Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis
We have previously demonstrated a close relationship between oleic acid (OA)-stimulated triglyceride (TG) synthesis and apolipoprotein B (apoB) secretion in HepG2 cells. However, other investigators studying the association between glucose-stimulated TG synthesis and apoB secretion have reported var...
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Elsevier
1998-11-01
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Series: | Journal of Lipid Research |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S0022227520324834 |
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author | Hongshi Jiang Henry N. Ginsberg Xujun Wu |
author_facet | Hongshi Jiang Henry N. Ginsberg Xujun Wu |
author_sort | Hongshi Jiang |
collection | DOAJ |
description | We have previously demonstrated a close relationship between oleic acid (OA)-stimulated triglyceride (TG) synthesis and apolipoprotein B (apoB) secretion in HepG2 cells. However, other investigators studying the association between glucose-stimulated TG synthesis and apoB secretion have reported variable results. The present study was carried out to answer the question: does TG derived from glucose have different effects on apoB secretion from HepG2 cells compared to TG derived from oleate? We observed that incubations of HepG2 cells for as long as 48 h in 30 mm glucose did not increase apoB secretion. We then demonstrated that the failure of glucose to stimulate apoB secretion from HepG2 cells results from insufficient stimulation of TG synthesis by glucose. Thus, incorporation of [3H]glycerol into [3H]TG in the presence of 30 mm glucose for up till 48 h was not increased compared to basal conditions. The inability of glucose to stimulate TG synthesis was also evidenced by the inability of both 8-h and 24-h incubations with 30 mm glucose to increase cell TG mass; similar incubations with OA increased TG mass 50–100“%. Additional studies demonstrated that glucose conversion to either glycerol or fatty acids was minimal; this accounted for the lack of stimulation of TG synthesis. We conclude that in HepG2 cells, availability of high glucose levels in the media for as long as 48 h does not stimulate triglyceride synthesis, and that this is the basis for the failure of glucose to stimulate apoB secretion. —Jiang, H., H. N. Ginsberg, and X. Wu. Glucose does not stimulate apolipoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis. J. Lipid Res. 1998. 39: 2277–2285. |
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spelling | doaj.art-9ee53284736e490eacd29ae2dfff55f92022-12-21T19:36:36ZengElsevierJournal of Lipid Research0022-22751998-11-01391122772285Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesisHongshi Jiang0Henry N. Ginsberg1Xujun Wu2Department of Medicine, Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032To whom correspondence should be addressed.; Department of Medicine, Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032Department of Medicine, Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032We have previously demonstrated a close relationship between oleic acid (OA)-stimulated triglyceride (TG) synthesis and apolipoprotein B (apoB) secretion in HepG2 cells. However, other investigators studying the association between glucose-stimulated TG synthesis and apoB secretion have reported variable results. The present study was carried out to answer the question: does TG derived from glucose have different effects on apoB secretion from HepG2 cells compared to TG derived from oleate? We observed that incubations of HepG2 cells for as long as 48 h in 30 mm glucose did not increase apoB secretion. We then demonstrated that the failure of glucose to stimulate apoB secretion from HepG2 cells results from insufficient stimulation of TG synthesis by glucose. Thus, incorporation of [3H]glycerol into [3H]TG in the presence of 30 mm glucose for up till 48 h was not increased compared to basal conditions. The inability of glucose to stimulate TG synthesis was also evidenced by the inability of both 8-h and 24-h incubations with 30 mm glucose to increase cell TG mass; similar incubations with OA increased TG mass 50–100“%. Additional studies demonstrated that glucose conversion to either glycerol or fatty acids was minimal; this accounted for the lack of stimulation of TG synthesis. We conclude that in HepG2 cells, availability of high glucose levels in the media for as long as 48 h does not stimulate triglyceride synthesis, and that this is the basis for the failure of glucose to stimulate apoB secretion. —Jiang, H., H. N. Ginsberg, and X. Wu. Glucose does not stimulate apolipoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis. J. Lipid Res. 1998. 39: 2277–2285.http://www.sciencedirect.com/science/article/pii/S0022227520324834apoprotein BHepG2 cellstriglycerideglucosefatty acidsoleic acid |
spellingShingle | Hongshi Jiang Henry N. Ginsberg Xujun Wu Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis Journal of Lipid Research apoprotein B HepG2 cells triglyceride glucose fatty acids oleic acid |
title | Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis |
title_full | Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis |
title_fullStr | Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis |
title_full_unstemmed | Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis |
title_short | Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis |
title_sort | glucose does not stimulate apoprotein b secretion from hepg2 cells because of insufficient stimulation of triglyceride synthesis |
topic | apoprotein B HepG2 cells triglyceride glucose fatty acids oleic acid |
url | http://www.sciencedirect.com/science/article/pii/S0022227520324834 |
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