Department of Anatomy & Embryology, NUTRIM School for Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands.
Department of Anatomy & Embryology, NUTRIM School for Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands; Nutrigenomics Consortium, Top Institute Food and Nutrition, Wageningen, The Netherlands.
Biochim Biophys Acta Mol Basis Dis. 2017 Jul;1863(7):1789-1804. doi: 10.1016/j.bbadis.2017.04.022. Epub 2017 Apr 28.
Few studies have assessed the effect of changing ratios of dietary macronutrients on fat accumulation in adipose tissue and organs such as the liver in a 3×n(n≥3) factorial design. We investigated the effects of 7 diets from a single manufacturer containing 11-58en% protein (casein), 0-81en% carbohydrates (CHO; sucrose, maltrodextrin-10 and corn starch), and 8-42en% fat (triheptanoin, olive oil or cocoa butter) in C57BL/6J mice, a good model for diet-induced obesity and fatty liver. The diets were fed for 3weeks to wild-type and hyperlipidemic male and female mice. Caloric intake was mainly determined by dietary fat. Body weight, liver lipid and cholesterol content, NFκB activation, and fat-pad size decreased only in mice fed a high-protein diet. A high dietary protein:CHO ratio reduced plasma FGF21 concentration, and increased liver PCK1 protein content and plasma triglyceride concentration. The dietary protein:CHO ratio determined hepatic expression of Pck1 and Ppargc1a in males, and Fgf21 in females, whereas the dietary CHO:fat ratio determined that of Fasn, Acaca1, and Scd1 in females. Hepatic glycogen content was determined by all three dietary components. Both hepatic PCK1 and plasma FGF21 correlated strongly and inversely with hepatic TG content, suggesting a key role for PCK1 and increased gluconeogenesis in resolving steatosis with a high-protein diet, with FGF21 expression reflecting declining cell stress. We propose that a diet containing ~35en% protein, 5-10en% fat, and 55-60en% carbohydrate will prevent fatty liver in mice without inducing side effects.
很少有研究评估在 3×n(n≥3)析因设计中改变膳食宏量营养素比例对脂肪在脂肪组织和器官（如肝脏）中积累的影响。我们研究了来自单一制造商的 7 种饮食的影响，这些饮食含有 11-58en%的蛋白质（酪蛋白）、0-81en%的碳水化合物（CHO；蔗糖、麦芽糊精-10 和玉米淀粉）和 8-42en%的脂肪（三庚酸甘油酯、橄榄油或可可脂），在 C57BL/6J 小鼠中，C57BL/6J 小鼠是饮食诱导肥胖和脂肪肝的良好模型。这些饮食喂养了 3 周的野生型和高脂血症雄性和雌性小鼠。热量摄入主要由膳食脂肪决定。体重、肝脂质和胆固醇含量、NFκB 激活和脂肪垫大小仅在喂食高蛋白饮食的小鼠中降低。高膳食蛋白质：CHO 比降低了血浆 FGF21 浓度，增加了肝 PCK1 蛋白含量和血浆甘油三酯浓度。膳食蛋白质：CHO 比决定了雄性小鼠的肝 Pck1 和 Ppargc1a 的表达，以及雌性小鼠的 Fgf21 表达，而膳食 CHO：fat 比决定了雌性小鼠的 Fasn、Acaca1 和 Scd1 的表达。肝糖原含量由这三种膳食成分决定。肝 PCK1 和血浆 FGF21 均与肝 TG 含量呈强烈负相关，表明高蛋白饮食中 PCK1 和增加的糖异生在解决脂肪肝中起关键作用，FGF21 表达反映了细胞应激的下降。我们提出，含有约 35en%蛋白质、5-10en%脂肪和 55-60en%碳水化合物的饮食将预防小鼠的脂肪肝，而不会引起副作用。
