A lard-rich, high-fat diet increases hepatic PPARs in endotoxemic rats

• Published in: The Journal of surgical research
• Main Authors: Kai, Motoki, MT, MS, Miyoshi, Makoto, MT, PhD, Fujiwara, Mayu, MT, PhD, Nishiyama, Yuya, MT, MS, Inoue, Taketo, MT, Ph.D, Maeshige, Noriaki, PT, PhD, Hamada, Yasuhiro, MD, PhD, Usami, Makoto, MD, PhD
• Format: Journal Article
• Language: English
• Published: 2016
• Subjects: Surgery; Lard; Peroxisome proliferator-activated receptor; High-fat diet; Lipopolysaccharide; Lipid metabolism; Liver injury
• ISSN: 0022-4804
• DOI: 10.1016/j.jss.2016.11.048

Abstract Background Diets high in saturated fatty acids activate chronic inflammation. We previously reported that, in even acute inflammation caused by lipopolysaccharide (LPS), liver injury was exacerbated in rats fed a lard-rich diet. Peroxisome proliferator-activated receptors (PPARs) are related to inflammation and are also key regulators of lipid metabolism. In this study, we examined effects of high-fat diet on liver injury and hepatic lipid metabolism during endotoxemia, measuring hepatic PPARs and other markers. Materials and Methods Male Wistar rats were fed a high-fat diet (HFD, 60 kcal% fat) or control diet (CD, 10 kcal% fat) for 4 or 12 wk, injected with LPS and sacrificed at 0, 1.5 or 6 h. Analyses included plasma aspartate transaminase (AST) and alanine transaminase (ALT) levels, mRNA and protein levels of hepatic PPARα and PPARγ and mRNA levels of enzymes related to fatty acid oxidation and synthesis. Results Endotoxemic rats on HFD for 12 wk, but not 4 wk, had higher mRNA and protein levels for hepatic PPARs, than did those on CD ( p < 0.01–0.05). Similarly, these rats had increased mRNA expression of hepatic fatty acid oxidation- and synthesis-related enzymes ( p < 0.01–0.05). Rats injected with LPS had more severe liver injury, indicated by plasma AST/ALT, if on the HFD for 12 wk, compared with for 4 wk. Conclusions Consumption of a lard-rich diet for 12 wk worsened liver injury and increased hepatic PPARα and PPARγ expression in endotoxemic rats.