scholarly journals Dietary cholesterol does not affect the synthesis of apolipoproteins B and E by rat hepatocytes

1985 ◽  
Vol 227 (1) ◽  
pp. 29-35 ◽  
Author(s):  
R A Davis ◽  
M Malone-McNeal
Keyword(s):  
Apolipoprotein E ◽  
Apolipoprotein B ◽  
Lipid Droplets ◽  
Monolayer Culture ◽  
De Novo ◽  
Dietary Cholesterol ◽  
Rat Hepatocytes ◽  
Experimental Period ◽  
Serum Concentrations ◽  
Hepatic Apolipoprotein

To examine the unproved hypothesis that dietary cholesterol affects the synthesis of apolipoprotein B and E, we fed rats a cholesterol-rich diet that has been shown to alter dramatically the serum concentrations of these apolipoproteins. Rats fed for 4 weeks on a cholesterol-rich diet accumulate increased concentrations of low Mr apolipoprotein B (+2.7-fold) and decreased concentrations of apolipoprotein E (-40%) in their serum. Hepatocytes obtained from similarly treated rats were placed in monolayer culture and the rate of synthesis de novo of apolipoproteins was determined. Although cells from cholesterol-fed rats remained filled with lipid droplets throughout the experimental period, there was no difference in plating efficiency or viability, compared with cells obtained from chow-fed control rats. Both groups of cells synthesized and secreted immunoprecipitable apolipoproteins B and E at similar rates throughout the 18 h experiment. Thus there was a discordance between the effects of dietary cholesterol on serum apolipoprotein concentrations and hepatocyte synthesis and secretion. The data indicate that altered hepatic apolipoprotein synthesis cannot account for the changes in serum apolipoprotein concentrations caused by dietary cholesterol.

scholarly journals Hepatic apolipoprotein E expression promotes very low density lipoprotein-apolipoprotein B production in vivo in mice

2000 ◽  
Vol 41 (10) ◽  
pp. 1673-1679 ◽  
Author(s):  
Cyrille Maugeais ◽  
Uwe J.F. Tietge ◽  
Kazuhisa Tsukamoto ◽  
Jane M. Glick ◽  
Daniel J. Rader
Keyword(s):  
Apolipoprotein E ◽  
Apolipoprotein B ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Hepatic Apolipoprotein

Triacylglyceride physiology in the short-finned eel, Anguilla australis—changes throughout early oogenesis

2015 ◽  
Vol 308 (11) ◽  
pp. R935-R944 ◽  
Author(s):  
Erin L. Damsteegt ◽  
Ali Falahatimarvast ◽  
Sally P. A. McCormick ◽  
P. Mark Lokman
Keyword(s):  
Energy Balance ◽  
Apolipoprotein E ◽  
Lipoprotein Lipase ◽  
Apolipoprotein B ◽  
Serum Lipid ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
Anguilla Australis ◽  
Vitellogenin Receptor ◽  
Hepatic Apolipoprotein

During certain stages in an animal's life cycle, energy requirements may exceed energy intake from the diet. The spawning migration of temperate eels is a textbook example of negative energy balance, forcing these fish to rely on stored fats (triacylglycerides) to provide their muscles with energy for swimming and their growing oocytes with the nutrients needed to develop and support healthy offspring. We predicted broad implications of this great need for endogenous triacylglycerides in terms of their packaging, transport, and ovarian uptake. To test this, serum lipid concentrations and transcript abundances of intestinal and hepatic triacylglyceride packagers and ovarian triacylglyceride modifiers and receivers were investigated throughout previtellogenesis (feeding phase) and into early vitellogenesis (fasting phase) in short-finned eels. A switch from exogenous to endogenous triacylglyceride packaging was seen as the liver upregulated transcript levels of apolipoprotein B and microsomal triacylglyceride transport protein and downregulated those of apolipoprotein E and lipoprotein lipase. In the intestine, the reverse response was observed. Furthermore, ovarian transcript abundances of triacylglyceride modifiers and receivers increased (apolipoprotein E, lipoprotein lipase, and vitellogenin receptor), indicative of increased triacylglyceride uptake during previtellogenesis. We propose that increased hepatic apolipoprotein B production is a conserved vertebrate response to prolonged periods of negative energy balance.

Effects of extracellular ATP on hepatic fatty acid metabolism

1996 ◽  
Vol 270 (4) ◽  
pp. G701-G707 ◽  
Author(s):  
M. Guzman ◽  
G. Velasco ◽  
J. Castro
Keyword(s):  
Fatty Acid ◽  
De Novo ◽  
Specific Inhibitor ◽  
Rat Hepatocytes ◽  
Inhibitory Effect ◽  
Extracellular Atp ◽  
Acid Oxidation ◽  
A 23187 ◽  
Malonyl Coa ◽  
Cpt I

Incubation of rat hepatocytes with extracellular ATP inhibited acetyl-CoA carboxylase (ACC) activity and fatty acid synthesis de novo, with a concomitant decrease of intracellular malonyl-CoA concentration. However, both carnitine O-palmitoyltransferase I (CPT-I) activity and ketogenesis from palmitate were inhibited in parallel by extracellular ATP. The inhibitory effect of extracellular ATP on ACC and CPT-I activities was not evident in Ca2+ -depleted hepatocytes. Incubation of hepatocytes with thapsigargin, 2,5-di-(t-butyl)-1,4-benzohydroquinone (BHQ), or A-23187, compounds that increase cytosolic free Ca2+ concentration ([Ca2+]i), depressed ACC activity, whereas CPT-I activity was unaffected. The phorbol ester 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA) increased ACC activity, whereas it decreased CPT-I activity in a nonaddictive manner with respect to extracellular ATP. The inhibitory effect of extracellular ATP on ACC activity was also evident in the presence of bisindolyl-maleimide, a specific inhibitor of protein kinase C (PKC), whereas this compound abolished the extracellular ATP-mediated inhibition of CPT-I. In addition, the PMA-induced inhibition of CPT-I was not potentiated by thapsigargin, BHQ, or A-23187. Results thus show 1) that the intracellular concentration of malonyl-CoA is not the factor responsible for the inhibition of hepatic long-chain fatty acid oxidation by extracellular ATP, and 2) that the inhibition of ACC by extracellular ATP may be mediated by an elevation of [Ca2+]i, whereas CPT-I may be inhibited by extracellular ATP through a PKC-dependent mechanism.

Sign in / Sign up

Export Citation Format

Share Document