valinomycin and Starvation

The uptake of beta-hydroxy-beta-methyl-glutarate (HMG) and beta-hydroxy-butyrate (beta-HB) by renal brushborder membrane vesicles prepared from normal and starved rats was examined. HMG and beta-HB uptake show a Na+ gradient-induced overshoot, suggesting luminal cotransport of these organic acids. Kinetic analysis of HMG and beta-HB uptake revealed a single component carrier system and a diffusional component for each compound. Vesicles from starved rats exhibit the same transport characteristics as those from normal rats. The transport interactions of other organic acids with HMG were examined and revealed that citrate is a competitive inhibitor, which implies that the compounds share a common organic acid carrier.

Topics: 3-Hydroxybutyric Acid; Animals; Biological Transport; Citrates; Glutarates; Hydroxybutyrates; Kidney; Kinetics; Male; Meglutol; Microvilli; Rats; Rats, Inbred Strains; Sodium; Starvation; Time Factors; Valinomycin

The ability of liver efficiently to take up amino acids, particularly l-alanine, during starvation was studied in a cell-free system by isolating plasma-membrane vesicles in a transport-competent state from rat liver parenchymal cells. These membrane vesicles have the capacity to accumulate l-alanine against an apparent concentration gradient when exposed to an artificial and transient transmembrane Na(+) gradient (extravesicular Na(+) concentration greater than inside). The rate of accumulation of l-alanine is dependent on the plasma-membrane vesicle concentration, and the steady-state concentration attained is inversely related to the osmolarity of the medium. The Na(+)-mediated stimulation is not exhibited if the membrane vesicles are pre-equilibrated with NaCl, if K(+) or Li(+) are substituted for Na(+), or if SO(4) (2-) replaces Cl(-) as the counterion. The apparent active transport of l-alanine into the membrane vesicles appears to occur by an electrogenic mechanism: (1) the use of NaSCN significantly heightens the early concentrative phase of transport when compared with the effect of NaCl; (2) an enhanced active transport is also observed when a valinomycin-induced K(+) efflux occurs concomitant with Na(+) and l-alanine influx. Plasma-membrane vesicles isolated from liver parenchymal cells of a 24 h-starved rat exhibit an initial l-alanine transport rate that is 3-4 times that for membrane vesicles derived from a fed animal. The increased rate of l-alanine transport by plasma-membrane vesicles from starved animals can be obliterated by adrenalectomy and restored by administration of glucocorticoid. These results establish that stimulation of the gluconeogenic pathway by starvation involves a plasma-membrane-localized change affecting l-alanine transport which is regulated in part by the glucocorticoid hormones.

Topics: Adrenalectomy; Alanine; Animals; Biological Transport; Cell Membrane; Dexamethasone; Glucocorticoids; In Vitro Techniques; Liver; Rats; Sodium; Starvation; Stimulation, Chemical; Valinomycin