vasoactive-intestinal-peptide has been researched along with fructose-2-6-diphosphate* in 2 studies
2 other study(ies) available for vasoactive-intestinal-peptide and fructose-2-6-diphosphate
| Article | Year |
|---|---|
Short-term regulation of glycolysis by vasoactive intestinal peptide in epithelial cells isolated from rat small intestine.
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. Topics: 3-O-Methylglucose; Animals; Bucladesine; Cell Separation; Epithelium; Fructosediphosphates; Glycolysis; Intestine, Small; Male; Methylglucosides; Rats; Vasoactive Intestinal Peptide | 1989 |
Hormonal control of fructose 2,6-bisphosphate concentration in the HT29 human colon adenocarcinoma cell line. Alpha 2-adrenergic agonists counteract effect of vasoactive intestinal peptide.
Vasoactive intestinal peptide (VIP) was found to cause a dose-dependent decrease in fructose 2,6-bisphosphatase concomitant with an increase in cyclic AMP in cultured HT29 cancer cells from human colon. The maximum effect was a 41% decrease obtained with 10 nM-VIP, and half-maximum effect was obtained with 0.75 nM-VIP. The effect of 2.5 nM-VIP was almost totally counteracted (i.e. fructose 2,6-bisphosphate concentration was restored) by either adrenaline (1 microM) or the alpha 2-adrenergic agonist UK-14304 (1 microM); the alpha 2-agonist clonidine (1 microM) was less efficient, since the VIP effect was decreased by 72% only. The adrenaline effect was totally antagonized by 1 microM-yohimbine. It is concluded that, in the HT29 cancer cells, the fructose 2,6-bisphosphate-producing system is sensitive to variations of cyclic AMP concentration and is under the dual control of VIP and alpha 2-adrenergic receptors. Topics: Adenocarcinoma; Brimonidine Tartrate; Cell Line; Clonidine; Colonic Neoplasms; Cyclic AMP; Epinephrine; Fructosediphosphates; Hexosediphosphates; Humans; Quinoxalines; Vasoactive Intestinal Peptide; Yohimbine | 1986 |