Allopurinol Ameliorates High Fructose Diet-Induced Metabolic Syndrome via up-regulation of Adiponectin Receptors and Heme oxygenase-1 Expressions in Rats

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). Meanwhil...

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Published in:Biomedical & pharmacology journal 2017, Vol.10 (4), p.1685-1694
Main Authors: Mostafa-Hedeab, G., Shahataa, Mary, Fouaad Ali, E., Sabry, Dina, EL-Nahass, EL-Shaymaa, Hassan, Manal, Mahmoud, Fatma
Format: Article
Language:English
Subjects:
Adiponectin
Allopurinol
Blood pressure
Body weight
Cholesterol
Creatinine
Diet
Fructose
Heart
Heme
Heme oxygenase (decyclizing)
High density lipoprotein
Insulin
Insulin resistance
Kidneys
Kinases
Liver
Low density lipoprotein
Metabolic syndrome
Nitric oxide
Nitric-oxide synthase
Oxygenase
Pancreas
Rodents
Triglycerides
Up-regulation
Urea
Uric acid
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Summary: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.
ISSN:0974-6242
2456-2610
DOI:10.13005/bpj/1280