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Glucose Transporters

Glucose Transporters

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:

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FSH isoform pattern in classic galactosemia.

Cynthia S Gubbels¹, Chris M G Thomas, Will K W H Wodzig

¹Department of Pediatrics, Maastricht University Medical Center, Maastricht, The Netherlands.

Journal of Inherited Metabolic Disease

|September 4, 2010

Summary

Female classic galactosemia patients often experience primary ovarian insufficiency (POI). This study found no evidence that altered follicle-stimulating hormone (FSH) glycosylation causes POI in galactosemia patients.

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Area of Science:

Endocrinology
Metabolic Disorders
Reproductive Biology

Background:

Classic galactosemia is a metabolic disorder with known complications including primary ovarian insufficiency (POI) in females.
Hypoglycosylation of molecules, a secondary effect of galactosemia, has been proposed to cause FSH dysfunction leading to POI.
Previous studies suggested altered FSH isoforms in galactosemia patients, hinting at hypoglycosylation.

Purpose of the Study:

To investigate the role of follicle-stimulating hormone (FSH) isoform patterns in primary ovarian insufficiency (POI) among patients with classic galactosemia.
To determine if hypoglycosylation-induced FSH dysfunction is a primary mechanism underlying POI in galactosemia.

Main Methods:

Compared FSH isoform patterns in five classic galactosemia patients with POI.
Included patients with phosphomannomutase-2-deficient congenital disorders of glycosylation (PMM2-CDG) and POI, and postmenopausal women as controls.
Utilized fast protein liquid chromatography (FPLC) chromatofocussing to measure FSH concentration across different fractions.

Main Results:

No significant differences were observed in FSH isoform patterns between galactosemia patients, PMM2-CDG patients, and postmenopausal controls.
The study did not find evidence supporting FSH dysfunction due to less acidic isoforms as a key mechanism for POI in galactosemia.

Conclusions:

The findings do not support the hypothesis that altered FSH glycosylation is the primary cause of primary ovarian insufficiency in classic galactosemia.
Further research is needed to elucidate the exact mechanisms of POI in galactosemia patients.