Fontana L, Moreira E, Torres M I, Fernández I, Ríos A, Sánchez de Medina F, Gil A
Department of Biochemistry and Molecular Biology, School of Pharmacy, University of Granada, Spain.
J Hepatol. 1998 Apr;28(4):662-9. doi: 10.1016/s0168-8278(98)80291-2.
BACKGROUND/AIMS: Dietary nucleotides modulate a number of metabolic processes, including long-chain polyunsaturated fatty acid metabolism. In this study, we evaluated the effect of dietary nucleotides on plasma and liver microsomal fatty acid profiles in a rat model of liver cirrhosis induced by oral intake of thioacetamide.
Fifty-four female Wistar rats were assigned to one of the following groups: rats in the thioacetamide group (n=45) were given 300 mg thioacetamide/l in their drinking water for 4 months, and rats in the control group (n=9) received water during the same period. After 4 months of treatment, 9 rats in each group were killed. The remaining rats in the thioacetamide group were divided into two new groups, and the animals in each were allowed to recover for 1 or 2 weeks on either a nucleotide-free diet or the same diet supplemented with 50 mg of each of the following: AMP, GMP, CMP, IMP and UMP per 100 g diet.
Saturated (mainly stearic acid), monounsaturated, and n-6 long-chain polyunsaturated fatty acids (mainly arachidonic acid), and also the unsaturation index decreased in plasma of rats with experimental cirrhosis. Administration of the diet supplemented with nucleotides to thioacetamide-treated rats corrected plasma levels of saturated, n-6 long-chain polyunsaturated fatty acids and the unsaturation index. In liver microsomes, the cirrhotic rats showed lower levels of protein and higher levels of palmitic, oleic, linoleic and arachidonic acids. Protein concentrations and levels of all the above-mentioned fatty acids were corrected with the nucleotide-enriched diet.
Dietary nucleotides contribute to correcting plasma and liver microsomal fatty acid alterations in rats with liver cirrhosis induced by chronic oral administration of thioacetamide.
背景/目的:膳食核苷酸可调节多种代谢过程,包括长链多不饱和脂肪酸代谢。在本研究中,我们评估了膳食核苷酸对口服硫代乙酰胺诱导的肝硬化大鼠模型血浆和肝脏微粒体脂肪酸谱的影响。
将54只雌性Wistar大鼠分为以下几组:硫代乙酰胺组(n = 45)大鼠饮用含300 mg硫代乙酰胺/升的水4个月,对照组(n = 9)大鼠在同一时期饮用清水。治疗4个月后,每组处死9只大鼠。硫代乙酰胺组中剩余的大鼠分为两个新组,每组动物分别在无核苷酸饮食或补充了以下物质的相同饮食中恢复1或2周:每100克饮食中含50毫克AMP、GMP、CMP、IMP和UMP。
实验性肝硬化大鼠血浆中的饱和脂肪酸(主要是硬脂酸)、单不饱和脂肪酸和n-6长链多不饱和脂肪酸(主要是花生四烯酸)以及不饱和指数均降低。给硫代乙酰胺处理的大鼠补充核苷酸饮食可纠正血浆中饱和脂肪酸、n-6长链多不饱和脂肪酸水平及不饱和指数。在肝脏微粒体中,肝硬化大鼠的蛋白质水平较低,棕榈酸、油酸、亚油酸和花生四烯酸水平较高。富含核苷酸的饮食可纠正蛋白质浓度及上述所有脂肪酸的水平。
膳食核苷酸有助于纠正慢性口服硫代乙酰胺诱导的肝硬化大鼠血浆和肝脏微粒体脂肪酸的改变。