Menhaden Oil Decreases High-Fat Diet-Induced Markers of Hepatic Damage, Steatosis, Inflammation, and Fibrosis in Obese Ldlr-/- Mice
Menhaden Oil Decreases High-Fat Diet-Induced Markers of Hepatic Damage, Steatosis, Inflammation, and Fibrosis in Obese Ldlr-/- Mice
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DOI：
10.3945/jn.112.158865
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发表时间：
2012-08-01
影响因子：
4.2
通讯作者：
Jump, Donald B.
中科院分区：
文献类型：
--
作者：
Depner, Christopher M.;Torres-Gonzalez, Moises;Jump, Donald B.
在美国，非酒精性脂肪性肝病（NAFLD）和非酒精性脂肪性肝炎（NASH）的发病频率与肥胖同时增加。NASH是进行性的，以肝损伤、炎症、纤维化和氧化应激为特征。由于C20-22 (n-3) PUFA是脂质代谢和炎症的调节因子，我们验证了鲱鱼油（MO）中的C20-22 (n-3) PUFA可以预防小鼠高脂肪（HF）饮食引起的脂肪肝疾病的假设。野生型（WT）和Ldlr(-/-) C57BL/6J小鼠喂食以下饲料12周：非纯化（NP）、HF +猪油（60%的能量来自脂肪）、HF-高胆固醇+橄榄油（HFHC-OO； 54.4%的能量来自脂肪，0.5%的胆固醇）或HFHC-OO添加MO （HFHC-MO）。与NP饲粮相比，HFHC-OO饲粮诱导Ldlr（-/-）小鼠肝内炎症标志物（单核细胞趋化蛋白-1）、纤维化标志物（前胶原-1 α 1）和氧化应激标志物（血红素加氧酶-1）肝脏胆固醇表达（P < 0.05, P < 140%）升高（P < 0.05）， Ldlr（-/-）小鼠肝内损伤[血浆丙氨酸转氨酶（ALT）和谷草转氨酶升高]。与HFHC-OO相比，饲喂HFHC-MO的WT和Ldlr（-/-）小鼠的血浆和肝脏标志物肝损伤、脂肪变性、炎症和纤维化均较低，但不包括氧化应激（P < 0.05）。总之，MO[2%能量时的C20-22 (n-3) PUFA]降低了小鼠中许多（但不是全部）HF饮食诱导的脂肪性肝病标志物。中国生物医学工程学报，32(2):393 - 393,2012。
The frequency of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) has increased in parallel with obesity in the United States. NASH is progressive and characterized by hepatic damage, inflammation, fibrosis, and oxidative stress. Because C20-22 (n-3) PUFA are established regulators of lipid metabolism and inflammation, we tested the hypothesis that C20-22 (n-3) PUFA in menhaden oil (MO) prevent high-fat (HF) diet-induced fatty liver disease in mice. Wild-type (WT) and Ldlr(-/-) C57BL/6J mice were fed the following diets for 12 wk: nonpurified (NP), HF with lard (60% of energy from fat), HF-high-cholesterol with olive oil (HFHC-OO; 54.4% of energy from fat, 0.5% cholesterol), or HFHC-OO supplemented with MO (HFHC-MO). When compared with the NP diet, the HF and HFHC-OO diets induced hepatosteatosis and hepatic damage [elevated plasma alanine aminotransferase (ALT) and aspartate aminotransferases] and elevated hepatic expression of markers of inflammation (monocyte chemoattractant protein-1), fibrosis (procollagen 1 alpha 1), and oxidative stress (heme oxygenase-1) (P 140%, P < 0.05) hepatic cholesterol in Ldlr(-/-) mice fed the HFHC-OO diet than WT mice fed the HF or HFHC-OO diets. Plasma and hepatic markers of liver damage, steatosis, inflammation, and fibrosis, but not oxidative stress, were lower in WT and Ldlr(-/-) mice fed the HFHC-MO diet compared with the HFHC-OO diet (P < 0.05). In conclusion, MO [C20-22 (n-3) PUFA at 2% of energy] decreases many, but not all, HF diet-induced markers of fatty liver disease in mice. J. Nutr. 142: 1495-1503, 2012.