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D-glucose and other monosaccharides are hydrophilic substances
that cannot easily cross the lipophilic bilayer of the cell membrane. Since
carbohydrates are most important for supplying energy to essentially
all cell types, specific transport mechanisms have evolved. While
vesicle-associated glucose transport has been described only recently,1-4 transporter proteins
have been known for years. Such proteins are embedded into the cell
membrane and function as hydrophilic pores that allow cellular uptake
and release and allow transcellular transport of monosaccharides.
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Glucose transporter proteins can be divided into two groups:
(1) Sodium-dependent glucose transporters (SGLTs, symporter systems,
secondary “active” transporters), which are members
of the solute carrier family 5 (SLC5), couple sugar transport to
the electrochemical gradient of sodium and hence can transport glucose
against its own concentration gradient (eFig.
157.1); and (2) facilitative glucose transporters (GLUTs, uniporter
systems, “passive” transporters) are members of
the SLC2 family that can transport monosaccharides only along an
existing gradient (eFig. 157.2). To date,
five congenital defects of monosaccharide transport are known (Fig. 157-1). Their clinical picture is the
consequence of tissue-specific expression and substrate specificity
of the affected transporter.
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