In both herbivorous tilapia (Oreochromis mossambicus) and carnivorous rockfish (Sebastes caurinus) intestinal and pyloric cecal brush-border membrane vesicles (BBMV), [14C]glycylsarcosine ([14C]Gly-Sar) uptake was stimulated by a transmembrane proton gradient. A transmembrane K(+)-diffusion potential (inside negative) stimulated [14C]Gly-Sar uptake above that observed with short-circuited vesicles, whereas an inwardly directed Na+ gradient in both fishes had no effect on peptide uptake. In tilapia, [14C]Gly-Sar influx occurred by the combination of 1) a high-affinity, saturable, proton gradient-dependent carrier system [Kt [concentration that equals one-half of maximum influx (Jmax)] = 0.56 +/- 0.08 mM; Jmax = 1,945.0 +/- 174.6 pmol.mg protein-1.10 s-1]; 2) a low-affinity, nonsaturable (within 1-10 mM), proton gradient-dependent carrier system (nonsaturable carrier-mediated transport component = 4,514.0 +/- 28.1 pmol.mg protein-1.10 s-1.mM-1); and 3) a diffusional component accounting for < 10% of total influx within the concentration range tested. Influx (10 s) of 1-10 mM [14C]Gly-Sar in tilapia intestine was significantly (P < 0.01) inhibited by 10 mM diethylpyrocarbonate, a specific inhibitor of proton-coupled peptide transport systems. [14C]Gly-Sar influx into tilapia BBMV showed cis-inhibition and trans-stimulation by Gly-Pro, suggesting that [14C]Gly-Sar and Gly-Pro shared the same mucosal peptide transporter in fish. These observations strongly suggest that intestinal transport of peptides in herbivorous and carnivorous fishes is proton gradient dependent, electrogenic, sodium independent, and qualitatively resembles the peptide transport paradigm proposed for mammals.
Epidermal D-glucose transport was investigated in vivo in the brackish-water polychaete worm Nereis diversicolor. Transfer across the apical membrane is rate-limiting to D-glucose uptake, but the cuticle and/or mucus presents some resistance to D-glucose diffusion between bulk solution and transporting membrane. Maximal D-glucose influx is about 10(-12) mol sec-1 per cm2 of apical plasmalemma. Under natural conditions (approximately 1 microM D-glucose in the medium), backflux from the epidermal transport pool is negligible, but a significant paracellular outflux may occur. D-glucose influx across the apical membrane is Na+-dependent and completely inhibitable by phlorizin and harmaline; phloretin is less effective, and cytochalasin B has no effect. Influx is moderately depressed by KCN and iodoacetate, alpha-methyl-D-glucopyranoside is an effective substitute of D-glucose in transport. Animals acclimated to a low salinity, in which epidermal salt transport takes place, show a marked decrease of D-glucose transport capacity. On transfer of animals from a high to a low salinity, or vice versa, the corresponding change of influx occurs after a time-lag of at least an hour. Permeability of the epidermis to simple diffusion of D-glucose is 8 X 10(-8) cm sec-1 (on basis of gross epidermal area).
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