Department of Physiology, University of Lausanne, Lausanne, Switzerland (VL, GC, LE, C Binnert, and LT); the Service of Internal Medicine (GC) and the Service of Endocrinology, Diabetes and Metabolism (LT); Lausanne University Hospital, Lausanne, Switzerland; the Department of Clinical Research and Institute of Diagnostic, Interventional, and Pediatric Radiology, University Bern, Bern, Switzerland (AB, ELM, RK, and C Boesch); and Nutrition & Health Research, Nestlé Research Center, Nestec SA, Lausanne, Switzerland (C Binnert and CD).
Am J Clin Nutr. 2014 Feb;99(2):268-75. doi: 10.3945/ajcn.113.069526. Epub 2013 Nov 20.
Epidemiologic and experimental data have suggested that chlorogenic acid, which is a polyphenol contained in green coffee beans, prevents diet-induced hepatic steatosis and insulin resistance.
We assessed whether the consumption of chlorogenic acid-rich coffee attenuates the effects of short-term fructose overfeeding, dietary conditions known to increase intrahepatocellular lipids (IHCLs), and blood triglyceride concentrations and to decrease hepatic insulin sensitivity in healthy humans.
Effects of 3 different coffees were assessed in 10 healthy volunteers in a randomized, controlled, crossover trial. IHCLs, hepatic glucose production (HGP) (by 6,6-d2 glucose dilution), and fasting lipid oxidation were measured after 14 d of consumption of caffeinated coffee high in chlorogenic acid (C-HCA), decaffeinated coffee high in chlorogenic acid, or decaffeinated coffee with regular amounts of chlorogenic acid (D-RCA); during the last 6 d of the study, the weight-maintenance diet of subjects was supplemented with 4 g fructose · kg(-1) · d(-1) (total energy intake ± SD: 143 ± 1% of weight-maintenance requirements). All participants were also studied without coffee supplementation, either with 4 g fructose · kg(-1) · d(-1) (high fructose only) or without high fructose (control).
Compared with the control diet, the high-fructose diet significantly increased IHCLs by 102 ± 36% and HGP by 16 ± 3% and decreased fasting lipid oxidation by 100 ± 29% (all P < 0.05). All 3 coffees significantly decreased HGP. Fasting lipid oxidation increased with C-HCA and D-RCA (P < 0.05). None of the 3 coffees significantly altered IHCLs.
Coffee consumption attenuates hepatic insulin resistance but not the increase of IHCLs induced by fructose overfeeding. This effect does not appear to be mediated by differences in the caffeine or chlorogenic acid content. This trial was registered at clinicaltrials.gov as NCT00827450.
流行病学和实验数据表明，绿咖啡豆中含有的多酚类物质——绿原酸可预防饮食诱导的肝脂肪变性和胰岛素抵抗。
我们评估富含绿原酸的咖啡的摄入是否能减弱短期果糖过食的影响，果糖过食已知会增加肝细胞内脂质（IHCL）和血液甘油三酯浓度，并降低健康人群的肝胰岛素敏感性。
在一项随机、对照、交叉试验中，我们评估了 10 名健康志愿者在饮用含咖啡因的绿原酸含量高的咖啡（C-HCA）、含咖啡因的脱咖啡因咖啡、或含常规绿原酸含量的脱咖啡因咖啡（D-RCA）14 天后的 IHCLs、肝葡萄糖生成（HGP）（通过 6,6-d2 葡萄糖稀释）和空腹脂质氧化情况。在研究的最后 6 天，受试者的维持体重饮食中补充 4 g 果糖·kg(-1)·d(-1)（总能量摄入 ± SD：143 ± 1%维持体重需求）。所有参与者还在不补充咖啡的情况下进行了研究，要么补充 4 g 果糖·kg(-1)·d(-1)（仅高果糖），要么不补充高果糖（对照）。
与对照饮食相比，高果糖饮食显著增加 IHCLs 102 ± 36%，HGP 增加 16 ± 3%，空腹脂质氧化减少 100 ± 29%（均 P < 0.05）。三种咖啡均显著降低 HGP。C-HCA 和 D-RCA 增加了空腹脂质氧化（P < 0.05）。三种咖啡均未显著改变 IHCLs。
咖啡的摄入可减弱肝胰岛素抵抗，但不能减弱果糖过食引起的 IHCLs 增加。这种作用似乎不是由咖啡因或绿原酸含量的差异介导的。该试验在 clinicaltrials.gov 注册为 NCT00827450。
