Abstract

Metabolic inflammation (low-grade inflammation) remains an etiopathogenic key factor in the development of metabolic syndrome. Nuclear Factor Kappa Beta (NF-κβ) is a transcription regulator of genes having a role in immunity, the inflammatory response which can be associated with obesity-related pathological conditions like nonalcoholic fatty liver (NAFLD). Various stimuli, such as metabolic stress (hyperglycemia, ROS, fat metabolism) and proinflammatory cytokines (TNF-α, IL-6, IL-1β) could activate NF-κβ. This study was aimed to investigate the underlying molecular mechanisms of NAFLD in rats fed a modified AIN-93M HFHF (High Fat High Fructose) diet. The design of this study was experimental post-test only controlled group design. Thirty male Sprague Dawley rats were distributed into 2 treatment groups by a completely randomized design (CRD) technique. The sacrifice was performed after 17 weeks of treatment. NF-κβ expression was assessed by an immunohistochemical method (IRS score). The results showed there were significant differences in feed intake and energy intake between groups P1 and P2 (p = 0,000, p = 0,000). The average NF-κβ expression in the P2 group was significantly higher (p = 0.000) compared to the control group (P1). The correlation test between dietary intake and NF-κβ expression proved that there was a positive correlation between energy, carbohydrate and fat intake on NF-κβ expression (p = 0.001, 0.000, 0.046). However, there was a negative relationship between protein intake and NF-κβ expression (p = 0.000). This study concluded the modified AIN-93M HFHF diet increased NF-κβ expression in the liver tissue of male Sprague Dawley rats.

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