scholarly journals Interaction of non-esterified fatty acid and insulin in control of triacylglycerol secretion by Hep G2 cells

1991 ◽  
Vol 280 (1) ◽  
pp. 99-104 ◽  
Author(s):  
C D Byrne ◽  
N P J Brindle ◽  
T W M Wang ◽  
C N Hales
Keyword(s):  
Oleic Acid ◽  
Fatty Acid ◽  
Acid Uptake ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Initial Concentration ◽  
Triacylglycerol Metabolism ◽  
Triacylglycerol Synthesis ◽  
Rat Liver Cells ◽  
G2 Cells

The role of insulin in the regulation of plasma triacylglycerol is poorly understood. Conflicting actions of insulin on rat liver cells have been reported, insulin inhibiting triacylglycerol secretion in short incubations (less than 24 h) and stimulating triacylglycerol secretion in longer incubations (48-72 h). The present study was undertaken to examine regulation of triacylglycerol secretion by insulin and investigate the interaction between insulin and non-esterified fatty acid over 72 h in human hepatoblastoma (Hep G2) cells. Insulin inhibited triacylglycerol secretion throughout the 72 h period. The inhibition increased from 66% in the first 24 h to 88% in the final 24 h. Increasing the initial concentration of oleic acid from 200 microM to 1000 microM resulted in a 358% increase in triacylglycerol secretion and a 712% increase in accumulation over 24 h. Oleic acid uptake by the cells was rapid, with only 2.4% of the initial concentration (500 microM) remaining after 24 h. Supplementation of the medium with oleic acid to maintain the concentration between 750 microM and 1000 microM throughout a 5 h period resulted in a 350% increase in triacylglycerol secretion. Supplementation also decreased the insulin-induced inhibition of triacylglycerol secretion (18.2 to 7.8%; P less than 0.001). These results demonstrate that there is not a biphasic action of insulin on triacylglycerol secretion by Hep G2 cells. Experiments of this nature have not previously taken into account the rapid uptake of non-esterified fatty acid by hepatocytes and have consequently underestimated the effect of a sustained concentration on triacylglycerol metabolism. Oleic acid is therefore an even more potent stimulus to triacylglycerol synthesis and secretion than has previously been recognized. In addition, in the presence of a sustained increase in oleic acid concentration, there is a decrease in the action of insulin to inhibit triacylglycerol secretion.

Glutamic Acid Uptake Inhibition Assay in Cultured Hep G2 Cells as an Alternative Method for Evaluating Potential In Vivo Eye Irritation

1989 ◽  
Vol 16 (4) ◽  
pp. 344-352
Author(s):  
Paul J. Dierickx
Keyword(s):  
Glutamic Acid ◽  
Corneal Opacity ◽  
Acid Uptake ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Eye Irritation ◽  
Uptake Inhibition ◽  
Range Finding ◽  
G2 Cells

Glutamic acid (GA) content was measured in cultured Hep G2 cells, after treatment of the cells with test compounds. The results with 37 chemicals were compared with their respective rabbit eye irritation data, of which 17 were determined according to the OECD test, and the other 20 in range-finding studies. The chemicals were mainly organic solvents (alcohols, esters, amines, acids and others). The xenobiotics were applied to the cells for 4 hours at 5 different concentrations. The cells were then incubated for 15 minutes with tritiated GA. GA uptake inhibition was measured by liquid scintillation counting, and the results were expressed as the GI50 value, which is the concentration of test compound required to induce a 50% reduction in GA uptake. A linear correlation coefficient r = 0.66 was found between the log GI50 and the mean corneal opacity scores. This value is comparable to that obtained in total protein and uridine uptake inhibition studies. However, r = 0.81 was found when the log GI50 was compared with range-finding scores, indicating that a closer relationship exists between cytotoxicity and the latter.

scholarly journals Apolipoprotein B synthesized by Hep G2 cells undergoes fatty acid acylation.

1988 ◽  
Vol 29 (9) ◽  
pp. 1215-1220
Author(s):  
J M Hoeg ◽  
M S Meng ◽  
R Ronan ◽  
S J Demosky ◽  
T Fairwell ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Apolipoprotein B ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
G2 Cells

Quantitation of the Mass of Fatty Acid Ethyl Esters Synthesized by Hep G2 Cells Incubated with Ethanol

1998 ◽  
Vol 22 (5) ◽  
pp. 1125-1131 ◽  
Author(s):  
Li Dan ◽  
Joanne E. Cluette-Brown ◽  
Ayman Kabakibi ◽  
Michael Laposata
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Ethyl Esters ◽  
Ethyl Esters ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
G2 Cells

scholarly journals Triacylglycerol metabolism in isolated rat kidney cortex tubules

1980 ◽  
Vol 186 (1) ◽  
pp. 317-324 ◽  
Author(s):  
Gabriele Wirthensohn ◽  
Walter G. Guder
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Kidney Cortex ◽  
Acid Uptake ◽  
Rat Kidney Cortex ◽  
Glycerol Moiety ◽  
Triacylglycerol Metabolism ◽  
Triacylglycerol Synthesis ◽  
Lipid Formation ◽  
Gluconeogenic Substrates

Triacylglycerol metabolism has been studied in kidney cortex tubules from starved rats, prepared by collagenase treatment. Triacylglycerol was determined by a newly developed fully enzymic method. Incubation of tubules in the absence of fatty acids led to a decrease of endogenous triacylglycerol by about 50% in 1h. Addition of albuminbound oleate or palmitate resulted in a steady increase of tissue triacylglycerol over 2h. The rate of triacylglycerol synthesis was linearly dependent on oleate concentration up to 0.8mm, reaching a saturation at higher concentrations. Triacylglycerol formation from palmitate was less than that from oleate. This difference was qualitatively the same when net synthesis was compared with incorporation of labelled fatty acids. Quantitatively, however, the difference was less with the incorporation technique. Gluconeogenic substrates, which by themselves had no effect on triacylglycerol concentrations, stimulated neutral lipid formation from fatty acids. Glucose and lysine did not have such a stimulatory effect. Inhibition of gluconeogenesis from lactate by mercaptopicolinic acid likewise inhibited triacylglycerol formation. This inhibitory effect was seen with oleate as well as with oleate plus lactate. When [2-14C]lactate was used the incorporation of label into triacylglycerol was found in the glycerol moiety exclusively. Addition of dl-β-hydroxybutyrate (5mm) to the incubation medium in the presence of oleate or oleate plus lactate led to a significant increase in triacylglycerol formation. In contrast with the gluconeogenic substrates, dl-β-hydroxybutyrate had no stimulatory effect on fatty acid uptake. The results suggest that renal triacylglycerol formation is a quantitatively important metabolic process. The finding that gluconeogenic substrates, but not glucose, increase lipid formation, indicates that the glycerol moiety is formed by glyceroneogenesis in the proximal tubules. The effect of ketone bodies seems to be caused by the sparing action of these substrates on fatty acid oxidation. The decrease of triacylglycerol in the absence of exogenous substrates confirms previous conclusions that endogenous lipids provide fatty acids for renal energy metabolism.

Hovenia DulcisExtract Reduces Lipid Accumulation in Oleic Acid-Induced Steatosis of Hep G2 Cells via Activation of AMPK and PPARα/CPT-1 Pathway and in Acute Hyperlipidemia Mouse Model

2016 ◽  
Vol 31 (1) ◽  
pp. 132-139 ◽  
Author(s):  
Bonglee Kim ◽  
Moon-Jea Woo ◽  
Chul-Soo Park ◽  
Sang-Hun Lee ◽  
Jin-Soo Kim ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Mouse Model ◽  
Lipid Accumulation ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
G2 Cells

Insulin increases fatty acid synthase gene transcription in human adipocytes

1998 ◽  
Vol 274 (5) ◽  
pp. R1253-R1259 ◽  
Author(s):  
Kate J. Claycombe ◽  
Brynn H. Jones ◽  
Melissa K. Standridge ◽  
Yingshi Guo ◽  
Joseph T. Chun ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthase ◽  
Hepatoma Cells ◽  
Human Adipocytes ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Mrna Stabilization ◽  
Fas Mrna ◽  
Mrna Content ◽  
G2 Cells

The purpose of this study was to investigate the molecular mechanism whereby insulin increases expression of a key de novo lipogenic gene, fatty acid synthase ( FAS), in cultured human adipocytes and hepatoma cells. RNA isolated from cultured adipocytes or from Hep G2 cells treated with or without insulin (20 nM) was analyzed. In addition, run-on transcription assays and measurements of RNA half-life were performed to determine the controlled step in FAS gene regulation by insulin. We demonstrated that FAS mRNA was expressed in both Hep G2 cells and human adipocytes. Insulin induced an approximately five- and threefold increase in FAS mRNA content in adipocytes and hepatoma cells, respectively. Similar regulation of FAS was observed in adipocytes from lean and obese human subjects. Furthermore, we demonstrated that the induction of human FAS expression by insulin was due to increased transcription rate of the FAS gene in human adipocytes, whereas mRNA stabilization accounted for increased FAS mRNA content in hepatoma cells. In conclusion, we report here for the first time expression of human FAS mRNA and its specific transcriptional induction by insulin in cultured human adipocytes.

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