Furthermore, triglycerides (TGs) and low-density lipoprotein cholesterol (LDL-c) were significantly decreased with normalized high-density lipoprotein cholesterol (HDL-c), total cholesterol, creatinine, blood urea nitrogen (BUN), and serum uric acid (SUA) levels. Surprisingly, allopurinol significantly up regulate adiponectin receptor one and two (adipo R1/R2) and heme oxygenase-1 (HO-1) in heart, liver and kidneys pancreas associated with up regulation of endothelial nitric oxide synthase (eNOS) expression in liver, kidneys, heart only associating with amelioration of the fibrotic changes in different tissue studied. Moreover, it normalized IR, pancreatic AdipoR2, and HO-1 expression. Conclusion: allopurinol could be considered an ideal agent for an amelioration of MS components possibly through up regulation of adipo R1/R2, HO-1 and eNOS in different tissues; however more experimental and clinical studies are needed to weight the expected allopurinol benefit against its long term use related side effects.

Keywords: Allopurinol; Metabolic Syndrome; Adiponectin R1/R2; Heme Oxygenase-1

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