Sources of blood glycerol during fasting

2001 ◽  
Vol 281 (5) ◽  
pp. E998-E1004 ◽  
Author(s):  
Michael D. Jensen ◽  
Visvanathan Chandramouli ◽  
William C. Schumann ◽  
Karin Ekberg ◽  
Stephen F. Previs ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Free Glycerol ◽  
Isotopic Equilibrium ◽  
Significant Percentage ◽  
Adipose Tissue Triglyceride ◽  
Vldl Triglyceride ◽  
Hydrolysis Of

To determine the source(s) of blood and very low density lipoprotein (VLDL)-triglyceride glycerol during fasting, four men ingested 2H2O from 14 to 20 h into a 60-h fast to achieve ∼0.5% body water enrichment. At 60 h of fasting, glycerol flux was measured using [2-14C]glycerol. Blood was taken for measurement of2H enrichment at carbon 6 of glucose and at carbon 3 of free glycerol and VLDL-triglyceride glycerol. 2H enrichment of the 2 hydrogens bound to carbon 3 of VLDL-triglyceride glycerol was 105 ± 2% of the 2H enrichment of the 2 hydrogens bound to carbon 6 of glucose, indicating isotopic equilibrium between hepatic glyceraldehyde 3- P and glycerol 3- P. The2H enrichment of the 2 hydrogens bound to carbon 3 of free glycerol was 17 ± 3% of VLDL-triglyceride glycerol, indicating that a significant percentage of free glycerol in blood originated from the hydrolysis of circulating VLDL-triglyceride or a pool of glycerol with similar 2H enrichment. Glycerol flux was 6.3 ± 1.1 μmol · kg−1 · min−1. Glycerol appearing from nonadipose tissue sources was then ∼1.1 μmol · kg−1 · min−1. Seven other subjects were fasted for 12, 42, and 60 h. A small percentage of glycerol in the circulation after 12 h of fasting was enriched with 2H. The enrichment of the 2 hydrogens bound to carbon 3 of free glycerol in the longer periods of fasting was ∼16% of the enrichment of the 2 hydrogens bound to carbon 6 of glucose. Therefore, as much as 15–20% of systemic glycerol turnover during fasting is not from lipolysis of adipose tissue triglyceride.

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.

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.

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.

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.

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