Effects of moderate exercise on VLDL1and Intralipid kinetics in overweight/obese middle-aged men

2012 ◽  
Vol 302 (3) ◽  
pp. E349-E355 ◽  
Author(s):  
Iqbal A. R. Al-Shayji ◽  
Muriel J. Caslake ◽  
Jason M. R. Gill
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Kinetic Studies ◽  
Random Order ◽  
Moderate Exercise ◽  
Middle Aged ◽  
Production Rates ◽  
Multiple Blood ◽  
Exercise Induced ◽  
Induced Changes

Prior moderate exercise reduces plasma triglyceride (TG)-rich lipoprotein concentrations, mainly in the large very low-density lipoprotein (VLDL1) fraction, but the mechanism responsible is unclear. We investigated the effects of brisk walking on TG-rich lipoprotein kinetics using a novel method. Twelve overweight/obese middle-aged men underwent two kinetic studies, involving infusion of Intralipid to block VLDL1catabolism, in random order. On the afternoon prior to infusion, subjects either walked on a treadmill for 2 h at ∼50% maximal oxygen uptake or performed no exercise. Multiple blood samples were taken during and after infusion for separation of Intralipid (Sf400) and VLDL1(Sf60–400). VLDL1-TG and -apoB production rates were calculated from their linear rises during infusion; fractional catabolic rates (FCR) were calculated by dividing linear rises by fasting concentrations. Intralipid-TG FCR was determined from the postinfusion exponential decay. Exercise reduced fasting VLDL1-TG concentration by 30% ( P = 0.007) and increased TG enrichment of VLDL1particles [30% decrease in cholesteryl ester (CE)/TG ratio ( P = 0.007); 26% increase in TG/apoB ratio ( P = 0.059)]. Exercise also increased VLDL1-TG, VLDL1-apoB, and Intralipid-TG FCRs by 82, 146, and 43%, respectively (all P < 0.05), but had no significant effect on VLDL1-TG or -apoB production rates. The exercise-induced increase in VLDL1-apoB FCR correlated strongly with the exercise-induced changes in VLDL1CE/TG ( r = −0.659, r = 0.020) and TG/apoB ( r = 0.785, P = 0.002) ratios. Thus, exercise-induced reductions in VLDL1concentrations are mediated by increased catabolism, rather than reduced production, which may be facilitated by compositional changes to VLDL1particles that increase their affinity for clearance from the circulation.

scholarly journals Duration of coffee- and exercise-induced changes in the fatty acid profile of human serum

2003 ◽  
Vol 94 (2) ◽  
pp. 476-484 ◽  
Author(s):  
Vassilis Mougios ◽  
Susanne Ring ◽  
Anatoli Petridou ◽  
Michalis G. Nikolaidis
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Profile ◽  
Hdl Cholesterol ◽  
Random Order ◽  
Human Tissues ◽  
Moderate Exercise ◽  
Nonesterified Fatty Acids ◽  
Blood Samples ◽  
Exercise Induced ◽  
Induced Changes

Prolonged moderate exercise increases the concentration of nonesterified fatty acids (NEFA) and the ratio of unsaturated to saturated (U/S) NEFA in human plasma. The present study examined the duration of these effects and compared them with the effects of coffee ingestion. On separate days and in random order, seven men and six women 1) cycled for 1 h, 2) ingested coffee containing 5 mg caffeine/kg body mass, 3) ingested coffee followed by exercise 1 h later, and 4) did nothing. Blood samples were drawn at 0, 1, 2, 4, 8, 12, and 24 h. Serum was analyzed for lactate, glucose, glycerol, individual NEFA, triacylglycerols, total cholesterol, and HDL cholesterol. Exercise elevated the U/S NEFA and the percentage of oleate, while decreasing the percentages of palmitate and stearate, at the end of exercise but not subsequently. Consumption of coffee triggered a lower lipolytic response with no alterations in U/S or percentages of individual NEFA. These findings may prove useful in discovering mechanisms mediating the effects of exercise training on the fatty acid profile of human tissues.

Carbamazepine increases atherogenic lipoproteins: mechanism of action in male adults

2002 ◽  
Vol 282 (2) ◽  
pp. H704-H716 ◽  
Author(s):  
Susanne Brämswig ◽  
Anja Kerksiek ◽  
Thomas Sudhop ◽  
Claus Luers ◽  
Klaus Von Bergmann ◽  
...  
Keyword(s):  
Isotope Labeling ◽  
Low Density Lipoprotein ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Mevalonic Acid ◽  
Kinetic Studies ◽  
Low Density ◽  
Production Rates ◽  
Underlying Mechanisms ◽  
Cholesterol Precursors

Treatment with carbamazepine (CBZ) affects cholesterol concentrations, but little is known about the precise nature and underlying mechanisms of changes in lipoprotein metabolism. We investigated prospectively the effects of CBZ on lipid metabolism in normolipemic adults. In 21 healthy males, lipoprotein and noncholesterol sterol concentrations were measured before and during treatment with CBZ for 70 ± 18 days. Thirteen subjects underwent kinetic studies of apolipoprotein-B (ApoB) metabolism with the use of endogenous stable isotope labeling. Lipoprotein kinetic parameters were calculated by multicompartmental modeling. Significant increases in total cholesterol, in ApoB-containing lipoproteins [very-low-density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low-density lipoprotein (LDL)], and in triglycerides, but not in high-density lipoprotein (HDL), were observed. Lipoprotein particle composition remained unchanged. Mean fractional catabolic and production rates of ApoB-containing lipoproteins were not significantly different, although mean production rates of VLDL and IDL were substantially increased (+46 ± 139% and +30 ± 97%, respectively), whereas mean production of LDL remained unchanged (+2.1 ± 45.6%). Cholestanol in serum increased significantly but not the concentrations of plant sterols (campesterol, sitosterol) and the cholesterol precursors (lathosterol, mevalonic acid). There was a significant correlation between the decrease in free thyroxine and the increase in IDL cholesterol. Treatment with CBZ increases mainly ApoB-containing lipoproteins. CBZ seems not to influence endogenous cholesterol synthesis or intestinal absorption directly. The increase is neither related to increased ApoB production nor to decreased catabolism but is rather due to changes in the conversion cascade of IDL particles, most likely as an indirect effect through a decrease in thyroid hormones.

scholarly journals Development of Fatty Acid Reference Ranges and Relationship with Lipid Biomarkers in Middle-Aged Healthy Singaporean Men and Women

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 435
Author(s):  
Cody A. C. Lust ◽  
Xinyan Bi ◽  
Christiani Jeyakumar Henry ◽  
David W. L. Ma
Keyword(s):  
Disease Risk ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Multiple Regression Model ◽  
Dietary Fatty Acids ◽  
Lipid Biomarkers ◽  
Reference Ranges ◽  
Middle Aged ◽  
Serum Samples ◽  
Biologically Relevant

Dietary fatty acids (FA) are essential for overall human health, yet individual FA reference ranges have yet to be established. Developing individual FA reference ranges can provide context to reported concentrations and whether an individual displays deficient, or excess amounts of FA. Reference ranges of sixty-seven individual FA (μmol/L) were profiled and analyzed using gas chromatography with a flame ionization detector from serum samples collected from 476 middle-aged Singaporean males (BMI:23.3 ± 2.9) and females (BMI:21.8 ± 3.6). Measures of triglycerides (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), and total cholesterol (TC) (mmol/L) were also collected. The mean FA concentration seen in this cohort (11,458 ± 2478 was similar to that of overweight North American cohorts assessed in past studies. Ten biologically relevant FA were compared between sexes, with females exhibiting significantly higher concentrations in four FA (p < 0.05). A multiple regression model revealed the ten FA contributed significantly to nearly all lipid biomarkers (p < 0.05). A majority of participants who had FA concentrations in the ≥95th percentile also exhibited TG, HDL, LDL, and TC levels in the “high” risk classification of developing cardiovascular disease. Future studies profiling individual FA reference ranges in many unique, global cohorts are necessary to develop cut-off values of individual FA concentrations highly related to disease-risk.

scholarly journals The Importance of Fatty Acids as Nutrients during Post-Exercise Recovery

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 280 ◽  
Author(s):  
Anne-Marie Lundsgaard ◽  
Andreas M. Fritzen ◽  
Bente Kiens
Keyword(s):  
Skeletal Muscle ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Whole Body ◽  
Tissue Blood Flow ◽  
Peroxisome Proliferator ◽  
Early Recovery ◽  
Peroxisome Proliferator Activated Receptor ◽  
Post Exercise ◽  
Exercise Induced

It is well recognized that whole-body fatty acid (FA) oxidation remains increased for several hours following aerobic endurance exercise, even despite carbohydrate intake. However, the mechanisms involved herein have hitherto not been subject to a thorough evaluation. In immediate and early recovery (0–4 h), plasma FA availability is high, which seems mainly to be a result of hormonal factors and increased adipose tissue blood flow. The increased circulating availability of adipose-derived FA, coupled with FA from lipoprotein lipase (LPL)-derived very-low density lipoprotein (VLDL)-triacylglycerol (TG) hydrolysis in skeletal muscle capillaries and hydrolysis of TG within the muscle together act as substrates for the increased mitochondrial FA oxidation post-exercise. Within the skeletal muscle cells, increased reliance on FA oxidation likely results from enhanced FA uptake into the mitochondria through the carnitine palmitoyltransferase (CPT) 1 reaction, and concomitant AMP-activated protein kinase (AMPK)-mediated pyruvate dehydrogenase (PDH) inhibition of glucose oxidation. Together this allows glucose taken up by the skeletal muscles to be directed towards the resynthesis of glycogen. Besides being oxidized, FAs also seem to be crucial signaling molecules for peroxisome proliferator-activated receptor (PPAR) signaling post-exercise, and thus for induction of the exercise-induced FA oxidative gene adaptation program in skeletal muscle following exercise. Collectively, a high FA turnover in recovery seems essential to regain whole-body substrate homeostasis.

Physiological changes in hemostasis associated with acute exercise

1986 ◽  
Vol 60 (3) ◽  
pp. 986-990 ◽  
Author(s):  
M. E. Wheeler ◽  
G. L. Davis ◽  
W. J. Gillespie ◽  
M. M. Bern
Keyword(s):  
Factor Viii ◽  
Acute Exercise ◽  
Density Lipoprotein ◽  
Physiological Changes ◽  
Blood Samples ◽  
Maximum Effort ◽  
Exercise Induced ◽  
Induced Changes ◽  
Treadmill Protocol ◽  
Ristocetin Cofactor

Acute exercise enhances fibrinolytic (FA), factor VIII coagulant and factor VIII ristocetin cofactor activities, and increases the concentration of factor VIII-related antigen. Little is known concerning the mechanisms of these changes. To investigate possible relationships between exercise-induced changes in blood lactate, 2,3-diphosphoglycerate (DPG), and the hemostatic variables, a branching multistage treadmill protocol was used to exercise male volunteers to a maximum effort. Blood samples were drawn before, immediately post-, and 8 min postexercise. All hemostatic variables were significantly (P less than 0.05) increased postexercise. Highest values for factor VIII coagulant, factor VIII-related antigens and factor VIII ristocetin cofactor were observed at 8 min postexercise. Significant (P less than 0.001) correlations were found postexercise for lactate with factor VIII coagulant (r = 0.64), while no association between pre-, post-, or 8 min postexercise. Postexercise lactate demonstrated a significant correlation (r = +0.81), which was strengthened by including the preexercise high-density lipoprotein (HDL) concentrations (r = +0.87). Consequently, the expected postexercise FA may be calculated from the observed values for postexercise lactate and preexercise HDL. The correlations of lactate with postexercise FA and with postexercise factor VIII coagulant may reflect a common stimulus for these exercise-induced changes.

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.

scholarly journals Beta-very low density lipoprotein is sequestered in surface-connected tubules in mouse peritoneal macrophages.

1993 ◽  
Vol 123 (6) ◽  
pp. 1389-1402 ◽  
Author(s):  
J N Myers ◽  
I Tabas ◽  
N L Jones ◽  
F R Maxfield
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Kinetic Studies ◽  
Peritoneal Macrophages ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
The Novel ◽  
Mouse Macrophages ◽  
Tubular Surface ◽  
Fluorescence Quencher

beta-very low density lipoprotein (VLDL) is a large lipoprotein with multiple apoprotein E (apoE) molecules that bind to the LDL receptors on mouse macrophages. Even though they bind to the same receptor, the endocytic processing of beta-VLDL differs from low density lipoprotein (LDL). LDL is rapidly delivered to perinuclear lysosomes and degraded, but much of the beta-VLDL is retained in peripheral compartments for several minutes. We have investigated the properties of these peripheral compartments. Measurement of the pH was made using FITC-phosphatidylethanolamine incorporated into the beta-VLDL, and we found that the peripheral compartments were near neutral in pH. These peripheral, beta-VLDL containing compartments were poorly accessible to antibodies, but a low molecular weight fluorescence quencher (trypan blue) entered the compartments within a few seconds. Intermediate voltage EM of cells labeled with colloidal-gold-beta-VLDL revealed that the peripheral compartments are tubular, surface-connected invaginations. Kinetic studies with fluorescent beta-VLDL showed that the compartments become fully sealed with a half-time of 6 min, and the beta-VLDL is then delivered rapidly to perinuclear lysosomes. By monitoring fluorescence energy transfer between lipid analogs incorporated into the beta-VLDL, some processing of the lipoprotein in the peripheral tubular compartments is demonstrated. The novel mode of uptake of beta-VLDL may account for the high cholesterol ester accumulation induced by this lipoprotein.

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