scholarly journals Fasting Inhibits the Recruitment of Kinesin‐1 to Lipid Droplets and Stalls Hepatic Triglyceride Secretion

Hepatology ◽  
2018 ◽  
Author(s):  
Ryan J. Schulze ◽  
Mark A. McNiven
Keyword(s):  
Lipid Droplets ◽  
Hepatic Triglyceride ◽  
Triglyceride Secretion

Essential fatty acid deficiency and plasma triglyceride turnover in rats

1980 ◽  
Vol 238 (5) ◽  
pp. E499-E505 ◽  
Author(s):  
M. T. Huang ◽  
M. A. Williams
Keyword(s):  
Fatty Acid ◽  
Essential Fatty Acid ◽  
Essential Fatty Acid Deficiency ◽  
Plasma Triglyceride ◽  
Hepatic Triglyceride ◽  
Triglyceride Accumulation ◽  
Essential Fatty Acid Deficient ◽  
Triglyceride Secretion ◽  
Acid Deficiency ◽  
Fatty Acid Deficiency

Hepatic triglyceride secretion in essential fatty acid-deficient rats was examined by three separate techniques in an effort to resolve conflicting evidence on the question of whether essential fatty acid deficiency altered hepatic triglyceride secretion in vivo. First, plasma triglyceride turnover was measured by intravenous injection of [2-3H]glycerol trioleate. Equations of the kinetics were formulated based on a single, open pool model. Turnover rates and pool sizes of plasma triglyceride were calculated from these equations. Second, [2-3H]glycerol was injected, and apparent rate constants for plasma triglyceride secretion and clearance were calculated by kinetic analysis. Third, Triton WR-1339 was used to inhibit lipoprotein clearance from blood plasma, and rates of plasma triglyceride accumulation were measured. The results of these studies showed that the rate of hepatic triglyceride secretion was 2-3 times greater in essential fatty acid-deficient rats than in nondeficient controls. The increase in triglyceride secretion, as well as the higher level of liver triglyceride typical of essential fatty acid-deficient rats, could be caused by increased lipogenesis and increased mobilization of fatty acids from adipose tissues.

LIF and CNTF, which share the gp130 transduction system, stimulate hepatic lipid metabolism in rats

1996 ◽  
Vol 271 (3) ◽  
pp. E521-E528 ◽  
Author(s):  
K. Nonogaki ◽  
X. M. Pan ◽  
A. H. Moser ◽  
J. Shigenaga ◽  
I. Staprans ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Acid Synthesis ◽  
Interleukin 4 ◽  
Dependent Manner ◽  
Hepatic Triglyceride ◽  
Serum Triglycerides ◽  
Triglyceride Secretion

We determined the effects of leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) on lipid metabolism in intact rats. Administration of LIF and CNTF increased serum triglycerides in a dose-dependent manner with peak values at 2 h. The effects of LIF and CNTF on serum cholesterol were very small, and serum glucose was unaffected. Both LIF and CNTF stimulated hepatic triglyceride secretion, hepatic de novo fatty acid synthesis, and lipolysis. Pretreatment with phenylisopropyl adenosine, which inhibits lipolysis, partially inhibited LIF- and CNTF-induced hypertriglyceridemia. Interleukin-4, which inhibits cytokine-induced hepatic fatty acid synthesis, also partially inhibited LIF- and CNTF-induced hypertriglyceridemia. These results indicate that both lipolysis and de novo fatty acid synthesis play a role in providing fatty acids for the increase in hepatic triglyceride secretion. Neither indomethacin nor adrenergic receptor antagonists affected the hypertriglyceridemia. The combination of LIF plus CNTF showed no additive effects consistent with the action of both cytokines through the gp130 transduction system. Thus LIF and CNTF have similar effects on lipid metabolism; they join a growing list of cytokines that stimulate hepatic triglyceride secretion and may mediate the changes in lipid metabolism that accompany the acute phase response.

The role of dietary fat and hepatic triglyceride secretion in cancer-induced hypertriglyceridemia

Lipids ◽  
1978 ◽  
Vol 13 (12) ◽  
pp. 887-891 ◽  
Author(s):  
Ramaswamy Kannan ◽  
Leon Wilson ◽  
Nome Baker
Keyword(s):  
Dietary Fat ◽  
Hepatic Triglyceride ◽  
Triglyceride Secretion

Glucose-stimulated insulin secretion suppresses hepatic triglyceride-rich lipoprotein and apoB production

2000 ◽  
Vol 279 (5) ◽  
pp. E1003-E1011 ◽  
Author(s):  
Doru V. Chirieac ◽  
Lucian R. Chirieac ◽  
James P. Corsetti ◽  
Joanne Cianci ◽  
Charles E. Sparks ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Serum Triglyceride ◽  
Hepatic Triglyceride ◽  
Triglyceride Secretion ◽  
Triglyceride Rich Lipoprotein ◽  
Apob Secretion ◽  
Glucose Stimulated Insulin Secretion

The current study assessed in vivo the effect of insulin on triglyceride-rich lipoprotein (TRL) production by rat liver. Hepatic triglyceride and apolipoprotein B (apoB) production were measured in anesthetized, fasted rats injected intravenously with Triton WR-1339 (400 mg/kg). After intravascular catabolism was blocked by detergent treatment, glucose (500 mg/kg) was injected to elicit insulin secretion, and serum triglyceride and apoB accumulation were monitored over the next 3 h. In glucose-injected rats, triglyceride secretion averaged 22.5 ± 2.1 μg · ml−1· min−1, which was significantly less by 30% than that observed in saline-injected rats, which averaged 32.1 ± 1.4 μg · ml−1· min−1. ApoB secretion was also significantly reduced by 66% in glucose-injected rats. ApoB immunoblotting indicated that both B100 and B48 production were significantly reduced after glucose injection. Results support the conclusion that insulin acts in vivo to suppress hepatic very low density lipoprotein (VLDL) triglyceride and apoB secretion and strengthen the concept of a regulatory role for insulin in VLDL metabolism postprandially.

scholarly journals Brain leptin reduces liver lipids by increasing hepatic triglyceride secretion and lowering lipogenesis

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Martina Theresa Hackl ◽  
Clemens Fürnsinn ◽  
Christina Maria Schuh ◽  
Martin Krssak ◽  
Fabrizia Carli ◽  
...  
Keyword(s):  
Hepatic Triglyceride ◽  
Liver Lipids ◽  
Triglyceride Secretion

scholarly journals Cod Protein Lowers the Hepatic Triglyceride Secretion Rate in Rats

2003 ◽  
Vol 133 (5) ◽  
pp. 1398-1402 ◽  
Author(s):  
Isabelle Demonty ◽  
Yves Deshaies ◽  
Benoît Lamarche ◽  
Hélène Jacques
Keyword(s):  
Secretion Rate ◽  
Hepatic Triglyceride ◽  
Triglyceride Secretion

Effects of Intravenous versus intragastric glucose pretreatment on triglyceride secretion by perfused livers of fed rats

1981 ◽  
Vol 59 (8) ◽  
pp. 580-585 ◽  
Author(s):  
D. J. Semple ◽  
B. M. Wolfe
Keyword(s):  
Porcine Insulin ◽  
Water Soluble ◽  
Hepatic Glycogen ◽  
Glucose Load ◽  
Hepatic Triglyceride ◽  
Intravenous Glucose ◽  
Total Liver ◽  
Triglyceride Secretion ◽  
The Mean

The effects of the route of administration of 450 mg [U-14C]glucose to 250-g fed rats in vivo on the subsequent release of triglycerides from the perfused liver was studied. Livers were perfused for 180 min using a nonrecycling medium containing 10 mM glucose, 2 mM lactate, 0.2 mM pyruvate, and 100 μU/mL porcine insulin. Biopsies were obtained at the beginning and end of the perfusions. The perfusate was collected and the secreted triglycerides were analyzed.Slower absorption of the intragastric glucose load contrasted with the rapid entry of the intravenous load; however, the total liver counts were not significantly affected by the route of glucose delivery. Hepatic glycogen concentration was also not significantly different, but the percent of total liver counts which was present in glycogen was significantly higher after intravenous glucose. The majority of the radioactivity in the livers of both groups of rats was present in water-soluble metabolites, with lesser amounts in triglycerides and phospholipids. Radioactivity in hepatic triglycerides declined significantly during perfusion only in the rats which had received glucose intravenously. The mean rate of triglyceride secretion from the livers of rats receiving the glucose intravenously was significantly lower than that of the rats receiving glucose intragastrically (0.21 ± 0.05 vs. 0.97 ± 0.28 mg/g liver per 180 min, p < 0.05). The route of glucose administration affects both entry of glucose into the blood and subsequent hepatic triglyceride metabolism and secretion.

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