The following reply to the discussion topic on glucose transport in
schisto, composed by Eain Cornford, is forwarded to schistonet with his
approval. Please send future replies and additional discussion to the
schistonet community as a whole. Thanks, Chuck Shoemaker.
Dear Dr. Shoemaker
I recently received a message via Ray Damian, and I am responding
to your schistonet community suggestion that a discussion be initiated
regarding schistosome glucose transport. In response to your query A: Do
schistos use active transport?
PRO Although I have heard Gary Uglem tell audiences that this is the case,
I do not believe any of the three more common schistosome species possess
an active transporter. (I know of no reliable evidence supporting such a
notion.)
CON I would politely remind you that the glucose transporters your group
has identified from schisto share homologies with the GLUT1-like mammalian
transporter, and not with the sodium-dependent, active SGLT1 transporter
which Ernie Wright has sequenced. This you already know.
It is accepted that glucose is actively transported in the rat
tapeworm H. diminuta, but I do not believe the responsible transporter has
been identified. Data which I believe support the hypothesis that schisto
glucose transport is not active are from our work (JP 74:116-28, 1988; and
EP 73:489-99, 1991). We demonstrated that the initial rate influx of
glucose (at tracer concentrations) was greater than that of water in H.
diminuta. We measured the Tissue Uptake index (TUI) of glucose in both
species; the TUI measures the amount of 14-C glucose influx relative to
3-HOH influx in 5 seconds, with correction for surface-adherent isotopes.
In tapeworms the TUI was 120-130% at tracer concentrations. A TUI
of more than 100% means that glucose influx was greater than water, and is
consistent with an active transporter mechanism.
In schistosomes, the glucose influx rate (maximal at tracer
concentrations) is on the order of 30% relative to that of water, and the
data consistent with a facilitated diffusion mechanism.
Furthermore, we estimated the internal free glucose concentration
in schistosomes and showed that over the range of anticipated
physiological glucose levels, the male glucose content was approximately
20% of the external concentration and the female about 10% (Mol Biochem
Parasit 17:131, 1985). We could find no evidence for concentration of
glucose in the schistosomes. It seems unlikely that the schisto would need
an efflux mechanism for glucose.
I have wondered whether readers confuse the SGLT1 of the gut brush
border, with the SGTP isoforms of the schistosome, and I know that Ernie
always refers to "the sodium-dependent, active, SGLT1" in speaking to
audiences.
I hope this information is of use to you.
Regards
Eain
