Diet-Induced Rat Model of Gradual Development of Non-Alcoholic Fatty Liver Disease (NAFLD) with Lipopolysaccharides (LPS) Secretion - PubMed (original) (raw)

doi: 10.3390/diagnostics9040205.

Agnieszka Łukomska 2, Karolina Dec 1, Karolina Skonieczna-Żydecka 1, Izabela Gutowska 3, Marta Skórka-Majewicz 1, Daniel Styburski 1, Kamila Misiakiewicz-Has 4, Anna Pilutin 4, Joanna Palma 1, Katarzyna Sieletycka 5, Wojciech Marlicz 6, Ewa Stachowska 1

Affiliations

Diet-Induced Rat Model of Gradual Development of Non-Alcoholic Fatty Liver Disease (NAFLD) with Lipopolysaccharides (LPS) Secretion

Dominika Maciejewska et al. Diagnostics (Basel). 2019.

Abstract

Background: Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver disorders in industrialized Western countries. The prevalence of the disease is estimated to range from 4% to 46% worldwide. The aim of study was to develop an animal model with gradual NAFLD development.

Methods: Sprague-Dawley rats were fed a high-fat and high-cholesterol (HFHCh) diet. The rats from the study and control groups were sacrificed after 2, 4, 8, 12, 16, and 20 weeks of dietary exposure.

Results: Analysis of biochemical parameters showed that after only two weeks, ALT and cholesterol concentration in serum were elevated. After 4 weeks, TNF-α and HOMA-IR were significantly higher compared to the control group. NAFLD progression started after 12 weeks of diet-weight gain and increased LPS secretions were noticed. During the experiment, rats induced steatosis (from stage 0/1 after 4 weeks to stage 2/3 after 20 weeks), inflammation (from stage 0/1 after 4 weeks to stage 1/2 after 20 weeks), and fibrosis (from stage 1 after 12 weeks to stage 2 after 20 weeks).

Conclusion: We can assume that the presented model based on the HFHCh diet induced gradual development of NAFLD. We confirmed that the animal NAFLD model increases LPS secretions during disease progression.

Keywords: NAFLD animal model; NAFLD model; NAFLD rat model; NASH model.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1

Figure 1

Hematoxylin-eosin (HE) stain of liver tissue from control (A–C), HFD livers at weeks 2 (D), 4 (E), 8 (F), 12 (G), 16 (H), and 20 (I). Objective magnification: A,B ×20; C–I ×40.

Figure 2

Figure 2

Mallory trichrome stain of liver tissue from control (A) and HFD livers at weeks 12 (B), 16 (C), 20 (D). Objective magnification ×20.

Figure 3

Figure 3

Progression of liver steatosis.

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