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
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.