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Influence of Fructose Consumption on Inflammatory Gene Expression in Liver and Brain in a Pig Model of Juvenile Obesity
Author(s) -
Jang Saebyeol,
Molokin Aleksey,
Laskman Sukla,
Panickar Kiran,
Bruna Gonzalo,
Urban Joseph F,
Solano-Aguilar Gloria
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.824.9
Subject(s) - fructose , nefa , endocrinology , medicine , calorie , biology , weight gain , steatosis , insulin , body weight , biochemistry
Fructose intake has been associated with the prevalence of overweight and obese humans. Therefore, we studied the metabolic effects of added fructose consumption in young pigs as a model of juvenile obesity. Conventional crossbred pigs were randomized and fed 1) a basal calorie diet alone or 2) with added fructose (20% of total calories); or 3) a high calorie diet with added fat alone or 4) with added fat and fructose for 12 wk. Two‐way ANOVA revealed a significant main effect of fat and a fructose by fat interaction on body weight gain showing that fructose consumption increased body weight gain only when added to a basal calorie diet. Gene expression was increased for hepatic inflammatory genes TNF‐α, IL‐1β, COX‐2 and MCP‐1, and brain hippocampal IL‐6 by high fat consumption whereas gene expression for hippocampal brain derived neurotrophic factor (BDNF) was diminished. There was no significant effect of fructose on gene expression. Interestingly, correlation z test revealed a significant relationship between concentration of serum non‐esterified fatty acid (NEFA) and gene expression of hippocampal IL‐6 and BDNF suggesting that NEFA might be predictive of changes in gene expression in the brain. Overall, this study showed that increased fructose in the diet contributed to body weight gain in a lean condition, but did not negatively affect hepatic and hippocampal‐derived inflammatory gene expression.