Very-low-density lipoprotein triglyceride kinetics in acute and chronic carbohydrate-fed rats

1988 ◽  
Vol 255 (3) ◽  
pp. E236-E240 ◽  
Author(s):  
T. Hirano ◽  
J. Mamo ◽  
M. Poapst ◽  
G. Steiner
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Water Control ◽  
Catabolic Rate ◽  
Identical Manner ◽  
Vldl Triglyceride ◽  
Control Plasma ◽  
Drinking Solution

Very-low-density lipoprotein (VLDL)-triglyceride (TG) kinetics were examined in rats maintained on either chow and water (control) or chow and a 10% carbohydrate drinking solution (fructose or glucose). The hexose solutions were available for an acute (16 h) or chronic (14 day) period. The acute fructose (AF), acute glucose (AG), and chronic fructose (CF) groups were hypertriglyceridemic (HTG) compared with control. Plasma TG concentration in chronic glucose (CG)-fed rats was similar to control. VLDL-TG was endogenously radiolabeled in donor rats with [2-3H]-glycerol. The fractional catabolic rate (FCR) was then determined by monitoring the clearance of plasma [3H]VLDL-TG in recipient animals. Donors and recipients were treated in an identical manner. AF and CF groups had an FCR significantly lower than rats given glucose for comparable periods. Both fructose groups and the AG group also had a lower FCR than control. In contrast, FCR in the CG group was significantly higher than controls. TG production rate (TGPR) in both AF and CF fed rats did not significantly differ from controls, suggesting that the HTG observed in these animals was solely from a catabolic defect. AG- and CG-treated glucose animals both had TGPR significantly higher than controls. Therefore, overproduction of VLDL-TG contributed to the HTG associated with this carbohydrate.

Impaired very low-density lipoprotein-triglyceride catabolism in acute and chronic fructose-fed rats

1989 ◽  
Vol 256 (4) ◽  
pp. E559-E565 ◽  
Author(s):  
T. Hirano ◽  
J. C. Mamo ◽  
M. E. Poapst ◽  
A. Kuksis ◽  
G. Steiner
Keyword(s):  
Fatty Acid ◽  
Unsaturated Fatty Acid ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Acid Ratio ◽  
Apoprotein E ◽  
Vldl Triglyceride ◽  
Drinking Solution

Very low-density lipoprotein (VLDL)-triglyceride (TG) catabolism was compared in rats given chow and either a 10% fructose (F) or 10% glucose (G) drinking solution for both acute (A) (16 h) and chronic (C) (14 days) periods. VLDL-TG were labeled in F and G donor rats using different isotopic forms of glycerol. A mixture of the VLDLs was injected into F and G recipients and the decline in plasma TG radioactivities used as a measure of clearance. VLDL-TG from F donors was cleared more slowly than VLDL-TG from G donors. In F recipients, the half-life of VLDL-TG from either F or G donors was longer than that in G fed recipients. VLDL from the AF group, had a lower apoprotein E-to-C apoprotein ratio (E/C) than VLDL from the AG group. VLDL from both F groups had a lower E/C than did that from control rats. The E/C negatively correlated with plasma VLDL-TG. CF and CG VLDL had elevated CIII0 and lower CIII3 levels compared with their respective A groups and controls. The ratio of VLDL apoprotein B100, B95, and B48 did not differ between treatments. AF and AG VLDL were larger and enriched in TG compared with control or the CF and CG groups. The saturated fatty acid-to-unsaturated fatty acid ratio in VLDL-TG was higher in the G groups and AF group compared with controls. The present study suggests that the E/C may be lowered as a result of F consumption, thereby contributing to the impairment in VLDL-TG removal.

scholarly journals Reduced very-low-density lipoprotein fractional catabolic rate in apolipoprotein C1-deficient mice

1997 ◽  
Vol 321 (2) ◽  
pp. 445-450 ◽  
Author(s):  
Miek C. JONG ◽  
Janine H. van REE ◽  
Vivian E. H. DAHLMANS ◽  
Rune R. FRANTS ◽  
Marten H. HOFKER ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Fractional Catabolic Rate ◽  
Catabolic Rate ◽  
And Control ◽  
Deficient Mice

The function of apolipoprotein (apo) C1 in vivo is not clearly defined. Because transgenic mice overexpressing human apoC1 show elevated triacylglycerol (TG) levels [Simonet, Bucay, Pitas, Lauer and Taylor (1991) J. Biol. Chem. 266, 8651Ő8654], an as yet unknown role for apoC1 in TG metabolism has been suggested. Here we investigated directly the effect of the complete absence of apoC1 on very-low-density lipoprotein (VLDL)-TG lipolysis, clearance and production, by performing studies with the previously generated apoC1-deficient mice. On a sucrose-rich, low fat/low cholesterol (LFC) diet, apoC1-deficient mice accumulate in their circulation VLDL particles, which contain relatively lower amounts of lipids when compared with VLDL isolated from control mice. Lipolysis assays in vitro on VLDL from apoC1-deficient and control mice showed no differences in apparent Km and Vmax values (0.27ŷ0.06 versus 0.24ŷ0.03 mmol of TG/litre and 0.40ŷ0.03 versus 0.36ŷ0.03 mmol of non-esterified fatty acid (NEFA)/min per litre respectively). To correct for potential differences in the size of the VLDL particles, the resulting Km values were also expressed relative to apoB concentration. Under these conditions apoC1-deficient VLDL displayed a lower, but not significant, Km value when compared with control VLDL (3.44ŷ0.71 versus 4.44ŷ0.52 mmol of TG2/g apoB per litre). VLDL turnover studies with autologous injections of [3H]TG-VLDL in vivo showed that the VLDL fractional catabolic rate (FCR) was decreased by up to 50% in the apoC1-deficient mice when compared with control mice (10.5ŷ3.4 versus 21.0ŷ1.2/h of pool TG). No significant differences between apoC1-deficient and control mice were observed in the hepatic VLDL production estimated by Triton WR139 injections (0.19ŷ0.02 versus 0.21ŷ0.05 mmol/h of TG per kg) and in the extra-hepatic lipolysis of VLDL-TG (4.99ŷ1.62 versus 3.46ŷ1.52/h of pool TG) in vivo. Furthermore, [125I]VLDLŐapoB turnover experiments in vivo also showed a 50% decrease in the FCR of VLDL in apoC1-deficient mice when compared with control mice on the LFC diet (1.1ŷ0.3 versus 2.1ŷ0.1/h of pool apoB). When mice were fed a very high fat/high cholesterol (HFC) diet, the VLDLŐapoB FCR was further decreased in apoC1-deficient mice (0.4ŷ0.1 versus 1.4ŷ0.4/h of pool apoB). We conclude that, in apoC1-deficient mice, the FCR of VLDL is reduced because of impaired uptake of VLDL remnants by hepatic receptors, whereas the production and lipolysis of VLDL-TG is not affected.

Composition and metabolism of very low density lipoproteins in dog cardiaclymph

1981 ◽  
Vol 59 (8) ◽  
pp. 709-714 ◽  
Author(s):  
P. Julien ◽  
A. Angel
Keyword(s):  
Activity Ratio ◽  
Specific Activity ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Protein Ratio ◽  
Vldl Triglyceride

In the present study, very low density lipoprotein (VLDL, d < 1.006) in cardiac lymph was characterized to determine its role as a metabolic substrate in the interstitial compartment. A major efferent cardiac lymph trunk was cannulated in fasting (18 h) dogs (20–27 kg). Three to five millilitres of lymph were collected over 3–4 h at 4 °C. Cardiac lymph VLDL concentration was 1.7 ± 0.7 mg protein∙100 mL−1 compared with 1.8 ± 0.8 mg protein∙100 mL−1 in plasma. The VLDL triglyceride concentration in lymph was 1.0 ± 0.3 mg triglyceride∙100 mL−1 with triglyceride/protein ratio of 0.9 compared with plasma VLDL triglyceride of 5.0 ± 1.6 mg∙100 mL−1 with a triglyceride/protein ratio of 5.5. Electron microscopy of VLDL revealed globular particles with a mean diameter of 388 Å in lymph and 661 Å in plasma. Thus, cardiac lymph VLDL are smaller and contain less triglyceride per particle than plasma VLDL. Following i.v. administration of human 125I-labelled low density lipoprotein ([125I]LDL, d 1.025–1.045), cardiac lymph/plasma LDL specific activity ratio was 0.52 ± 0.15 (n = 3) and 0.55 ± 0.15 (n = 4) at 3 and 27 h, respectively. The fact that the specific activity ratio did not reach 1 at plateau suggests continuous addition of unlabelled LDL in the cardiac interstitium, presumably from VLDL precursors. These findings demonstrate that on a protein basis the concentration of VLDL in cardiac lymph equals that of plasma, and also suggests that VLDL degradation and LDL production occur in the cardiac interstitial space.

An approach to measuring the in vivo transformation of glycerol to a very low density lipoprotein triglyceride

1979 ◽  
Vol 57 (6) ◽  
pp. 613-617
Author(s):  
M. A. Kallai-Sanfaçon ◽  
K. H. Norwich ◽  
G. Steiner
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Steady State Rate ◽  
Serum Glycerol ◽  
State Rate ◽  
The Relationship ◽  
Vldl Triglyceride

This paper describes a new method which permits measurement of the steady-state rate of transformation of serum glycerol to a very low density lipoprotein (VLDL) triglyceride in vivo in dogs. Although the turnover of glycerol and the turnover of VLDL triglyceride glycerol have both been previously measured, the rate of transformation of the former into the latter has not. While there is considerable dog-to-dog variation in the absolute turnover and transformation rates, the relationship between the various rates is quite constant. Thus, 13% of the serum glycerol which normal fasting dogs utilize is converted to VLDL triglyceride. The remaining 87% is converted to other products. Also, 28% of VLDL triglyceride glycerol in these dogs is derived from serum glycerol. The balance, 72%, is derived from other sources. The procedure described here can be used to quantitate the contribution of glycerol to VLDL in a number of conditions in which glycerol and (or) VLDL triglyceride metabolism is altered, thereby providing another way to gain insight into the metabolism of VLDL. Even more generally, the principles developed here can be applied to estimate the transformation of other precursors to other products in vivo.

scholarly journals Decreased Efficiency of Very-Low-Density Lipoprotein Lipolysis Is Linked to Both Hypertriglyceridemia and Hypercholesterolemia, but It Can Be Counteracted by High-Density Lipoprotein

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1224
Author(s):  
Ewa Wieczorek ◽  
Agnieszka Ćwiklińska ◽  
Agnieszka Kuchta ◽  
Barbara Kortas-Stempak ◽  
Anna Gliwińska ◽  
...  
Keyword(s):  
High Density Lipoprotein ◽  
Electrophoretic Mobility ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Density ◽  
Lipid Lowering ◽  
Lower Percentage ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Vldl Triglyceride

Impaired triglyceride-rich lipoprotein plasma catabolism is considered the most important factor for hypertriglyceridemia development. The aim of this study was to evaluate the impact of hypercholesterolemia and hypertriglyceridemia on the efficiency of lipoprotein lipase (LPL)-mediated very-low-density lipoprotein (VLDL)-triglyceride lipolysis and the role of high-density lipoprotein (HDL) in this process. Subjects with no history of cardiovascular disease (CVD) and untreated with lipid-lowering agents were recruited into the study and divided into normolipidemic, hypercholesterolemic, and hyperlipidemic groups. VLDL was isolated from serum and incubated with LPL in the absence or presence of HDL. For the hypercholesterolemic and hyperlipidemic groups, a significantly lower percentage of hydrolyzed VLDL-triglyceride was achieved compared to the normolipidemic group (p < 0.01). HDL enhanced the lipolysis efficiency in the hypercholesterolemic and hyperlipidemic groups on average by ~7% (p < 0.001). The lowest electrophoretic mobility of the VLDL remnants indicating the most effective lipolysis was obtained in the normolipidemic group (p < 0.05). HDL presence significantly reduced the electrophoretic mobility of the VLDL remnants for the hypercholesterolemic and hyperlipidemic groups (p < 0.05). The results of our study indicate that VLDL obtained from hypercholesterolemic and hyperlipidemic subjects are more resistant to lipolysis and are additional evidence of the need for early implementation of hypocholesterolemic treatment, already in asymptomatic CVD subjects.

Effect of exogenous estrogens on catabolism of VLDL in cholesterol-fed rabbits

1981 ◽  
Vol 241 (5) ◽  
pp. E372-E377
Author(s):  
R. S. Kushwaha ◽  
W. R. Hazzard
Keyword(s):  
Apolipoprotein B ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Pool Size ◽  
Estrogen Treatment ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Fractional Catabolic Rate ◽  
Catabolic Rate ◽  
Metabolic Mechanism

To determine the metabolic mechanism of the hypolipidemic response to estrogen in cholesterol-fed rabbits, very low-density lipoprotein (VLDL) apolipoprotein B (apoB) turnover studies were conducted in cholesterol-fed animals with or without estrogen treatment. Autologous VLDL apoB had a more rapid fractional catabolic rate (FCR) in estrogen-treated than in untreated animals, but there was no difference in the radioactivity appearing in the intermediate-(IDL) and low- (LDL) density lipoproteins. Similar differences in the FCR were observed when isologous VLDL from donors in the opposite group was injected, suggesting that estrogen treatment in cholesterol-fed rabbits accelerated the catabolism of cholesterol- and apoE-rich lipoproteins by a mechanism that is not dependent on its conversion to LDL. Furthermore, VLDL apoB from normal untreated donor animals was catabolized more rapidly in the estrogen-treated animals, but most of the radioactivity appeared in LDL in both groups. These observations suggest that estrogen treatment of cholesterol-fed rabbits affected only the efficiency but not the completeness of catabolism of normal VLDL. Thus the catabolism of vLDL in cholesterol-fed animals treated with or without estrogen depended on the composition of VLDL injected and the pool size of plasma VLDL, which was reduced by estrogen treatment.

Metabolism of apoprotein B in cynomolgus monkey: evidence for independent production of low-density lipoprotein apoprotein B

1983 ◽  
Vol 244 (2) ◽  
pp. E196-E201
Author(s):  
I. J. Goldberg ◽  
N. A. Le ◽  
H. N. Ginsberg ◽  
J. R. Paterniti ◽  
W. V. Brown
Keyword(s):  
Cynomolgus Monkey ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Fractional Catabolic Rate ◽  
Catabolic Rate ◽  
Apoprotein B ◽  
The Mean

The catabolism of very-low-density lipoprotein apoprotein B and its conversion to low-density lipoprotein was studied in five chow-fed cynomolgus monkeys following injection of radioiodinated homologous very-low-density lipoproteins. The mean (+/- SD) fractional catabolic rate of very-low-density lipoprotein apoprotein B was 0.97 +/- 0.20 h-1 and the mean (+/- SD) production rate was 0.76 +/- 0.20 mg X kg-1 X h-1. The percent of conversion of very-low-density lipoprotein apoprotein B to low-density lipoprotein ranged from 33 to 59%. In separate studies of low-density lipoprotein apoprotein B turnover performed using homologous radiolabeled low-density lipoprotein in five additional animals, the mean (+/- SD) fractional catabolic rate for low-density lipoprotein apoprotein B was 0.050 +/- 0.017 h-1 and the mean (+/- SD) apoprotein B production rate was 0.70 +/- 0.18 mg X kg-1 X h-1. Comparison of the total low-density lipoprotein apoprotein B production with that derived from very-low-density lipoprotein apoprotein B suggested that a large fraction of plasma low-density lipoprotein apoprotein B was derived from a source exclusive of circulating very-low-density lipoprotein apoprotein B. This was confirmed in two animals by simultaneous injection of radiolabeled very-low-density and low-density lipoproteins. Thus, a significant proportion of cynomolgus monkey low-density lipoproteins are produced either by direct hepatic secretion or by rapid conversion of lower-density lipoproteins before they appear in the peripheral circulation.

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