UMR Physiologie de la Nutrition et du Comportement Alimentaire, AgroParisTech, INRA, Université Paris Saclay, Paris, France.
J Nutr. 2019 Feb 1;149(2):270-279. doi: 10.1093/jn/nxy262.
We have reported large differences in adiposity (fat mass/body weight) gain between rats fed a low-fat, high-starch diet, leading to their classification into carbohydrate "sensitive" and "resistant" rats. In sensitive animals, fat accumulates in visceral adipose tissues, leading to the suggestion that this form of obesity could be responsible for rapid development of metabolic syndrome.
We investigated whether increased amylase secretion by the pancreas and accelerated starch degradation in the intestine could be responsible for this phenotype.
Thirty-two male Wistar rats (7-wk-old) were fed a purified low-fat (10%), high-carbohydrate diet for 6 wk, in which most of the carbohydrate (64% by energy) was provided as corn starch. Meal tolerance tests of the Starch diet were performed to measure glucose and insulin responses to meal ingestion. Indirect calorimetry combined with use of 13C-labelled dietary starch was used to assess meal-induced changes in whole body and starch-derived glucose oxidation. Real-time polymerase chain reaction was used to assess mRNA expression in pancreas, liver, white and brown adipose tissues, and intestine. Amylase activity was measured in the duodenum, jejunum, and ileum contents. ANOVA and regression analyses were used for statistical comparisons.
"Resistant" and "sensitive" rats were separated according to adiposity gain during the study (1.73% ± 0.20% compared with 4.35% ± 0.36%). Breath recovery of 13CO2 from 13C-labelled dietary starch was higher in "sensitive" rats, indicating a larger increase in whole body glucose oxidation and, conversely, a larger decrease in lipid oxidation. Amylase mRNA expression in pancreas, and amylase activity in jejunum, were also higher in sensitive rats.
Differences in digestion of starch can promote visceral fat accumulation in rats when fed a low-fat, high-starch diet. This mechanism may have important implications in human obesity.
我们曾报道过,以低脂肪、高淀粉饮食喂养的大鼠,其体脂(脂肪量/体重)增加存在显著差异,可将这些大鼠分为碳水化合物“敏感”和“耐受”型。在敏感型动物中,脂肪堆积在内脏脂肪组织中,这表明这种肥胖形式可能是导致代谢综合征迅速发展的原因。
我们研究了胰腺淀粉酶分泌增加和肠道中淀粉降解加速是否是造成这种表型的原因。
32 只 7 周龄雄性 Wistar 大鼠用纯化的低脂肪(10%)、高碳水化合物饮食喂养 6 周,其中 64%的能量由玉米淀粉提供。进行淀粉饮食的摄食负荷试验,以测量进食后血糖和胰岛素的反应。使用 13C 标记的饮食淀粉进行间接测热法和全身及来源于淀粉的葡萄糖氧化的摄食诱导变化评估。实时聚合酶链反应用于评估胰腺、肝脏、白色和棕色脂肪组织以及肠道中的 mRNA 表达。在十二指肠、空肠和回肠内容物中测量淀粉酶活性。采用方差分析和回归分析进行统计比较。
根据研究期间的体脂增加,将大鼠分为“耐受”和“敏感”型(1.73%±0.20%比 4.35%±0.36%)。13C 标记饮食淀粉中 13CO2 的呼吸恢复率在敏感型大鼠中更高,表明全身葡萄糖氧化增加更大,相反,脂质氧化减少更大。敏感型大鼠胰腺中的淀粉酶 mRNA 表达和空肠中的淀粉酶活性也更高。
当用低脂肪、高淀粉饮食喂养时,淀粉消化的差异可促进大鼠内脏脂肪堆积。这种机制在人类肥胖中可能具有重要意义。