Effects of prior moderate exercise on exogenous and endogenous lipid metabolism and plasma factor VII activity

2001 ◽  
Vol 100 (5) ◽  
pp. 517-527 ◽  
Author(s):  
Jason M. R. GILL ◽  
Keith N. FRAYN ◽  
Stephen A. WOOTTON ◽  
George J. MILLER ◽  
Adrianne E. HARDMAN
Keyword(s):  
Lipid Metabolism ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Factor Vii ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Moderate Exercise ◽  
Prior Exercise ◽  
Plasma Factor ◽  
Plasma Triacylglycerol

Moderate exercise reduces postprandial triacylglycerol concentrations, which are a risk marker for coronary heart disease. The present study sought to determine the qualitative nature of exercise-induced changes in lipid metabolism and their association (if any) with changes in factor VII activation. Eleven normotriglyceridaemic men, aged 51.7±6.1 years (mean±S.D.), participated in two oral fat tolerance tests after different pre-conditions: control (no exercise), and exercise (90 min of brisk walking the day before). Venous blood samples were obtained in the fasted state and for 8 h after ingestion of a high-fat meal (1.32 g of fat, 1.36 g of carbohydrate, 0.30 g of protein and 10 mg of [1,1,1-13C] tripalmitin·kg-1 body mass). Prior exercise reduced postprandial plasma triacylglycerol concentrations by 25±3% (mean±S.E.M.), with lower concentrations in the Svedberg flotation rate (Sf) 20–400 (very-low-density lipoprotein) fraction accounting for 79±10% of this reduction. There was no effect on plasma factor VII coagulant activity or on the concentration of the active form of factor VIIa. Prior exercise increased postprandial serum 3-hydroxybutyrate and plasma fatty acid concentrations, decreased serum postprandial insulin concentrations and increased exogenous (8 h 13C breath excretion of 15.1±0.9% of ingested dose compared with 11.9±0.8%; P = 0.00001) and endogenous postprandial fat oxidation. These data raise the possibility that reduced hepatic secretion of very-low-density lipoprotein plays a role in the attenuation of plasma triacylglycerol concentrations seen after exercise, although it is possible that increased triacylglycerol clearance also contributes to this effect.

Very low density lipoprotein and low density lipoprotein isolated from patients with hepatitis C infection induce altered cellular lipid metabolism

2007 ◽  
Vol 79 (3) ◽  
pp. 254-258 ◽  
Author(s):  
Mariarosaria Napolitano ◽  
Alessandro Giuliani ◽  
Tonino Alonzi ◽  
Carmine Mancone ◽  
Gianpiero D'Offizi ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepatitis C ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Cellular Lipid ◽  
Hepatitis C Infection

scholarly journals Leptin Augments the Acute Suppressive Effects of Insulin on Hepatic Very Low-Density Lipoprotein Production in Rats

Endocrinology ◽  
2009 ◽  
Vol 150 (5) ◽  
pp. 2169-2174 ◽  
Author(s):  
Wan Huang ◽  
Anantha Metlakunta ◽  
Nikolas Dedousis ◽  
Heidi K. Ortmeyer ◽  
Maja Stefanovic-Racic ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Fatty Acid Oxidation ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Saline Control ◽  
Acid Oxidation ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Vldl Metabolism

It is well established that leptin increases the sensitivity of carbohydrate metabolism to the effects of insulin. Leptin and insulin also have potent effects on lipid metabolism. However, the effects of leptin on the regulation of liver lipid metabolism by insulin have not been investigated. The current study addressed the effects of leptin on insulin-regulated hepatic very low-density lipoprotein (VLDL) metabolism in vivo in rats. A 90-min hyperinsulinemic/euglycemic clamp (4 mU/kg · min−1) reduced plasma VLDL triglyceride (TG) by about 50% (P < 0.001 vs. saline control). Importantly, a leptin infusion (0.2 μg/kg · min−1) in combination with insulin reduced plasma VLDL-TG by about 80% (P < 0.001 vs. insulin alone). These effects did not require altered skeletal muscle lipoprotein lipase activity but did include differential effects of insulin and leptin on liver apolipoprotein (apo) B and TG metabolism. Thus, insulin decreased liver and plasma apoB100/B48 levels (∼50%, P < 0.01), increased liver TGs (∼20%, P < 0.05), and had no effect on fatty acid oxidation. Conversely, leptin decreased liver TGs (∼50%, P < 0.01) and increased fatty acid oxidation (∼50%, P < 0.01) but had no effects on liver or plasma apoB levels. Importantly, the TG-depleting and prooxidative effects of leptin were maintained in the presence of insulin. We conclude that leptin additively increases the suppressive effects of insulin on hepatic and systemic VLDL metabolism by stimulating depletion of liver TGs and increasing oxidative metabolism. The net effect of the combined actions of insulin and leptin is to decrease the production and TG content of VLDL particles.

scholarly journals miR-130b is a potent stimulator of hepatic very-low-density lipoprotein assembly and secretion via marked induction of microsomal triglyceride transfer protein

2020 ◽  
Vol 318 (2) ◽  
pp. E262-E275 ◽  
Author(s):  
Jing Zhang ◽  
Ferdous Rastgar Jazii ◽  
Mahdi Montazer Haghighi ◽  
Danielle Alvares ◽  
Lipei Liu ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepg2 Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Microsomal Triglyceride Transfer Protein ◽  
Luciferase Reporter ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Transfer Protein ◽  
Stimulation Of

miR-130b is a microRNA whose expression is particularly elevated within adipose tissue and in the circulation in diabetic states. Hepatic miR-130b expression has been linked to hepatocellular carcinoma and changes in lipid metabolism. Here, we investigated the role of miR-130b in hepatic lipid homeostasis and lipoprotein export. We observed that overexpression of miR-130b-3p or -5p in HepG2 cells markedly enhanced the secretion of very-low-density lipoprotein (VLDL) particles, enhanced the secretion of [3H]glycerol metabolically labeled triglyceride (TG), and significantly increased the number or the average size of lipid droplets (LDs), respectively. Overexpression of miR-130b also altered the expression of key genes involved in lipid metabolism and in particular markedly increased both mRNA and protein expression levels of microsomal triglyceride transfer protein (MTP). Conversely, the miR-130b inhibitor decreased mRNA levels of MTP and fatty acid synthase ( FAS) in HepG2 cells. However, dual-luciferase reporter assays indicated that MTP is not a direct target of miR-130b-3p. miR-130b overexpression did not alter de novo synthesized TG or the stability and secretion of apolipoprotein B 100. Interestingly, knockdown of phosphatase and tensin homolog ( PTEN) blocked the upregulation of MTP mRNA induced by miR-130b. Finally, miR-130b-induced stimulation of VLDL secretion was also observed in a second hepatocyte cell culture model, immortalized human hepatocytes, confirming the effects observed in HepG2 cells. Overall, these data suggest a potential role for miR-130b in promoting hepatic VLDL assembly and secretion mediated by marked stimulation of MTP expression and TG mobilization. Thus miR-130b overexpression corrects the defect in VLDL production in HepG2 cells.

A role for hepatic leptin signaling in lipid metabolism via altered very low density lipoprotein composition and liver lipase activity in mice

Hepatology ◽  
2012 ◽  
Vol 57 (2) ◽  
pp. 543-554 ◽  
Author(s):  
Frank K. Huynh ◽  
Ursula H. Neumann ◽  
Ying Wang ◽  
Brian Rodrigues ◽  
Timothy J. Kieffer ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Lipase Activity ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Leptin Signaling ◽  
Lipoprotein Composition

Effect of in vitro Cultured Anoectochilus formosanus on Lipid Metabolism in Clinical Uses

2007 ◽  
Vol 35 (05) ◽  
pp. 735-741 ◽  
Author(s):  
Xiao-Ming Du ◽  
Ning-Yi Sun ◽  
Norihiro Furusho ◽  
Jun Hayashi ◽  
Yukihiro Shoyama
Keyword(s):  
Lipid Metabolism ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Serum Levels ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
High Cholesterol ◽  
Anoectochilus Formosanus ◽  
High Triglyceride

A clinical study was performed on the effect of in vitro cultured Anoectochilus formosanus HAYATA on lipid-metabolism. Sixty-six volunteers, including 36 healthy, 14 high-triglyceride-, 11 high-cholesterol- and 5 high-triglyceride- and high cholesterol- subjects, were administrated with A. formosanus (450 mg/day) for 6 months or 12 months. A. formosanus significantly decreased the concentrations of the serum levels of cholesterol, low density lipoprotein and very low density lipoprotein in all volunteers. The results of the present study suggested that A. formosanus might function as a liver activator resulting in improvement of lipid-metabolism.

Peripheral triacylglycerol extraction in the fasting and post-prandial states

1991 ◽  
Vol 81 (5) ◽  
pp. 621-626 ◽  
Author(s):  
Jennifer L. Potts ◽  
Rachel M. Fisher ◽  
Sandy M. Humphreys ◽  
Simon W. Coppack ◽  
Geoffrey F. Gibbons ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Inverse Correlation ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Fasting Plasma ◽  
Triacylglycerol Concentration ◽  
Plasma Triacylglycerol ◽  
Forearm Muscle

1. Triacylglycerol extraction by subcutaneous adipose tissue and forearm muscle was studied in nine normal subjects after an overnight fast and after the consumption of a mixed meal. 2. There was an inverse correlation between the total plasma fractional triacylglycerol extraction across the adipose tissue and the fasting arterial plasma triacylglycerol concentration. In contrast, there was no correlation between the lower fractional triacylglycerol extraction across the forearm muscle and the fasting plasma triacylglycerol concentration. 3. Chylomicron-triacylglycerol concentrations in arterial(ized) plasma increased post-prandially and peaked at 240–300 min. There was a comparable increase in the very-low-density lipoprotein-triacylglycerol concentration, peaking at 300 min. 4. Clearance of chylomicron-triacylglycerol by adipose tissue increased after the meal (P <0.05). In contrast, the clearance of very-low-density lipoprotein-triacylglycerol by adipose tissue decreased post-prandially (P <0.05). 5. Although there was significant uptake of chylomicron-triacylglycerol by the forearm muscle post-prandially, this was less than by the adipose tissue. Very-low-density lipoprotein-triacylglycerol was unaffected by passage through the forearm muscle at any time. 6. We conclude that the extraction of lipoprotein-triacylglycerol by human adipose tissue is important in determining the fasting plasma triacylglycerol concentration. Chylomicron-triacylglycerol, appearing in the plasma post-prandially, may compete with very-low-density lipoprotein-triacylglycerol for clearance by adipose tissue lipoprotein lipase, and this mechanism may explain, at least in part, the post-prandial rise in very-low-density lipoprotein-triacylglycerol. Forearm muscle, in contrast, appears to play a much smaller role in the extraction of plasma triacylglycerol, especially that in the very-low-density lipoprotein fraction.

ARHGAP21 deficiency impairs hepatic lipid metabolism and improves insulin signaling in lean and obese mice

2019 ◽  
Vol 97 (11) ◽  
pp. 1018-1027 ◽  
Author(s):  
Lucas Zangerolamo ◽  
Gabriela Moreira Soares ◽  
Jean Franciesco Vettorazzi ◽  
Maria Esméria do Amaral ◽  
Everardo Magalhães Carneiro ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Protein Expression ◽  
Insulin Signaling ◽  
Liver Lipid ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Microsomal Triglyceride Transfer Protein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Gene And Protein Expression

ARHGAP21 is a Rho-GAP that controls GTPases activity in several tissues, but its role on liver lipid metabolism is unknown. Thus, to achieve the Rho-GAP role in the liver, control and ARHGAP21-haplodeficient mice were fed chow (Ctl and Het) or high-fat diet (Ctl-HFD and Het-HFD) for 12 weeks, and pyruvate and insulin tolerance tests, insulin signaling, liver glycogen and triglycerides content, gene and protein expression, and very-low-density lipoprotein secretion were measured. Het mice displayed reduced body weight and plasma triglycerides levels, and increased liver insulin signaling. Reduced gluconeogenesis and increased glycogen content were observed in Het-HFD mice. Gene and protein expression of microsomal triglyceride transfer protein were reduced in both Het mice, while the lipogenic genes SREBP-1c and ACC were increased. ARHGAP21 knockdown resulted in hepatic steatosis through increased hepatic lipogenesis activity coupled with decreases in CPT1a expression and very-low-density lipoprotein export. In conclusion, liver of ARHGAP21-haplodeficient mice are more insulin sensitive, associated with higher lipid synthesis and lower lipid export.

scholarly journals In vitro study of the effect of raloxifene on lipid metabolism compared with tamoxifen

2000 ◽  
Vol 143 (3) ◽  
pp. 427-430 ◽  
Author(s):  
Y Hozumi ◽  
M Kawano ◽  
VC Jordan
Keyword(s):  
Oleic Acid ◽  
Lipid Metabolism ◽  
Total Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Tamoxifen Treatment ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Intracellular Concentrations

OBJECTIVE: Tamoxifen and raloxifene, selective estrogen receptor modulators, decrease serum concentrations of total cholesterol; however, the effect of these drugs on triglyceride metabolism is unclear. In the present study, we investigated the in vitro effect of raloxifene on lipid metabolism and compared it with that of tamoxifen. DESIGN AND METHODS: Intracellular concentrations of total cholesterol and triglyceride in HepG2 cells were measured by an enzymatic method after tamoxifen or raloxifene treatment with or without oleic acid and with or without very low density lipoprotein. RESULTS: Intracellular concentrations of total cholesterol and triglyceride without oleic acid or very low density lipoprotein were not significantly different after treatment with tamoxifen or raloxifene. In contrast, although raloxifene with oleic acid did not increase the intracellular concentrations of triglyceride, tamoxifen treatment in the presence of oleic acid or very low density lipoprotein significantly increased (P<0.05) the triglyceride concentrations. CONCLUSION: The present study suggests that raloxifene does not increase intracellular triglyceride in the presence of oleic acid or very low density lipoprotein, in contrast to tamoxifen. Therefore, raloxifene might be safer than tamoxifen for treating patients with unstable triglyceride levels or a history of hypertriglyceridemia.

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