Department of Human Biology and Movement Sciences, School of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University Medical Center, Maastricht, P.O. Box 616, 6200 MD, The Netherlands.
Nutrition, Metabolism and Genomics Group, Wageningen University, Wageningen, The Netherlands.
Clin Nutr. 2018 Apr;37(2):719-727. doi: 10.1016/j.clnu.2017.06.007. Epub 2017 Jun 10.
BACKGROUND & AIMS: Chocolate consumption is associated with a decreased risk for CVD. Theobromine, a compound in cocoa, may explain these effects as it favorably affected fasting serum lipids. However, long-term effects of theobromine on postprandial metabolism as well as underlying mechanisms have never been studied. The objective was to evaluate the effects of 4-week theobromine consumption (500 mg/day) on fasting and postprandial lipid, lipoprotein and glucose metabolism, and duodenal gene expression.
In a randomized, double-blind crossover study, 44 healthy men and women, with low baseline HDL-C concentrations consumed 500 mg theobromine or placebo daily. After 4-weeks, fasting blood was sampled and subjects participated in a 4-h postprandial test. Blood was sampled frequently for analysis of lipid and glucose metabolism. In a subgroup of 10 men, 5 h after meal consumption duodenal biopsies were taken for microarray analysis.
4-weeks theobromine consumption lowered fasting LDL-C (-0.21 mmol/L; P = 0.006), and apoB100 (-0.04 g/L; P = 0.022), tended to increase HDL-C (0.03 mmol/L; P = 0.088) and increased hsCRP (1.2 mg/L; P = 0.017) concentrations. Fasting apoA-I, TAG, FFA, glucose and insulin concentrations were unchanged. In the postprandial phase, theobromine consumption increased glucose (P = 0.026), insulin (P = 0.011) and FFA (P = 0.003) concentrations, while lipids and (apo)lipoproteins were unchanged. In duodenal biopsies, microarray analysis showed no consistent changes in expression of genes, pathways or gene sets related to lipid, cholesterol or glucose metabolism.
It is not likely that the potential beneficial effects of cocoa on CVD can be ascribed to theobromine. Although theobromine lowers serum LDL-C concentrations, it did not change fasting HDL-C, apoA-I, or postprandial lipid concentrations and duodenal gene expression, and unfavorably affected postprandial glucose and insulin responses. This trial was registered on clinicaltrials.gov under study number NCT02209025.
巧克力的摄入与 CVD 风险降低有关。可可中的可可因可能是造成这种影响的原因，因为它能有利地影响空腹血清脂质。然而，可可因对餐后代谢的长期影响以及潜在的机制从未被研究过。本研究的目的是评估 4 周可可因（500mg/天）摄入对空腹和餐后脂质、脂蛋白和葡萄糖代谢以及十二指肠基因表达的影响。
在一项随机、双盲交叉研究中，44 名基线 HDL-C 浓度较低的健康男性和女性每天摄入 500mg 可可因或安慰剂。4 周后，采集空腹血样，受试者参加 4 小时的餐后测试。频繁采血分析脂质和葡萄糖代谢。在 10 名男性的亚组中，在餐后 5 小时采集十二指肠活检进行微阵列分析。
4 周可可因摄入可降低空腹 LDL-C（-0.21mmol/L；P=0.006）和 apoB100（-0.04g/L；P=0.022），并倾向于增加 HDL-C（0.03mmol/L；P=0.088）和 hsCRP（1.2mg/L；P=0.017）浓度。空腹 apoA-I、TAG、FFA、葡萄糖和胰岛素浓度不变。在餐后阶段，可可因摄入可增加葡萄糖（P=0.026）、胰岛素（P=0.011）和 FFA（P=0.003）浓度，而脂质和（apo）脂蛋白浓度不变。在十二指肠活检中，微阵列分析显示与脂质、胆固醇或葡萄糖代谢相关的基因、途径或基因集的表达没有一致的变化。
可可对 CVD 的潜在有益影响不太可能归因于可可因。尽管可可因降低血清 LDL-C 浓度，但它并没有改变空腹 HDL-C、apoA-I 或餐后脂质浓度和十二指肠基因表达，并且不利于餐后葡萄糖和胰岛素反应。本试验在 clinicaltrials.gov 上注册，注册号为 NCT02209025。
