Substitution of soy protein for casein prevents oxidative modification and inflammatory response induced in rats fed high fructose diet.

S Sreeja,Krishnamoorthy Bhavani,Rajagopalan Geetha,Carani Venkatraman Anuradha,Emayavaramban Priyadarshini

doi:10.1155/2014/641096

Abstract

Fructose-rich diet is known to cause metabolic dysregulation, oxidative stress, and inflammation. We aimed to compare the effects of two dietary proteins of animal and plant origins on fructose-induced oxidative stress and inflammatory changes in liver. Wistar rats were fed either starch or fructose (60%) diet with casein or soy protein (20%) as the protein source for 8 weeks. Glucose and insulin, glycated hemoglobin and fructosamine, AOPP, and FRAP were determined in circulation. Intracellular ROS, oxidatively modified proteins (4-HNE and 3-NT adducts), adiponectin, TNF-α, IL-6 and PAI-1 mRNA expression, phosphorylation and activation of JNK and IKKβ, and NF-κB binding activity were assayed in liver. In comparison with starch fed group, fructose + casein group registered significant decline in antioxidant potential and increase in plasma glucose, insulin, and glycated proteins. Increased ROS production, 4-HNE and 3-NT modified proteins, JNK and IKKβ activation, and NF-κB binding activity were observed in them along with increased gene expression of PAI-1, IL-6, and TNF-α and decreased adiponectin expression. Substitution of soy protein for casein reduced oxidative modification and inflammatory changes in fructose-fed rats. These data suggest that soy protein but not casein can avert the adverse effects elicited by chronic consumption of fructose.

Highlights

The consumption of fructose has increased greatly due to the widespread use of high fructose corn syrup as a sweetening agent in food industry
The findings reported here demonstrate that fructose + casein diet induced reactive oxygen species (ROS) generation, increased the accumulation of oxidatively modified proteins and the expression of proinflammatory cytokines, and activated NF-κB signaling, while soy protein substitution reduced the damaging effects of fructose and protected the cells
Decline in the ferric reducing ability of plasma (FRAP) value is responsible for the elevated intracellular levels of ROS and plasma advanced oxidation protein products (AOPP) levels in fructose + casein group

Summary

Introduction

The consumption of fructose has increased greatly due to the widespread use of high fructose corn syrup as a sweetening agent in food industry. This has received the attention of many investigators since obesity and several aspects of the metabolic syndrome, such as hypertension, dyslipidemia, and glucose intolerance, are strongly correlated with the consumption of high fructose diet. 4-Hydroxy-2,3-nonenal (HNE) and 4-hydroxy-2,3-alkenals of different chain length originate as a consequence of peroxidation of lipids. These molecules form aldehyde-protein adducts by interacting with reactive groups of cysteine, lysine, and histidine which produce damage to cells and tissues [4]. Nitration of tyrosine residues of proteins occurs during excessive formation of peroxynitrite [5]. 3-Nitrotyrosine (3-NT) modified protein

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