The Effect of High Fat High Fructose Diet (Modification of AIN-93M) on Nuclear Factor Kappa Beta Expression in the Liver Tissue of Male Sprague Dawley Rats

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.

Modulation activity of Vildagliptin on Hepatic Complications and Lipoprotein Abnormalities Associated with Insulin Resistance in Rats

“…Oral treatment of HFFD induced IR with VIL (10 mg/kg) for 8 consecutive weeks showed a prominent modulation in AST and ALT serum levels. Hepatocytes have a unique antioxidant cellular defenses strategy to overcome presence of reactive oxygen species (ROS) that are implicated in tissue injury, NASH and subsequently cell death (Engel et al, 2019). HFFD model is one of the highly valuable predisposing factors that responsible for an increment in ROS and lipid peroxidation products leading to exhaustion of cellular defenses strategy (Şahin et al, 2019).…”