scholarly journals Brain Oxidative Stress in Neural Mechanism of Programmed Hypertension to Maternal High Fructose Diet

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Kay Wu ◽  
You‐Lin Tain ◽  
Julie Chan
2021 ◽  
Author(s):  
Rodrigo Cardoso ◽  
Luiza Dias Moreira ◽  
Mirian Costa ◽  
Renata Celi Lopes Toledo ◽  
Mariana Grancieri ◽  
...  

The aim of this study was to evaluate the effect of green and black tea kombuchas consumption on adiposity, lipid metabolism, liver steatosis, oxidative stress, and inflammation in Wistar rats...


2022 ◽  
pp. 101728
Author(s):  
Patoomporn Prasartthong ◽  
Poungrat Pakdeechote ◽  
Putcharawipa Maneesai ◽  
Sariya Meephat ◽  
Siwayu Rattanakanokchai ◽  
...  

Author(s):  
PRIYA CHANDRASEKARAN SATHIYA ◽  
RAMACHANDRAN VIDHYA ◽  
KALIVARATHAN JAGAN ◽  
CARANI VENKATRAMAN ANURADHA

2007 ◽  
Vol 2007 ◽  
pp. 1-8 ◽  
Author(s):  
Panchamoorthy Rajasekar ◽  
Carani Venkatraman Anuradha

There is evidence that high-fructose diet induces insulin resistance, alterations in lipid metabolism, and oxidative stress in rat tissues. The purpose of this study was to evaluate the effect of L-carnitine (CAR) on lipid accumulation and peroxidative damage in skeletal muscle of rats fed high-fructose diet. Fructose-fed animals (60 g/100 g diet) displayed decreased glucose/insulin (G/I) ratio and insulin sensitivity index (ISI0,120) indicating the development of insulin resistance. Rats showed alterations in the levels of triglycerides, free fatty acids, cholesterol, and phospholipids in skeletal muscle. The condition was associated with oxidative stress as evidenced by the accumulation of lipid peroxidation products, protein carbonyls, and aldehydes along with depletion of both enzymic and nonenzymic antioxidants. Simultaneous intraperitoneal administration of CAR (300 mg/kg/day) to fructose-fed rats alleviated the effects of fructose. These rats showed near-normal levels of the parameters studied. The effects of CAR in this model suggest that CAR supplementation may have some benefits in patients suffering from insulin resistance.


Scientifica ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Kanokwan Jarukamjorn ◽  
Nattharat Jearapong ◽  
Charinya Pimson ◽  
Waranya Chatuphonprasert

Excessive fat liver is an important manifestation of nonalcoholic fatty liver disease (NAFLD), associated with obesity, insulin resistance, and oxidative stress. In the present study, the effects of a high-fat, high-fructose diet (HFFD) on mRNA levels and activities of the antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), were determined in mouse livers and brains. The histomorphology of the livers was examined and the state of nonenzymatic reducing system was evaluated by measuring the glutathione system and the lipid peroxidation. Histopathology of the liver showed that fat accumulation and inflammation depended on the period of the HFFD-consumption. The levels of mRNA and enzymatic activities of SOD, CAT, and GPx were raised, followed by the increases in malondialdehyde levels in livers and brains of the HFFD mice. The oxidized GSSG content was increased while the total GSH and the reduced GSH were decreased, resulting in the increase in the GSH/GSSG ratio in both livers and brains of the HFFD mice. These observations suggested that liver damage and oxidative stress in the significant organs were generated by continuous HFFD-consumption. Imbalance of antioxidant condition induced by long-term HFFD-consumption might increase the risk and progression of NAFLD.


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