Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.

Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:

• Class I comprises GLUT1 to GLUT4 and GLUT14.
• Class II has GLUT5, GLUT7, GLUT9, and GLUT11.
• Class III includes GLUT6, GLUT8, GLUT10, GLUT12, and GLUT13.

These GLUTs are found in several organs of the body, where they help maintain glucose levels. For example, GLUT 1 is ubiquitously expressed in all tissues but predominantly in the cell membrane of erythrocytes and endothelial cells of the blood-brain barrier. GLUT3 is mainly present in the brain. Interestingly, GLUT7 and 11, in addition to glucose, can also transport fructose.

Sodium-linked glucose transporters (SGLTs) are secondary active transporters where the protein does not directly utilize ATP. The energy for glucose transport (against its concentration gradient) is provided by the sodium gradient across the cell membrane and is maintained by the sodium-potassium pump. The human genome contains 12 members in this gene family, of which 6 are SGLTs encoded by SLC5A.

The SLC50 encodes a recently discovered "Sugars Will Eventually Be Exported Transporter" (SWEET) protein. These are expressed in plants, animals, protozoans, and bacteria and help transport sugars driven by their concentration gradient.

Disorders associated with glucose transporters

Although not completely understood, GLUT1 deficiency syndrome may be due to a de novo mutation in the gene SLC2A1. This mutation is thought to be inherited in an autosomal dominant manner. It impairs glucose transport at the blood-brain barrier. Clinical symptoms arising from this mutation include early-onset epileptic encephalopathy, microcephaly, and seizures.

Fanconi-Bickel syndrome, a rare autosomal recessive condition, is caused by mutations of GLUT2 either due to its decreased expression or an impaired function of the gene. Patients with this condition typically show a combination of hepatomegaly due to increased glycogen storage, nephropathy with severe glucosuria, fasting hypoglycemia, and glucose and galactose intolerance in the fed state.

Intestinal glucose-galactose malabsorption, an autosomal recessive disorder, results from a defect in the SGLT1 gene. It causes severe osmotic diarrhea and dehydration soon after birth.

SGLT2 mutations result in renal glucosuria, where glucose is excreted in the urine. A renal transport defect affects the tubular glucose reabsorption at the proximal tubules but does not affect other kidney functions. Hence, patients could present with normal blood glucose levels.