Plasma lipids, lipoproteins, and triglyceride turnover in eu- and hypo-thyroid rats and rats on a hypocaloric diet

1981 ◽  
Vol 59 (8) ◽  
pp. 715-721 ◽  
Author(s):  
Ladislav Dory ◽  
Brian R. Krause ◽  
Paul S. Roheim

Lipid and lipoprotein concentration, and triglyceride turnover were studied in control, thyroidectomized, and pair-fed control rats (pair-fed to match the food intake of the thyroidectomized rats). Thyroidectomy induced a significant increase in plasma cholesterol (and low density lipoprotein) concentrations and a decrease in plasma triglyceride (and very low density lipoprotein) concentrations. Changes in similar direction but of smaller magnitude were observed in the plasma of the pair-fed control rats. To further investigate triglyceride metabolism in these three groups of animals, triglyceride turnover was studied in fasted, unrestrained, and unanesthetized rats, following injection of [2-3H]glycerol. Peak incorporation of [2-3H]glycerol into plasma triglyceride occurred in all three groups of animals at 25 min after precursor administration, although the maximal incorporation was substantially lower in the thyroidectomized group than in either of the control groups. Thereafter, plasma triglyceride radioactivity decayed monoexponentially with a half-life of 24 ± 1 min for both normal and pair-fed control rats, compared with the half-life of 41 ± 3 min observed in the thyroidectomized rats. The calculated apparent fractional catabolic rates were thus 0.029 min−1 for both control groups and only 0.017 min−1 for the thyroidectomized animals. The apparent total catabolic rates of plasma triglyceride were 299 ± 11, 138 ± 11, and 48 ± 4 μg triglyceride∙min−1 for the normal controls, pair-fed controls, and thyroidectomized rats, respectively. These data further emphasize the importance of thyroid hormones in regulating plasma lipid and lipoprotein metabolism and, specifically, indicate that hypothyroidism results in a reduction of triglyceride secretion into, and the removal from, circulation. Furthermore, evidence was presented that the decreased caloric intake of the hypothyroid animals cannot, in itself, account for this observation.

2021 ◽  
Vol 8 ◽  
Author(s):  
Dien Ye ◽  
Xiaofei Yang ◽  
Liwei Ren ◽  
Hong S. Lu ◽  
Yuan Sun ◽  
...  

Objective: Elevated plasma cholesterol concentrations contributes to ischemic cardiovascular diseases. Recently, we showed that inhibiting hepatic (pro)renin receptor [(P)RR] attenuated diet-induced hypercholesterolemia and hypertriglyceridemia in low-density lipoprotein receptor (LDLR) deficient mice. The purpose of this study was to determine whether inhibiting hepatic (P)RR could attenuate atherosclerosis.Approach and Results: Eight-week-old male LDLR−/− mice were injected with either saline or N-acetylgalactosamine-modified antisense oligonucleotides (G-ASOs) primarily targeting hepatic (P)RR and were fed a western-type diet (WTD) for 16 weeks. (P)RR G-ASOs markedly reduced plasma cholesterol concentrations from 2,211 ± 146 to 1,128 ± 121 mg/dL. Fast protein liquid chromatography (FPLC) analyses revealed that cholesterol in very low-density lipoprotein (VLDL) and intermediate density lipoprotein (IDL)/LDL fraction were potently reduced by (P)RR G-ASOs. Moreover, (P)RR G-ASOs reduced plasma triglyceride concentrations by more than 80%. Strikingly, despite marked reduction in plasma lipid concentrations, atherosclerosis was not reduced but rather increased in these mice. Further testing in ApoE−/− mice confirmed that (P)RR G-ASOs reduced plasma lipid concentrations but not atherosclerosis. Transcriptomic analysis of the aortas revealed that (P)RR G-ASOs induced the expression of the genes involved in immune responses and inflammation. Further investigation revealed that (P)RR G-ASOs also inhibited (P)RR in macrophages and in enhanced inflammatory responses to exogenous stimuli. Moreover, deleting the (P)RR in macrophages resulted in accelerated atherosclerosis in WTD fed ApoE−/− mice.Conclusion: (P)RR G-ASOs reduced the plasma lipids in atherosclerotic mice due to hepatic (P)RR deficiency. However, augmented pro-inflammatory responses in macrophages due to (P)RR downregulation counteracted the beneficial effects of lowered plasma lipid concentrations on atherosclerosis. Our study demonstrated that hepatic (P)RR and macrophage (P)RR played a counteracting role in atherosclerosis.


1973 ◽  
Vol 45 (5) ◽  
pp. 583-592 ◽  
Author(s):  
Gilbert R. Thompson ◽  
J. Paul Miller

1. Plasma lipids and lipoproteins have been studied in control subjects and patients with various types of steatorrhoea. 2. Low plasma cholesterol levels were found in malabsorbers and were associated with decreased amounts of low-density lipoprotein (LDL) in males and high-density lipoprotein (HDL) in females. 3. Serum triglyceride levels were normal in males, but exceeded control values in some of the females, due to an increase in very-low-density lipoprotein. 4. LDL composition was abnormal in both male and female malabsorbers, with a decreased proportion of cholesterol ester and an increased proportion of triglyceride. There was also an increased proportion of triglyceride in HDL. 5. These findings show that malabsorption markedly influences not only the concentration but also the composition of plasma lipoproteins.


1992 ◽  
Vol 262 (6) ◽  
pp. R947-R954 ◽  
Author(s):  
C. K. Fujihara ◽  
D. M. Limongi ◽  
H. C. De Oliveira ◽  
R. Zatz

The Nagase analbuminemic rat (NAR), a mutant of the Sprague-Dawley (SD) strain, exhibits high levels of plasma cholesterol (Chol), thrombocytosis, and enhanced platelet aggregability, which might promote glomerulosclerosis (GS). To determine whether NAR are more susceptible than SD rats to aging GS, young (3-mo-old) and aging (18-mo-old) SD rats and NAR were studied. In young NAR, glomerular pressure and glomerular volume were lower, whereas total and high-density lipoprotein plasma Chol levels were higher than in young SD rats. Aging SD rats developed glomerular hypertension and hypertrophy. Less glomerular enlargement and subnormal glomerular pressures were seen in aging NAR. Enhanced platelet aggregation developed in aging SD rats, approaching the values seen in NAR. Similarly elevated levels of low-density lipoprotein Chol were seen in additional SD rats and NAR studied at 12 mo of age. Plasma triglyceride (TG) levels were lower in NAR at this age. Only SD rats developed proteinuria and exhibited GS and glomerular lipid deposits at 18 mo of age. Reduced glomerular wall stress due to lower glomerular pressure and volume as well as lower TG levels may explain the absence of GS in aging NAR despite plasma lipid and platelet abnormalities.


Author(s):  
Raveenan Mingpakanee ◽  
Chatchanok Chaisitthichai ◽  
Nattaporn Wichitamporn ◽  
Paradee Sappittayakorn ◽  
Suparnnikar Phongphanwatana

Objective: The aim of the study was to investigate the effect of quail egg and hen egg supplements on lipoprotein profiles, low-density lipoprotein (LDL) oxidation and small dense LDL cholesterol (sd-LDL-C) in young healthy people, compared with hen eggs. Material and Methods: Twenty-three healthy volunteers (11 men and 12 women) were randomly assigned to consume 3 whole hen eggs per day (hen group, n=11) (total cholesterol 633 mg) or 9 quail eggs per day (quail group, n=12) (total cholesterol 459 mg) for 30 days. The plasma cholesterol and plasma triglyceride concentrations and lipoprotein fractions (Triglyceride-rich lipoprotein; TRL, LDL and high-density lipoprotein; HDL) were determined at baseline and after the 30-day period of egg consumption. The LDL oxidation (lag time) was measured by the increase of conjugated diene production. Sd-LDL-C was calculated from the major lipid and lipoprotein parameters. Results: In the quail group, plasma triglyceride (TG) and LDL-TG were significantly decreased, whereas the plasma cholesterol and HDL-C were unchanged. There was no alteration in lipoprotein profiles in the hen group. The LDL lag time of the quail group was longer than at baseline. There were no significant changes in sd-LDL-C levels in both groups during the study.Conclusion: Quail egg and hen egg consumptions for 30 days did not change the lipoprotein profiles, sd-LDL as well as the LDL-oxidation, which not modified the cardiovascular disease risk factor.


1994 ◽  
Vol 86 (3) ◽  
pp. 323-329 ◽  
Author(s):  
Shui-Ping Zhao ◽  
Arn M. J. M. Van den Maagdenberg ◽  
Ton F. F. P. Vroom ◽  
Ferdinand M. Van't Hooft ◽  
Jan A. Gevers Leuven ◽  
...  

1. The plasma lipoprotein profiles of eight members of a Dutch pedigree spanning three generations where two rare apolipoprotein E mutants, APOE*3(Cys-112→Arg; Arg-251→Gly) and APOE*2(Val-236 →Glu), segregate were analysed to determine whether the APOE mutants were associated with dyslipidaemia. 2. The proband, a 51-year-old Caucasian male, was a carrier of APOE*3(Cys-112→Arg; Arg-251→Gly) and his spouse was a carrier of APOE*2(Val-236→Glu). Four other family members were carriers of one or both of the mutant APOE genes. 3. The plasma cholesterol and triacylglycerol concentrations were markedly elevated in the proband and were classified as type IV hyperlipoproteinaemia. The plasma triacylglycerol concentration was moderately increased in a sister, who was a carrier of APOE*3(Cys-112→Arg; Arg-251→Gly), and in the son, who was a compound heterozygote for both mutant APOE alleles. Normal plasma lipid levels were observed in all other family members. In the plasma samples of the proband and his family members β-very-low-density lipoprotein was not detectable and the molar ratio of very-low-density lipoprotein-cholesterol to very-low-density lipoprotein-triacylglycerol was less than 0.9. The concentration of intermediate-density lipoprotein was within normal limits. 4. None of the family members carrying APOE*3-(Cys-112→Arg; Arg-251→Gly) and/or APOE*2(Val-236→Glu) exhibited lipoprotein abnormalities characteristic of familial dysbetalipoproteinaemia, although three family members carrying APOE*3-(Cys-112→Arg; Arg-251→Gly) showed hypertriglyceridaemia.


1993 ◽  
Vol 85 (2) ◽  
pp. 183-188 ◽  
Author(s):  
Marcus H. Howell ◽  
Michael M. Adams ◽  
Mary S. Wolfe ◽  
Marie L. Foegh ◽  
Peter W. Ramwell

1. Currently, a wide range of drugs is being evaluated for the ability to prevent the restenosis which frequently accompanies percutaneous transluminal coronary angioplasty. Patients undergoing angioplasty are generally hypercholesterolaemic and therefore the possibility that plasma lipids may compromise the efficacy of anti-restenotic drugs must be assessed. A promising drug in several clinical trials for the prevention of restenosis is angiopeptin, an octapeptide analogue of somatostatin that possesses a highly lipophilic terminal. 2. The effect of angiopeptin on myointimal hyperplasia was studied in a rabbit model of arterial balloon catheter injury where the rabbits were made hypercholesterolaemic by a 0.5% cholesterol diet. The degree of subsequent myointimal thickening was measured by morphometry. 3. Angiopeptin (20 μg day−1 kg−1) significantly inhibited myointimal thickening by an average of 47% in the infrarenal aorta and both the common and external iliac arteries in the presence of elevated plasma lipids concentrations. Low dose angiopeptin (2 μg day−1 kg−1) significantly inhibited myointimal thickening in the external iliac artery but not in the other two vessels. 4. Angiopeptin treatment (20 μg day−1 kg−1) did not significantly modify the plasma cholesterol, very-low-density lipoprotein, intermediate-sized low-density lipoprotein, low-density lipoprotein and high-density lipoprotein concentrations that were elevated by the 0.5% cholesterol diet. 5. We conclude that the inhibitory effect of angiopeptin is largely unaffected by elevated plasma lipid concentrations and that this drug did not modify plasma lipid concentrations in rabbits.


1980 ◽  
Vol 29 (4) ◽  
pp. 299-302 ◽  
Author(s):  
Jean Milner ◽  
Joe C. Christian ◽  
David Hewitt

Plasma lipids were studied on 92 pairs of twins (66 MZ and 26 like-sexed DZ). The DZ twins had significantly greater total variance than the MZ twins for total plasma cholesterol but not for triglycerides or the high, low, and very low-density lipoprotein cholesterol fractions.


1976 ◽  
Vol 50 (5) ◽  
pp. 349-353 ◽  
Author(s):  
P. N. Durrington ◽  
C. J. C. Roberts ◽  
Lyn Jackson ◽  
R. A. Branch ◽  
M. Hartog

1. Phenobarbitone in a dose of 180 mg daily was administered to ten normal subjects for 3 weeks. There was a significant increase in total plasma cholesterol, plasma low-density-lipoprotein cholesterol, plasma low-density-lipoprotein (LDL) triglycerides and plasma LDL protein. The increase in plasma LDL cholesterol accounted for the increase in total plasma cholesterol. There was a significant reduction in the ratio of LDL cholesterol to LDL protein. 2. No significant changes were observed in total plasma triglycerides, plasma very-low-density-lipoprotein (VLDL) triglycerides, plasma VLDL cholesterol or plasma VLDL protein. 3. Evidence that drug-metabolizing enzymes were induced by phenobarbitone was provided by an increase in antipyrine clearance. No relationship was observed between changes in plasma cholesterol and changes in antipyrine clearance. Serum γ-glutamyl transpeptidase was also increased after phenobarbitone administration, the increase being unrelated to changes in antipyrine clearance or plasma cholesterol.


Author(s):  
D. A. Helen Sheeba ◽  
R. Gandhimathi

Introduction: Hyperlipidemia is a medical condition indicated by an increase in one or more plasma lipids, such as triglycerides, cholesterol, cholesterol esters, phospholipids, and/or plasma lipoproteins, such as very low-density lipoprotein and low-density lipoprotein, as well as decreased levels of high-density lipoprotein. This increase in plasma lipids is one of the most important risk factors for cardiovascular disease. In the meanwhile, statins and fibrates remain the most common anti-hyperlipidemic drugs for treating high plasma cholesterol and triglycerides. Conclusion: Hence this review focused to study of hyperlipidemia. This review is useful to research work in hyperlididemia.


1984 ◽  
Vol 51 (02) ◽  
pp. 186-188 ◽  
Author(s):  
A Szczeklik ◽  
R J Gryglewski ◽  
K Sladek ◽  
E Kostka-Trąbka ◽  
A Żmuda

SummaryDihomo-γ-linolenic acid (DHLA), a precursor of monoenoic anti-aggregatory prostaglandins (PGE1, PGD2), was administered for 4 weeks in a daily dose of 1.0 g into 33 patients with atherosclerosis on a basis of a double-blind trial. Comparison of treatment and placebo groups revealed elevation of DHLA in red cell lipids in DHLA-treated subjects. No differences, however, between the two groups could be observed in platelet aggregability, thromboxane A2 generation by platelets, serum cholesterol, PGE1 and PGE2 levels, and in inhibitory activity of low-density lipoproteins against prostacyclin synthetizing system in arteries. The dietary supplementation used did not lead to distinct antithrombotic effects.


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