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Protective potential of fish oil supplementation against insulin resistance and pancreatic islet damage in STZ-induced Wistar rats


Nurina Titisari
Ahmad Fauzi
Intan Shameha Abdul Razak
Nurdiana Samsulrizal
Hafandi Ahmad

Abstract

Background: Fish oil, which is regarded as the primary source of omega-3 fatty acids, has been long studied for its  potential as an antidiabetic therapy. However, its protective ability against insulin resistance and pancreatic islet alteration remains unclear and controversial.


Aim: To investigate the beneficial effects of fish oil consumption on the progression of insulin resistance and pancreatic islet dysfunction in a rat model of diabetes.


Methods: Diabetic rats model (n = 30) were divided into five groups and received; 1) NS injection + NS oral (normal control); 2) NS injection + 3 g/kg fish oil (fish oil control); 3) streptozotocin (STZ) injection + NS oral [diabetes control (DC)]; 4) STZ injection + 1 g/kg fish oil (DFO1); and 5) STZ injection + 3 g/kg fish oil (DFO3). Fasting blood insulin was  analyzed by commercial rat insulin enzyme-linked immunosorbent assay; meanwhile, the determination of insulin sensitivity was calculated by homeostatic model assessment of insulin resistance (HOMA-IR) and homeostatic model assessment of beta-cell function. A histological study was conducted on pancreas tissue using H and E staining.


Results:  Fish oil supplementation reduced hyperglycemia and ameliorated HOMA-IR in STZ-induced animal models indicating that fish oil supplementation improved insulin sensitivity. Furthermore, animals treated with fish oil at a dose  of 3 g/kg (DFO3) showed an enhancement in pancreatic islets, which was displayed by less abnormal structures than DC  animals. This could imply that the administration of fish oil, especially rich in bioactive omega-3 fatty acids effectively  inhibits insulin resistance and restore islet of Langerhans alteration in rats injected with STZ.


Conclusion: Thus, the  current study suggested that fish oil supplementation could support the treatment of diabetes but should not be  considered as an alternative therapy 


Journal Identifiers


eISSN: 2218-6050
print ISSN: 2226-4485