ABSTRACT

This study was designed to investigate the effects of green tea on lipid profile, liver tissue damage, and oxidative stress in rats fed a diet including high fructose. Sprague-Dawley rats were randomly divided into four groups: Control (C), Fructose (F), Green Tea (GT), and F+GT. F and F+GT groups were given 20% fructose in the drinking water for eight weeks. Green tea (2 mg kg−1) was administrated to GT and F+GT groups by oral gavage for eight weeks. Biochemical parameters in serum and oxidative stress markers in the liver were analysed. The liver sections were stained with haematoxylin-eosin. As of the 3rd week of the experiment, the body weight of rats in the F group showed a statistically significant increase in comparison with the F+GT group. The serum glucose and triglyceride levels of the F+GT group significantly decreased when compared with the F group. The fructose-induced degenerative changes in the liver were reduced with green tea. Green tea may serve a protective role against hyperlipidaemia and liver injury in rats fed a high fructose diet.

Fructose is the natural sugar found in fruits. This sugar is widely used in all ready-made foods, especially in soft drinks. The study aims to examine how fructose consumption affects biochemical parameters in blood and whether it causes endoplasmic reticulum (ER) stress-caused cell death in pancreatic tissue. Sprague-Dawley rats were separated into control and fructose groups. Control animals (n=7) had free access to tap water, and standard pellet, fructose group (n=7) was given 20% fructose in drinking water for eight weeks. The consumption of food and fluid of the rats were measured daily during the experiment. The lipid levels and total oxidant/antioxidant statuses in serum were analyzed. Grp-78, IRE1-α, PERK, ATF-4, and -6, CHOP, and Caspase (Cas)-3/-8/-9/-12 mRNA expression levels in pancreas were detected. Fructose intake increased TG and VLDL levels in serum, and the mRNA expression levels of Grp-78, IRE-1α, PERK, ATF-4, -6 and Cas-3/-8/-9/-12 in pancreas with fructose consumption as compared with control group. Fructose consumption may cause disruption of lipid profile and oxidant/antioxidant balance, as well as trigger ER stress and thus cause programmed cell death. This will lead to the development of many diseases.