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High-fat diet modifies cytokine gene expression and exacerbates the effects of acute pancreatitis in the liver of rats.
Journal of Basic and Clinical Physiology and Pharmacology 2018 November 28
BACKGROUND: Obese patients have a higher risk of developing different metabolic syndromes (MeS), including acute pancreatitis (AP). Although obese individuals are more prone to MeS and more susceptible to local and systemic inflammation in response to AP, thus causing long-lasting hospitalization, higher morbidity and mortality, their underlying mechanisms remain unclear. This study aimed to investigate the relationship between obesity and the outcomes of AP in the rat model of AP.
METHODS: To assess the link between obesity and AP, 40 male albino rats were divided into two groups: control and those given a high-fat diet for 12 weeks. This was followed by the injection of a single dose of L-arginine (250 mg/100 gm) in half of each group to induce AP.
RESULTS: Data evaluation was done using 2-way ANOVA. Values were considered significant when p≤0.05. Markers of AP were evaluated in the serum and ascitic fluid. Moreover, the systemic inflammatory markers, such as IL-6, TNF-α, HMGB1 and TLR4, were quantified in the liver of all groups. Results showed that the OAP group had the highest levels of liver enzymes and amylase aside from several signs of liver damage, such as fat necrosis and steatosis.
CONCLUSIONS: The inflammatory cytokine levels are synchronized, creating an early responsive stage and late inflammatory stage to realize the best defense mechanism. Results also indicate that obesity is a main determinant of the severity of AP at the late stage.
METHODS: To assess the link between obesity and AP, 40 male albino rats were divided into two groups: control and those given a high-fat diet for 12 weeks. This was followed by the injection of a single dose of L-arginine (250 mg/100 gm) in half of each group to induce AP.
RESULTS: Data evaluation was done using 2-way ANOVA. Values were considered significant when p≤0.05. Markers of AP were evaluated in the serum and ascitic fluid. Moreover, the systemic inflammatory markers, such as IL-6, TNF-α, HMGB1 and TLR4, were quantified in the liver of all groups. Results showed that the OAP group had the highest levels of liver enzymes and amylase aside from several signs of liver damage, such as fat necrosis and steatosis.
CONCLUSIONS: The inflammatory cytokine levels are synchronized, creating an early responsive stage and late inflammatory stage to realize the best defense mechanism. Results also indicate that obesity is a main determinant of the severity of AP at the late stage.
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