Abstract

The objective of this study was to evaluate the influence of high-fat (HF) and cafeteria diet (CAF) diets and sex on the metabolism of important fatty acids in the liver and perirenal fat tissue. Dietary treatments induced changes in the fatty acid profile in comparison to the untreated group, but the characteristic differences between treated groups were also observable. The HF diet induced an increase in the content of C16:1n-7 and C18:1n-7 in the liver phospholipids (PL) and triglycerides (TG) and perirenal fat tissue compared to the control and CAF diet. The CAF diet induced a more drastic decrease in both n-3 and n-6 polyunsaturated fatty acids (PUFA), including depletion of eicosapentaenoic acid (EPA). The CAF diet also increased the content of n-6 docosapentaenoic acid (DPAn-6) in the liver and decreased it in the perirenal fat. Sex also had a significant influence on the fatty acid profile, but the variables with the highest differences between the CAF and HF treatments were identical in the male and female rats. In this study, we have established that two dietary models of non-alcoholic fatty liver disease (NAFLD) led to characteristic changes in the hepatic and perirenal fat fatty acid profile, in contrast to the control diet and in comparison with each other. These differences could play an important role in the interpretation of the experimental results of nutritional studies.

Highlights

  • Non-alcoholic fatty liver disease (NAFLD) is simple to severe steatosis and consequent hepatitis, fibrosis, and cirrhosis [1]

  • The exact pathology of NAFLD is still unclear, and animal models still play an important role in attempts to elucidate NAFLD pathogenesis and find effective prevention and treatment methods [4]

  • We investigated initial sex how differences differences in the tissue fatty content, which exist between males and females, are reflected in the in the tissue fatty content, which exist between males and females, are reflected in the fatty acid content fatty acid content during during NAFLD progression

Read more

Summary

Introduction

Non-alcoholic fatty liver disease (NAFLD) is simple to severe steatosis and consequent hepatitis, fibrosis, and cirrhosis [1]. NAFLD may progress further to hepatocellular carcinoma [2]. The importance of NAFLD lies in the trend of its increasing prevalence, alongside diabetes and metabolic syndrome [3]. The exact pathology of NAFLD is still unclear, and animal models still play an important role in attempts to elucidate NAFLD pathogenesis and find effective prevention and treatment methods [4]. High-fructose (HF) and high-fat diets (in different forms) are widely used dietary models of rodent NAFLD. One of the possible forms is a “cafeteria diet” (CAF) where animals are allowed free access to highly palatable and energy-dense “unhealthy” human food. The CAF model is a robust rodent model that creates obesity, glucose intolerance, and inflammation [5]

Objectives
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call