Schwarz Jean-Marc, Noworolski Susan M, Wen Michael J, Dyachenko Artem, Prior Jessica L, Weinberg Melissa E, Herraiz Laurie A, Tai Viva W, Bergeron Nathalie, Bersot Thomas P, Rao Madhu N, Schambelan Morris, Mulligan Kathleen
Touro University (J.M.S., A.D., J.L.P., N.B.), Vallejo, California 94594; Department of Medicine (J.M.S., M.E.W., T.P.B., M.N.R., M.S., K.M.), University of California, San Francisco, San Francisco, California 94143; Division of Endocrinology (J.M.S., M.J.W., M.E.W., V.W.T., M.N.R., M.S., K.M.), San Francisco General Hospital, San Francisco, California 94110; Department of Radiology and Biomedical Imaging (S.M.N.), University of California, San Francisco, San Francisco, California 94143; UCSF Clinical and Translational Science Institute Clinical Research Center (L.A.H., V.W.T.), San Francisco, California 94143; and The Gladstone Institute of Cardiovascular Disease (T.P.B.), San Francisco, California 94158.
J Clin Endocrinol Metab. 2015 Jun;100(6):2434-42. doi: 10.1210/jc.2014-3678. Epub 2015 Mar 31.
Consumption of high-fructose diets promotes hepatic fatty acid synthesis (de novo lipogenesis [DNL]) and an atherogenic lipid profile. It is unclear whether these effects occur independent of positive energy balance and weight gain.
We compared the effects of a high-fructose, (25% of energy content) weight-maintaining diet to those of an isocaloric diet with the same macronutrient distribution but in which complex carbohydrate (CCHO) was substituted for fructose.
DESIGN, SETTING, AND PARTICIPANTS: Eight healthy men were studied as inpatients for consecutive 9-day periods. Stable isotope tracers were used to measure fractional hepatic DNL and endogenous glucose production (EGP) and its suppression during a euglycemic-hyperinsulinemic clamp. Liver fat was measured by magnetic resonance spectroscopy.
Weight remained stable. Regardless of the order in which the diets were fed, the high-fructose diet was associated with both higher DNL (average, 18.6 ± 1.4% vs 11.0 ± 1.4% for CCHO; P = .001) and higher liver fat (median, +137% of CCHO; P = .016) in all participants. Fasting EGP and insulin-mediated glucose disposal did not differ significantly, but EGP during hyperinsulinemia was greater (0.60 ± 0.07 vs 0.46 ± 0.06 mg/kg/min; P = .013) with the high-fructose diet, suggesting blunted suppression of EGP.
Short-term high-fructose intake was associated with increased DNL and liver fat in healthy men fed weight-maintaining diets.
高果糖饮食会促进肝脏脂肪酸合成（从头脂肪生成[DNL]）以及形成致动脉粥样硬化的脂质谱。目前尚不清楚这些影响是否独立于正能量平衡和体重增加而发生。
我们比较了高果糖（占能量的25%）维持体重饮食与等热量饮食的效果，后者具有相同的宏量营养素分布，但用复合碳水化合物（CCHO）替代了果糖。
设计、地点和参与者：8名健康男性作为住院患者连续接受为期9天的研究。使用稳定同位素示踪剂测量肝脏DNL分数、内源性葡萄糖生成（EGP）及其在正常血糖-高胰岛素钳夹期间的抑制情况。通过磁共振波谱法测量肝脏脂肪。
体重保持稳定。无论饮食顺序如何，高果糖饮食在所有参与者中均与更高的DNL（平均，CCHO组为11.0±1.4%，高果糖组为18.6±1.4%；P = 0.001）和更高的肝脏脂肪（中位数，CCHO组的+137%；P = 0.016）相关。空腹EGP和胰岛素介导的葡萄糖处置无显著差异，但高果糖饮食时高胰岛素血症期间的EGP更高（0.60±0.07 vs 0.46±0.06 mg/kg/min；P = 0.013），提示EGP抑制减弱。
在维持体重饮食的健康男性中，短期高果糖摄入与DNL增加和肝脏脂肪增加有关。
