Rossi I, Monge L, Feliu J E
Servicio de Gastroenterología, Clínica Puerta de Hierro, Facultad de Medicina, Universidad Autónoma de Madrid, Spain.
Biochem J. 1989 Sep 1;262(2):397-402. doi: 10.1042/bj2620397.
In epithelial cells isolated from rat small intestine, we have studied the influence of vasoactive intestinal peptide (VIP), a neurotransmitter which markedly increases enterocyte cyclic AMP, and of two cyclic AMP analogues (8-bromo cyclic AMP and N6,2'-O-dibutyryl cyclic AMP) on the rate of glycolysis, fructose 2,6-bisphosphate concentration and 6-phosphofructo-2-kinase activity, as well as on the rate of 3-O-methyl-D-[14C]glucose uptake. Our results show that, without affecting the rate of 3-O-methyl-D-[14C]glucose accumulation, VIP and cyclic AMP analogues were able to inhibit glucose consumption and L-lactate formation by isolated rat enterocytes. These effects occurred parallel to a significant decrease in the cellular concentration of fructose 2,6-bisphosphate and to a partial inactivation of 6-phosphofructo-2-kinase. These findings support the hypothesis that VIP inhibits glycolysis in rat enterocytes through a cyclic AMP-dependent mechanism.
在从大鼠小肠分离出的上皮细胞中，我们研究了血管活性肠肽（VIP）（一种能显著提高肠上皮细胞环磷酸腺苷水平的神经递质）以及两种环磷酸腺苷类似物（8-溴环磷酸腺苷和N6,2'-O-二丁酰环磷酸腺苷）对糖酵解速率、果糖2,6-二磷酸浓度和6-磷酸果糖-2-激酶活性的影响，以及对3-O-甲基-D-[14C]葡萄糖摄取速率的影响。我们的结果表明，在不影响3-O-甲基-D-[14C]葡萄糖积累速率的情况下，VIP和环磷酸腺苷类似物能够抑制分离的大鼠肠上皮细胞的葡萄糖消耗和L-乳酸生成。这些效应伴随着细胞内果糖2,6-二磷酸浓度的显著降低以及6-磷酸果糖-2-激酶的部分失活而出现。这些发现支持了VIP通过环磷酸腺苷依赖机制抑制大鼠肠上皮细胞糖酵解的假说。
