GLYCOGEN - A CARBOHYDRATE SOURCE FOR GLUT-1 GLYCOSYLATION DURING GLUCOSE DEPRIVATION OF 3T3-L1 ADIPOCYTES

Citation
Rj. Mcmahon et Sc. Frost, GLYCOGEN - A CARBOHYDRATE SOURCE FOR GLUT-1 GLYCOSYLATION DURING GLUCOSE DEPRIVATION OF 3T3-L1 ADIPOCYTES, American journal of physiology: endocrinology and metabolism, 33(4), 1996, pp. 640-645
Citations number
22
Categorie Soggetti
Physiology
ISSN journal
01931849
Volume
33
Issue
4
Year of publication
1996
Pages
640 - 645
Database
ISI
SICI code
0193-1849(1996)33:4<640:G-ACSF>2.0.ZU;2-D
Abstract
In 3T3-L1 adipocytes, the glycosylation of the GLUT-1 transporter is a ltered beyond 12 h of glucose deprivation. To determine whether glycog en degradation provides substrate for normal protein glycosylation dur ing this delay, we measured the glycogen content of 3T3-L1 adipocytes. From an initial value of 0.537 +/- 0.097 pmol glucose/10(6) cells, gl ycogen was depleted in a time-dependent manner in response to glucose deprivation, exhibiting a half-time of 6 h. Surprisingly, fructose did not prevent glycogen depletion. However, in such glycogen-depleted ad ipocytes, the alteration of GLUT-1 glycosylation in response to glucos e deprivation was more rapid than in normal adipocytes. Chinese hamste r ovary (CHO) cells, which synthesize abbreviated dolichol-linked olig osaccharides within minutes of glucose deprivation (J. I. Rearick, A. Chapman, and S. Kornfeld. J. Biol. Chem. 256: 6255-6261, 1981), contai ned only 1% of the level of glycogen found in 3T3-L1 adipocytes. Glyco sylation of GLUT-1 was altered in CHO cells within 3 h of glucose depr ivation. These data demonstrate that, during glucose stress, glycogen may serve as a buffer for oligosaccharide biosynthesis and provide a p otential explanation for varying sensitivities of different cell types to glucose deprivation.