Potential-dependent D-glucose uptake by renal brush border membrane vesicles in the absence of sodium

Abstract

The uptake of D-glucose by renal brush border membrane vesicles was studied in the absence of Na+. Uptake of the sugar was membrane potential dependent (inside negative), inhibited by phlorizin, sugar and stereospecific, accelerated by exchange diffusion, saturable, and temperature dependent. The binding of phlorizin in the absence of Na+ was also increased by a membrane potential (inside negative). Thus, the properties of this membrane potential-dependent, Na+-independent sugar transport system resembled those described for the Na+-D-glucose cotransport system. In the absence of Na+ but in the presence of a valinomycin-induced K+ diffusion potential the apparent Km for D-glucose was 43 mM. This contrasted with an apparent Km of 1.8 mM for the Na+ chemical gradient system. Therefore, the Na+-independent uptake system represented a low-affinity transport mechanism. It is suggested that the same carrier mediated the Na+-independent and Na+-dependent transport systems. A hypothetical model for the membrane potential-dependent stimulation of D-glucose uptake in the absence of Na+ is proposed.

The small-intestinal Na+,d-glucose cotransporter: An asymmetric gated channel (or pore) responsive to ΔΨ

“…(For a discussion of the quantitative differences between these two transport systems, see Toggenburger et al, 1982.) Also a recent, independent observation of Hilden and Sacktor (1982) on the kidney cotransporter(s) fits beautifully in the mechanistic model of Fig. 9.…”

“…(v) Finally, A0 (negative inside) accelerates D-glucose influx into and increases phlorizin binding onto the (renal) brush border cotransporter even in the absence of Na + (Hilden & Sacktor, 1982). Phlorizin binds to the (intestinal) cotransporter in the neutral form (Toggenburger et al, 1978) and, of course, so does D-glucose.…”

“…This is not to say that the translocation probabilities of the parially occupied complexes always need be equal to zero. Indeed, Hilden and Sacktor (1982) have recently shown that A ~ (negative inside the vesicles) accelerates the out ---, in transport of D-glucose by the renal cotransporter even in the absence of Na +. Thus, at least the out ~ in translocation probability of the D-glucose loaded (renal) cotransporter(s) must be of detectable (albeit small) magnitude.…”

Proton-coupled transport of organic solutes in animal cell membranes and its relation to Na+ transport.

“…In regard to these problems, the role of H+ in usual Nat-dependent cotransport system, particularly under Na+-free conditions is of special interest. HILDEN and SACKTOR [28] demonstrated that D-glucose transport across renal brush border membrane vesicles in the absence of Na+ was stimulated by inside-negative K+ diffusion potential though the mechanism of stimulation was unknown. Interestingly, it was observed that Na+-independent d cp m-stimulated D-glucose transport across the same membranes was dependent on the pH gradient (Takuwa and Hoshi, unpublished observation).…”

Kinetics of the sodium/beta‐methyl‐D‐glucoside co‐transport system in the guinea‐pig small intestine.

“…With the aid of membrane vesicle preparations in which the microenvironment -and thus the reservoirsurrounding the brush-border membrane in intact tissue has been destroyed, it has been shown that the mediated uptake of sugars and amino acids is strongly dependent on the presence of sodium ions (Murer & Hopfer, 1974). Although widely accepted, even this doctrine has however recently been questioned (Hilden & Sacktor, 1982). An absolute dependence on sodium would imply that only the ternary complex (SCA in Fig.…”