Delzenne N M, Hernaux N A, Taper H S
Département des sciences pharmaceutiques, Université catholique de Louvain, Brussels, Belgium.
Food Chem Toxicol. 1998 Jul;36(7):555-61. doi: 10.1016/s0278-6915(98)00023-4.
Liver steatosis is often attributed to dietary habits. Our previous results have shown that fatty acid synthesis is considerably increased by high carbohydrates-fat free diet (HCFF) given to rats after fasting, and leads to lipid accumulation and morphological alterations in the liver, defined as steatosis. As n-3 polyunsaturated fatty acids are able to counteract lipogenesis induction in vivo and in vitro, we hypothesized that the addition of menhaden oil in a carbohydrate-rich diet might be able to protect the liver against steatosis induced by a fasting-re-feeding transition. Male Wistar rats were first fasted for 48 hr, then re-fed ad lib. for 24 hr with either (1) standard diet; (2) high carbohydrates-fat free diet (HCFF), containing 40% (w/w) starch, 40% saccharose, 16% casein and 4% vitamin mineral mix; or (3) the latter diet containing additionally 5% menhaden oil (HCMO) for 24 hr. Triglyceride (TG) accumulation occurred in liver tissue of rats re-fed with HCFF and HCMO diets after fasting. The addition of menhaden oil led to a strong decrease in serum TG; however, both TG and phospholipid (PL) levels, as well as fatty acid synthase activity, were increased in the liver of HCMO rats as compared with the values obtained in HCFF re-fed rats. Histologically diagnosed steatosis was even more severe when rats received HCMO than HCFF. These results indicate that menhaden oil supplementation does not avoid, but even increases, the degree of steatosis generated in vivo by re-feeding a high carbohydrate diet after fasting.
肝脂肪变性通常归因于饮食习惯。我们之前的研究结果表明,禁食后的大鼠给予高碳水化合物无脂饮食(HCFF)会使脂肪酸合成显著增加,并导致肝脏脂质蓄积和形态改变,即脂肪变性。由于n-3多不饱和脂肪酸能够在体内和体外对抗脂肪生成诱导作用,我们推测在富含碳水化合物的饮食中添加鲱鱼油可能能够保护肝脏免受禁食-再喂食转变诱导的脂肪变性。雄性Wistar大鼠首先禁食48小时,然后随意再喂食24小时,分别给予:(1)标准饮食;(2)高碳水化合物无脂饮食(HCFF),含40%(w/w)淀粉、40%蔗糖、16%酪蛋白和4%维生素矿物质混合物;或(3)后一种饮食额外添加5%鲱鱼油(HCMO),持续24小时。禁食后再喂食HCFF和HCMO饮食的大鼠肝脏组织中出现甘油三酯(TG)蓄积。添加鲱鱼油导致血清TG显著降低;然而,与再喂食HCFF的大鼠相比,HCMO大鼠肝脏中的TG和磷脂(PL)水平以及脂肪酸合酶活性均升高。组织学诊断的脂肪变性在接受HCMO的大鼠中比接受HCFF的大鼠更严重。这些结果表明,补充鲱鱼油并不能避免,反而会增加禁食后再喂食高碳水化合物饮食在体内产生的脂肪变性程度。