High-fat diet decreases anti-inflammatory activities due to the disturbance of hepatic lipid metabolism accompanied by intestinal microbiota and EGCG regulation in broilers

Author:

Dou Xiujing1,Cui Ying1,Wu Jiaqi1,Zhang Man1,Shan Anshan1

Affiliation:

1. Northeast Agricultural University

Abstract

Abstract Background: Long or short-term high-fat diets often lead to adverse effects in the body, such as metabolic disorders, changes in the intestinal flora, and even cause inflammation. It also increases the risk of developing diseases like dyslipidemia, type 2 diabetes mellitus (T2DM), and fatty liver disease. The inflammatory links between a high-fat diet and diseases are currently unknown entirely. (-) - Epigallocatechin-3-gallate (EGCG), a major bioactive chemical substance extracted from green tea, is well-established in nutrient metabolism and lessens the occurrence. This study aims to demonstrate that high fat decreases disease tolerance, evaluate the alleviative effect of EGCG and explore the protective mechanism of EGCG from liver lipid metabolism and intestinal microflora. Results: We found that when broilers were fed a high-fat diet, they had symptoms such as liver hypertrophy, increased abdominal fat deposition, lipid metabolism disorder and changes in intestinal microbial structure. In addition, when broilers were fed with high fat for some time, lipopolysaccharide injection would expose more disadvantages of high fat, including increased oxidative damage and inflammatory damage. After administration of EGCG, liver hypertrophy, abdominal fat deposition, and liver lipid metabolism disorder were slowed down, and intestinal flora changes caused by a high-fat diet were regulated. Conclusions: The study showed that a high-fat diet decreases anti-inflammatory activities due to hepatic lipid metabolism and intestinal microbiota disturbances. EGCG alleviates the disorder of liver lipid metabolism and intestinal microbial structure in broilers, which is critical to maintaining lipid and microbial homeostasis during the pathogenesis of inflammation.

Publisher

Research Square Platform LLC

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