Breusing Nicolle, Lagerpusch Merit, Engstler Anna Janina, Bergheim Ina, Mueller Manfred J, Bosy-Westphal Anja
a University of Hohenheim, Institute of Nutritional Medicine , Stuttgart , GERMANY.
b Friedrich Schiller University, Institute of Nutrition , Jena , GERMANY.
J Am Coll Nutr. 2017 Jan;36(1):72-79. doi: 10.1080/07315724.2016.1156036. Epub 2017 Jan 6.
Overfeeding with a high-fat and/or high-carbohydrate (CHO) diet is known to increase plasma concentrations of endotoxin (lipopolysaccharide [LPS]) that may lead to metabolic disturbances like insulin resistance. The impact of CHO quality (i.e., the glycemic index [GI]) independent of fat intake on metabolic endotoxemia remains unclear. In the present study, the effects of changes in energy balance and GI on plasma endotoxin were studied.
Fifteen healthy young men overconsumed diets containing 65% CHO and 20% fat for 1 week (OF; +50% of energy requirement) followed by 3 weeks of caloric restriction (CR; -50% of energy requirement) and were then randomized to 2 weeks hypercaloric refeeding (RF, +50% of energy requirement) with either a low- or high-GI (40 vs 74) diet.
During OF, subjects gained 1.9 ± 0.7 kg body weight (+0.6 ± 0.8% fat mass) followed by a weight loss of 6.1 ± 0.8 kg (-2.0 ± 0.6% fat mass) and weight regain of 4.0 ± 0.6 kg (0.9 ± 0.8% fat mass). Fasting insulin and homeostasis model assessment-insulin resistance (HOMA) increased with OF and RF and decreased with CR, Matsuda decreased by 37% after RF (all p < 0.05). Endotoxin significantly increased by 30.8% with OF and by 24.7% with RF (both p < 0.05), whereas CR normalized endotoxin levels. No difference in endotoxin levels was observed between refeeding a hypercaloric high- or low-GI diet. Changes in endotoxin levels with RF were not related to changes in insulin sensitivity.
A hypercaloric diet (OF and RF) increased plasma endotoxin irrespective of GI, whereas a negative energy balance did not reduce endotoxemia. Impaired insulin sensitivity with hypercaloric refeeding on a high-GI diet was not explained by metabolic endotoxemia.
已知高脂和/或高碳水化合物（CHO）饮食过量会增加血浆内毒素（脂多糖[LPS]）浓度，这可能导致如胰岛素抵抗等代谢紊乱。CHO质量（即血糖生成指数[GI]）独立于脂肪摄入量对代谢性内毒素血症的影响仍不清楚。在本研究中，研究了能量平衡和GI变化对血浆内毒素的影响。
15名健康年轻男性过量摄入含65%CHO和20%脂肪的饮食1周（OF；能量需求的+50%），随后进行3周的热量限制（CR；能量需求的-50%），然后随机分为两组，进行为期2周的高热量再喂养（RF，能量需求的+50%），分别给予低GI或高GI（40对74）饮食。
在OF期间，受试者体重增加1.9±0.7kg（脂肪量增加0.6±0.8%），随后体重减轻6.1±0.8kg（脂肪量减少2.0±0.6%），体重恢复4.0±0.6kg（脂肪量增加0.9±0.8%）。空腹胰岛素和稳态模型评估-胰岛素抵抗（HOMA）在OF和RF时升高，在CR时降低，RF后松田指数降低37%（均p<0.05）。内毒素在OF时显著增加30.8%，在RF时增加24.7%（均p<0.05），而CR使内毒素水平恢复正常。高热量高GI或低GI饮食再喂养时内毒素水平无差异。RF时内毒素水平的变化与胰岛素敏感性的变化无关。
高热量饮食（OF和RF）会增加血浆内毒素，与GI无关，而负能量平衡并未降低内毒素血症。高热量高GI饮食再喂养时胰岛素敏感性受损并非由代谢性内毒素血症所致。
