Goda T, Yasutake H, Suzuki Y, Takase S, Koldovský O
Department of Nutrition, School of Food and Nutritional Sciences, University of Shizuoka, Japan.
Am J Physiol. 1995 Jun;268(6 Pt 1):G1066-73. doi: 10.1152/ajpgi.1995.268.6.G1066.
To explore the mechanisms by which jejunal lactase activity is modified by carbohydrate and/or fat intake, mRNA levels and the absolute synthesis rate of lactase-phlorizin hydrolase (LPH) were determined in 6-wk-old rats that were fed either low-starch diets containing long-chain triacylglycerol (LCT, 73% energy as corn oil) or medium-chain triacylglycerol (MCT, 66% energy as MCT, 7% energy as corn oil), or a high-starch diet (70% energy as cornstarch) for 7 days. LPH mRNA levels in the jejunum were similar between LCT-fed and MCT-fed rats, but animals fed the high-starch diet exhibited a greater (2x) LPH mRNA level than other groups. The absolute synthesis rate of LPH, estimated by the flooding dose technique using [3H]phenylalanine, was greater (2.4x) in rats fed the high-starch diet than in other groups. A short-term force-feeding experiment revealed that sucrose was able to evoke LPH mRNA levels within 12 h but that a nonmetabolizable sugar (alpha-methylglucoside) was unable to enhance it. By contrast, animals fed the high-LCT diet showed a lower (by 30%) lactase activity than rats fed the low-starch, high-MCT diet, which was accompanied by not only a reduction of immunoreactive LPH in brush-border membranes but also a reduction in lactase activity per unit weight of immunoreactive LPH. These results suggest that both gene expression and posttranslational events of LPH might be influenced by dietary manipulations; carbohydrate intake primarily increases LPH mRNA levels, and LCT accelerates inactivation and/or degradation of lactase.
为探究碳水化合物和/或脂肪摄入对空肠乳糖酶活性的调节机制,对6周龄大鼠进行了研究。这些大鼠被分别喂食含长链三酰甘油(LCT,73%能量来自玉米油)或中链三酰甘油(MCT,66%能量来自MCT,7%能量来自玉米油)的低淀粉饮食,或高淀粉饮食(70%能量来自玉米淀粉),持续7天。喂食LCT和MCT的大鼠空肠中LPH mRNA水平相似,但喂食高淀粉饮食的动物LPH mRNA水平比其他组高(2倍)。通过使用[3H]苯丙氨酸的灌流剂量技术估算,喂食高淀粉饮食的大鼠中LPH的绝对合成率比其他组高(2.4倍)。一项短期强制喂食实验表明,蔗糖能够在12小时内引起LPH mRNA水平升高,但不可代谢的糖(α-甲基葡糖苷)无法增强其水平。相比之下,喂食高LCT饮食的动物乳糖酶活性比喂食低淀粉、高MCT饮食的大鼠低(30%),这不仅伴随着刷状缘膜中免疫反应性LPH的减少,还伴随着单位重量免疫反应性LPH中乳糖酶活性的降低。这些结果表明,LPH的基因表达和翻译后事件可能都受到饮食调控的影响;碳水化合物摄入主要增加LPH mRNA水平,而LCT加速乳糖酶的失活和/或降解。