The therapeutic effects of fructose on rat model of non-alcoholic fatty liver disease

  • سال انتشار: 1398
  • محل انتشار: پنجمین کنگره کشوری کمیته تحقیقات دانشجویی دانشگاه علوم پزشکی رفسنجان
  • کد COI اختصاصی: SRCCG05_027
  • زبان مقاله: انگلیسی
  • تعداد مشاهده: 593
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نویسندگان

Babak Hassankhan

Department of Biology, Faculty of Basic Sciences, Science and Research Branch, Islamic Azad University, Tehran, Iran.

Parichehreh Yaghmaei

Department of Biology, Faculty of Basic Sciences, Science and Research Branch, Islamic Azad University, Tehran, Iran.

Kazem Parivar

Department of Biology, Faculty of Basic Sciences, Science and Research Branch, Islamic Azad University, Tehran, Iran.

Azadeh Ebrahim-Habibi

Endocrinology and Metabolism Research Center, Tehran University of Medical Sciences,Tehran, Iran.

چکیده

Background and Aim: Excessive dietary fructose consumption may be a risk factor for the development of Non-alcoholic fatty liver disease NAFLD . High fructose diet can promote lipogenesis, oxidative stress and insulin resistance. Although fructose produces deleterious metabolic effects, fructose-1-phosphate as a metabolite of it, increases activity of glucokinase as an enzyme that plays a key role in the control of glucose homeostasis. In this study, a low-fructose diet was used to evaluate its effect on insulin resistance, hepatic activity of superoxide dismutase SOD , hepatic malondialdehyde MDA and some parameters of NAFLD due to high fat diet in the Sprague-Dawley rats.Materials and Methods: Male rats were divided into normal control group, high fat diet group and fructose group n=8 . The high fat control group was orally treated with the high fat emulsion diet HFD and fructose group orally treated with the HFD plus fructose 1g/kg once per day via gavage for six weeks. Results: After six weeks, in fructose group receiving fructose at a dose of 1 g/kg , serum glucose, insulin, insulin resistance and serum lipid profile significantly decreased. In addition, hepatic malondialdehyde and serum adiponectin level increased and hepatic activity of superoxide dismutase and serum TNFα level decreased. PGC-1α gene expression in adipose tissue of fructose group significantly increased compared to the high fat control group P< 0/05 . Conclusion: Our results showed that a low-fructose diet could prevent insulin resistance, oxidative stress, hypoadiponectinemia and TNFα activation that they are features of nonalcoholic steatohepatitis NASH . These data also indicate that the low-fructose diet might provide a beneficial treatment for oxidative stress, insulin resistance and NAFLD.

کلیدواژه ها

Non-alcoholic fatty liver disease, Adiponectin, TNFα, Fructose, Low-fructose diet , Insulin resistance.

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