未经批准:高碳水化合物,即,糖,糖摄入可能会驱使肝脏进入脂肪生成状态,导致血浆脂肪酸升高。过量摄入饱和脂肪和含糖苏打会导致肝脏脂肪积累,但在长期随机试验中缺乏研究高摄入量的含糖苏打对从头脂肪生成(DNL)脂肪酸的影响。
未经批准:为了研究每天食用1升含糖苏打的效果,半脱脂牛奶(牛奶),在DNL衍生脂肪酸上超过24周的阿斯巴甜加糖苏打或水(即,棕榈酸盐(主要结果)和其他饱和和单不饱和脂肪酸),和血浆磷脂(PL)中硬脂酰辅酶A去饱和酶活性(SCD1)的标记,胆固醇酯(CE),和甘油三酯(TG)。
UNASSIGNED:一项随机平行研究同时在奥胡斯大学医院和哥本哈根大学进行,丹麦,包括(n=41)20-50岁的个人,BMI为26-40kg/m2,无糖尿病。这些小组由9个人在含糖苏打水中组成,10在牛奶中,11在阿斯巴甜加糖的苏打水中,11在水中使用ANCOVA和混合效应模型评估并比较各组在24周时的变化。探讨了脂肪酸变化与肝脏脂肪积累(磁共振成像)的相关性。
未经批准:24周后,各组在PL中棕榈酸酯比例不同,CE和PL中的油酸酯,以及所有组分中的棕榈油酸盐和SCD1(p<0.05)。与水相比,在含糖苏打(p=0.011)和牛奶(p=0.006)期间,PL中棕榈酸酯的相对比例增加了约1%,而油酸盐和棕榈油酸盐仅在含糖苏打期间增加(CE2.77%,p<0.001;PL1.51%,p=0.002和CE1.46%,PL0.24%,TG1.31%,所有p分别<0.001)。肝脏脂肪积累与棕榈油酸盐的变化一致相关,而与棕榈酸盐和油酸盐的相关性在脂质组分之间不一致。
未经证实:尽管含糖苏打和牛奶都增加了PL中的棕榈酸,仅摄入过量的含糖苏打会增加所有脂质成分中的棕榈油酸盐,并与肝脏脂肪相关。相比之下,等热量牛奶的摄入不会增加血浆单不饱和脂肪酸。
UNASSIGNED:[https://clinicaltrials.gov/ct2/show/NCT00777647],标识符[NCT00777647]。
UNASSIGNED: High carbohydrate, i.e., sugars, intake potentially drives the liver into a lipogenic state leading to elevated plasma fatty acids. Excessive intake of saturated fat and sugar-sweetened soda induces liver fat accumulation, but studying the effect of high intake from sugar-sweetened soda on the de novo lipogenesis (DNL) fatty acids in long-term randomized trials is lacking.
UNASSIGNED: To
study the effect of consuming 1 L/day of sugar-sweetened soda, semi-skimmed milk (milk), aspartame-sweetened soda or water over 24 weeks on DNL-derived fatty acids (i.e., palmitate (primary outcome) and other saturated and monounsaturated fatty acids), and markers of stearoyl-CoA desaturase activity (SCD1) in plasma phospholipids (PL), cholesteryl esters (CE), and triglycerides (TG).
UNASSIGNED: A randomized parallel
study was conducted simultaneously at Aarhus University Hospital and Copenhagen University, Denmark, including (n = 41) individuals aged 20-50 years, with BMI of 26-40 kg/m2, and without diabetes. The groups consisted of 9 individuals in the sugar-sweetened soda, 10 in the milk, 11 in the aspartame-sweetened soda, and 11 in the water. The change at 24 weeks was assessed and compared across the groups using ANCOVA and mixed-effects models. Correlations of fatty acid changes with liver fat accumulation (magnetic resonance imaging) were explored.
UNASSIGNED: After 24 weeks, the groups differed in palmitate proportions in PL, oleate in CE and PL, and palmitoleate and SCD1 in all fractions (p < 0.05). Compared with water, the relative proportion of palmitate in PL increased by approximately 1% during both sugar-sweetened soda (p = 0.011) and milk (p = 0.006), whereas oleate and palmitoleate increased only during sugar-sweetened soda (CE 2.77%, p < 0.001; PL 1.51%, p = 0.002 and CE 1.46%, PL 0.24%, TG 1.31%, all p < 0.001, respectively). Liver fat accumulation correlated consistently with changes in palmitoleate, whereas correlations with palmitate and oleate were inconsistent across lipid fractions.
UNASSIGNED: Although both sugar-sweetened soda and milk increased palmitate in PL, only excess intake of sugar-sweetened soda increased palmitoleate in all lipid fractions and correlated with liver fat. In contrast, isocaloric milk intake did not increase plasma monounsaturated fatty acids.
UNASSIGNED: [https://clinicaltrials.gov/ct2/show/NCT00777647], identifier [NCT00777647].