Secretion of apolipoproteins A-I and B by HepG2 cells: regulation by substrates and metabolic inhibitors.

Kempen, H.J.M.; Imbach, Alexander; Giller, Thomas; Neumann, W J; Hennes, U.; Nakada, Naoki

doi:10.1016/s0022-2275(20)41498-1

Cited by 19 publications

(5 citation statements)

References 38 publications

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“…In conclusion, our new experimental results with glucose provide further evidence that, in the HepG2 cell model of assembly and secretion of apoB-containing lipoproteins, TG synthesis is tightly linked to apoB secretion. These results are in accord with those of Kempen et al (33) who under somewhat differing conditions (DMEM rather than MEM in the culture media) found parallel increase in both apoB and TG secretion and with the recent report from . This model still leaves us without an explanation for the dissociation of apoB and TG secretion observed in vivo, in humans fed high carbohydrate diets, by Melish et al (49).…”

Section: Discussionsupporting

confidence: 93%

“…Unfortunately, no data for TG synthesis or cell mass was given by Arrol et al (51). Finally, Kempen et al (33) reported that glucose increased apoB secretion after incubations of 48 and 72 h, but not after a 24-h incubation. Kempen et al (33) stated that cell TG content was also increased after prolonged glucose treatment and, most importantly, demonstrated that inhibition of lipogenesis by either 8-Br-cyclic AMP or 5-(tetradecyloxy)-2-furancarboxylic acid inhibited apoB secretion.…”

Section: Discussionmentioning

confidence: 99%

“…Kempen et al (33) stated that cell TG content was also increased after prolonged glucose treatment and, most importantly, demonstrated that inhibition of lipogenesis by either 8-Br-cyclic AMP or 5-(tetradecyloxy)-2-furancarboxylic acid inhibited apoB secretion. Of interest, Kempen et al (33) conducted their studies in DMEM and found that when the HepG2 cells were incubated in MEM, basal rates of apoB secretion were higher, but the response to glucose, although still significant, was blunted. Kempen (33).…”

Section: Discussionmentioning

confidence: 99%

“…Of interest, Kempen et al (33) conducted their studies in DMEM and found that when the HepG2 cells were incubated in MEM, basal rates of apoB secretion were higher, but the response to glucose, although still significant, was blunted. Kempen (33). However, both our present data (negative for glucose effects on both TG synthesis and apoB secretion), and the data of Kempen et al (positive for effects of glucose on both TG synthesis and apoB secretion) demonstrate concordance between glucose effects on TG synthesis and apoB secretion.…”

Section: Discussionmentioning

confidence: 99%

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Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis

Jiang

Ginsberg²,

Wu³

1998

Journal of Lipid Research

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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 m m 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 [ 3 H]glycerol into [ 3 H]TG in the presence of 30 m m 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 m m 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.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis

Jiang

Ginsberg²,

Wu³

1998

Journal of Lipid Research

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“…TOFA (5-(tetradecyloxy)-2-furancarboxylic acid) is a representative of fatty acyl-CoA mimetics, reducing fatty acid synthesis by inhibiting ACCs when converted to a CoA derivative (TOFyl-CoA) (19,33,130,131). It has been demonstrated that TOFA can reduce lipid synthesis and TG secretion in cultured hepatic cells and the plasma TG levels and body weight in animals (130)(131)(132)(133)(134)(135). As a hypolipidemic agent, TOFA shows more potent inhibition than natural fatty acid, oleate (136).…”

Section: Acca As a Potential Target For Cancer Therapeuticsmentioning

confidence: 99%

Acetyl-CoA carboxylase-a as a novel target for cancer therapy

Wang

Rajput²,

Watabe³

et al. 2010

Front Biosci

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Acetyl-CoA carboxylases (ACC) are rate-limiting enzymes in de novo fatty acid synthesis, catalyzing ATP-dependent carboxylation of acetyl-CoA to form malonyl-CoA. Malonyl-CoA is a critical bi-functional molecule, i.e., a substrate of fatty acid synthase (FAS) for acyl chain elongation (fatty acid synthesis) and an inhibitor of carnitine palmitoyltransferase I (CPT-I) for fatty acid beta-oxidation. Two ACC isoforms have been identified in mammals, i.e. ACC-alpha (ACCA, also termed ACC1) and ACC-beta (ACCB, also designated ACC2). ACC has long been used as a target for the management of metabolic diseases, such as obesity and metabolic syndrome, and various inhibitors have been developed in clinical trials. Recently, ACCA up-regulation has been recognized in multiple human cancers, promoting lipogenesis to meet the need of cancer cells for rapid growth and proliferation. Therefore, ACCA might be effective as a potent target for cancer intervention, and the inhibitors developed for the treatment of metabolic diseases would be potential therapeutic agents for cancer therapy. This review summarizes our recent findings and updates the current understanding of the ACCA with focus on cancer research.

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Requirement of cytosolic phospholipase A2 gamma in lipid droplet formation

Liu

Zhang

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Secretion of apolipoproteins A-I and B by HepG2 cells: regulation by substrates and metabolic inhibitors.

Cited by 19 publications

References 38 publications

Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis

Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis

Acetyl-CoA carboxylase-a as a novel target for cancer therapy

Requirement of cytosolic phospholipase A2 gamma in lipid droplet formation

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