Research Programs Unit, Diabetes and Obesity, University of Helsinki and Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland.
Institute for Molecular Medicine FIMM, Helsinki, Finland.
J Intern Med. 2017 Aug;282(2):187-201. doi: 10.1111/joim.12632. Epub 2017 Jun 27.
Overconsumption of dietary sugars, fructose in particular, is linked to cardiovascular risk factors such as type 2 diabetes, obesity, dyslipidemia and nonalcoholic fatty liver disease. However, clinical studies have to date not clarified whether these adverse cardiometabolic effects are induced directly by dietary sugars, or whether they are secondary to weight gain.
To assess the effects of fructose (75 g day ), served with their habitual diet over 12 weeks, on liver fat content and other cardiometabolic risk factors in a large cohort (n = 71) of abdominally obese men.
We analysed changes in body composition, dietary intake, an extensive panel of cardiometabolic risk markers, hepatic de novo lipogenesis (DNL), liver fat content and postprandial lipid responses after a standardized oral fat tolerance test (OFTT).
Fructose consumption had modest adverse effects on cardiometabolic risk factors. However, fructose consumption significantly increased liver fat content and hepatic DNL and decreased β-hydroxybutyrate (a measure of β-oxidation). The individual changes in liver fat were highly variable in subjects matched for the same level of weight change. The increase in liver fat content was significantly more pronounced than the weight gain. The increase in DNL correlated positively with triglyceride area under the curve responses after an OFTT.
Our data demonstrated adverse effects of moderate fructose consumption for 12 weeks on multiple cardiometabolic risk factors in particular on liver fat content despite only relative low increases in weight and waist circumference. Our study also indicates that there are remarkable individual differences in susceptibility to visceral adiposity/liver fat after real-world daily consumption of fructose-sweetened beverages over 12 weeks.
过量摄入膳食糖,尤其是果糖,与 2 型糖尿病、肥胖、血脂异常和非酒精性脂肪肝等心血管危险因素有关。然而,迄今为止,临床研究仍未明确这些不良的代谢心血管效应是直接由膳食糖引起的,还是由体重增加引起的。
评估在 12 周内用习惯性饮食摄入 75 克果糖对 71 例腹型肥胖男性的肝脏脂肪含量和其他代谢心血管危险因素的影响。
我们分析了身体成分、饮食摄入、广泛的代谢心血管风险标志物、肝脏从头合成脂肪(DNL)、肝脏脂肪含量以及标准化口服脂肪耐量试验(OFTT)后的餐后脂质反应的变化。
果糖摄入对代谢心血管危险因素有适度的不良影响。然而,果糖摄入显著增加了肝脏脂肪含量和肝脏 DNL,降低了β-羟丁酸(β-氧化的一种衡量指标)。在体重变化相同的受试者中,肝脏脂肪的个体变化差异很大。肝脏脂肪含量的增加明显大于体重的增加。DNL 的增加与 OFTT 后甘油三酯曲线下面积的增加呈正相关。
我们的数据表明,在 12 周内摄入适量的果糖对多种代谢心血管危险因素,特别是肝脏脂肪含量,有不良影响,尽管体重和腰围的相对增加较低。我们的研究还表明,在现实生活中每天摄入果糖饮料 12 周后,个体对内脏脂肪/肝脏脂肪的易感性存在显著差异。