Karasov W H, Pond R S, Solberg D H, Diamond J M
Proc Natl Acad Sci U S A. 1983 Dec;80(24):7674-7. doi: 10.1073/pnas.80.24.7674.
Active uptake of D-glucose and L-proline at 50 mM was measured in everted intestinal sleeves of mice whose dietary carbohydrate and protein levels were being varied experimentally. Compared to a nearly carbohydrate-free meat diet, a 50% carbohydrate laboratory chow diet stimulated active glucose uptake in the proximal intestine without affecting proline uptake, passive glucose permeability, or several measures of mucosal mass. Switching from a low-protein high-carbohydrate to a high-protein no-carbohydrate diet reversibly stimulated proline uptake while inhibiting glucose uptake. For each solute and diet switch, the stimulation of transport was complete within 1 day, while the inhibition required several days. The results imply induction and repression of intestinal glucose and proline transport by dietary substrate levels. This mechanism, in conjunction with the normal gradient of nutrient concentrations along the intestine, is probably largely responsible for the gradient in nutrient transport along the intestine.
在通过实验改变饮食中碳水化合物和蛋白质水平的小鼠外翻肠套中,测定了50 mM浓度下D-葡萄糖和L-脯氨酸的主动摄取。与几乎不含碳水化合物的肉类饮食相比,50%碳水化合物的实验室常规饮食刺激了近端肠道中葡萄糖的主动摄取,而不影响脯氨酸摄取、葡萄糖的被动通透性或几种黏膜质量指标。从低蛋白高碳水化合物饮食转变为高蛋白无碳水化合物饮食,可可逆地刺激脯氨酸摄取,同时抑制葡萄糖摄取。对于每种溶质和饮食转变,转运的刺激在1天内完成,而抑制则需要几天时间。结果表明饮食底物水平可诱导和抑制肠道葡萄糖和脯氨酸的转运。这种机制,连同沿肠道营养物质浓度的正常梯度,可能在很大程度上导致了沿肠道营养物质转运的梯度。