富含猪油的高脂饮食会增加内毒素血症大鼠肝脏中的过氧化物酶体增殖物激活受体。
A lard-rich high-fat diet increases hepatic peroxisome proliferator-activated receptors in endotoxemic rats.
作者信息
Kai Motoki, Miyoshi Makoto, Fujiwara Mayu, Nishiyama Yuya, Inoue Taketo, Maeshige Noriaki, Hamada Yasuhiro, Usami Makoto
机构信息
Division of Nutrition and Metabolism, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Department of Therapeutic Nutrition, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.
出版信息
J Surg Res. 2017 May 15;212:22-32. doi: 10.1016/j.jss.2016.11.048. Epub 2016 Dec 7.
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, messenger RNA (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.
背景
富含饱和脂肪酸的饮食会引发慢性炎症。我们之前报道过，即使在脂多糖（LPS）引起的急性炎症中，喂食富含猪油饮食的大鼠肝脏损伤也会加剧。过氧化物酶体增殖物激活受体（PPARs）与炎症相关，也是脂质代谢的关键调节因子。在本研究中，我们通过检测肝脏PPARs及其他标志物，研究了高脂饮食对内毒素血症期间肝脏损伤和肝脏脂质代谢的影响。
材料与方法
雄性Wistar大鼠分别喂食高脂饮食（HFD，脂肪含量60千卡%）或对照饮食（CD，脂肪含量10千卡%）4周或12周，注射LPS，并在0、1.5或6小时后处死。分析指标包括血浆天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）水平、肝脏PPARα和PPARγ的信使核糖核酸（mRNA）和蛋白质水平，以及与脂肪酸氧化和合成相关的酶的mRNA水平。
结果
喂食12周而非4周高脂饮食的内毒素血症大鼠，其肝脏PPARs的mRNA和蛋白质水平高于对照饮食组大鼠（P < 0.01 - 0.05）。同样，这些大鼠肝脏脂肪酸氧化和合成相关酶的mRNA表达增加（P < 0.01 - 0.05）。与喂食4周高脂饮食的大鼠相比，喂食12周高脂饮食且注射LPS的大鼠，血浆AST/ALT显示其肝脏损伤更严重。
结论
喂食富含猪油的饮食12周会加重内毒素血症大鼠的肝脏损伤，并增加肝脏PPARα和PPARγ的表达。
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