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At least 19 recordsLinked to original sources
PubMed1992

The effect of bezafibrate on very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low density lipoprotein (LDL) composition in type 1 diabetes associated with hypercholesterolaemia or combined hyperlipidaemia.

Lipoprotein composition was examined in type 1 diabetic subjects with hypercholesterolaemia +/- hypertriglyceridaemia during a 3-month double-blind placebo controlled assessment of bezafibrate therapy. The predominant effect was on lipoprotein lipid content. In those with hypercholesterolaemia alone, bezafibrate significantly reduced the cholesterol (particularly esterified cholesterol) and triglyceride content of large very low density lipoprotein (VLDL) (Svedberg flotation units (Sf) 60-400) in comparison to the placebo group (P less than 0.05), and a trend towards a reduction in free and esterified cholesterol within the intermediate density lipoprotein fraction (IDL) (Sf 12-20) was noted. Low density lipoprotein (LDL) composition was unaltered and in general phospholipid and protein concentrations and cholesteryl ester/protein ratios within the lipoprotein fractions were unaffected. Large VLDL cholesterol and triglyceride concentrations in those with combined hyperlipidaemia were significantly decreased following bezafibrate therapy, both in comparison to placebo-treated subjects and to baseline concentrations (P less than 0.05). An additional significant reduction in small VLDL (Sf 20-60) free cholesterol was recorded (P less than 0.05). Average reductions of large and small VLDL protein of 50-56% were not significant because of wide variation in responses. Bezafibrate had no effect on the abnormal composition of IDL and LDL, characteristic of Type 1 diabetes, regardless of whether or not hypertriglyceridaemia was associated with hypercholesterolaemia. Its major action was to lower VLDL lipid concentrations, but it may also reduce the lipid content of intermediate density lipoprotein in Type 1 diabetes.

Adolescent↗
PubMed1991

Influence of early diabetic nephropathy on very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low density lipoprotein (LDL) composition.

The procedure of discontinuous gradient ultracentrifugation (DGU) was used to characterize the influence of early diabetic nephropathy on the composition of very low density lipoprotein (VLDL, flotation density 60-400 Svedberg (Sf) units), low density lipoprotein (LDL, flotation density 0-12 Sf) and subfractions of intermediate density lipoprotein (IDL1 and IDL2, 20-60 and 12-20 Sf, respectively). Forty-six subjects with type 1 (insulin-dependent) diabetes and serum creatinine, less than 140 mumol/l were studied, of whom 23 consistently had normal rates of albumin excretion (AER less than 15 micrograms/min), and 23 had persistent albuminuria (AER 20.0-960.6 micrograms/min). The two groups were similar with respect to total serum lipids, glycaemic control, age and body mass. The composition (lipid, protein and phospholipid) and mass of VLDL, LDL and IDL2 was not appreciably altered by early nephropathy, but free and total cholesterol concentration in IDL1 (Sf 20-60) was increased (total cholesterol 0.68 (0.09) (mean (SE)) vs. 0.47 (0.07) mmol/l, and free cholesterol 0.27 (0.04) vs. 0.17 (0.03) mmol/l, both P less than 0.05). The explanation of these findings was probably an accumulation in the circulation of the remnants of chylomicron metabolism and/or intermediates in the conversion from VLDL to IDL1. In addition, there was a decrease in serum high density lipoprotein (HDL) cholesterol in early nephropathy (1.27 (0.06) vs. 1.38 (0.10) mmol/l, P less than 0.05), due to a decrease in the HDL2 cholesterol subfraction (P less than 0.05). These findings may in part explain the increased risk of premature atherosclerosis associated with the development of albuminuria.

Adolescent↗
PubMed2003

The very low density lipoprotein (VLDL) receptor--a peripheral lipoprotein receptor for remnant lipoproteins into fatty acid active tissues.

The VLDL (very low density lipoprotein) receptor is a member of the LDL (low density lipoprotein) receptor family. The VLDL receptor binds apolipoprotein (apo) E but not apo B, and is expressed in fatty acid active tissues (heart, muscle, adipose) and macrophages abundantly. Lipoprotein lipase (LPL) modulates the binding of triglyceride (TG)-rich lipoprotein particles to the VLDL receptor. By the unique ligand specificity, VLDL receptor practically appeared to function as IDL (intermediate density lipoprotein) and chylomicron remnant receptor in peripheral tissues in concert with LPL. In contrast to LDL receptor, the VLDL receptor expression is not down regulated by lipoproteins. Recently several possible functions of the VLDL receptor have been reported in lipoprotein metabolism, atherosclerosis, obesity/insulin resistance, cardiac fatty acid metabolism and neuronal migration. The gene therapy of VLDL receptor into the LDL receptor knockout mice liver showed a benefit effect for lipoprotein metabolism and atherosclerosis. Further researches about the VLDL receptor function will be needed in the future.

Animals↗
PubMed1992

Apolipoprotein E and lipoprotein lipase reduce macrophage degradation of oxidized very-low-density lipoprotein (VLDL), but increase cellular degradation of native VLDL.

Oxidized low-density lipoprotein (Ox-LDL) has been shown to be taken up by the macrophage-scavenger receptor at an enhanced rate in comparison to native LDL, with consequent cellular cholesterol accumulation. In the present study, we analyzed macrophage interaction with very-low-density lipoprotein (VLDL) from normolipidemic subjects (N-VLDL) that was oxidized in the presence of 10 mumol/L copper ions. Oxidized VLDL (Ox-VLDL) contained increased conjugated dienes and malondialdehyde (MDA) equivalents and showed increased electrophoretic mobility. Gradual fragmentation of VLDL apolipoproteins (apo) was noted, with apo B-100 being the first to be fragmented, followed by apo E and apo C. Degradation of Ox-VLDL by mouse peritoneal macrophages (MPM) was increased almost twofold in comparison to N-VLDL. Upon incubation of VLDL with lipoprotein lipase (LPL), the LPL-treated lipoprotein demonstrated up to 50% increased degradation by macrophages in comparison to control N-VLDL. However, the degradation of LPL-treated Ox-VLDL was decreased by up to 20% in comparison to control Ox-VLDL. Similarly, the addition of apo E to VLDL enhanced its cellular degradation by 56%, whereas a 20% reduction in the degradation of apo E-treated Ox-VLDL was demonstrated in comparison to nontreated Ox-VLDL. These results showed that LPL and apo E, two important regulatory substances in cellular metabolism of plasma lipoproteins, increased macrophage degradation of native VLDL, but reduced the degradation of Ox-VLDL. These inhibitory effects on macrophage uptake of Ox-VLDL suggest that apo E and LPL may possess antiatherogenic potential.

Animals↗
PubMed2004

The very low-density lipoprotein (VLDL) receptor: characterization and functions as a peripheral lipoprotein receptor.

The very low-density lipoprotein (VLDL) receptor is a member of the low-density lipoprotein (LDL) receptor family. In vitro and in vivo studies have shown that VLDL receptor binds triglyceride (TG)-rich lipoproteins but not LDL, and functions as a peripheral remnant lipoprotein receptor. VLDL receptor is expressed abundantly in fatty acid-active tissues (heart, skeletal muscle and fat), the brain and macrophages. It is likely that VLDL receptor functions in concert with lipoprotein lipase (LPL), which hydrolyses TG in VLDL and chylomicron. In contrast to the LDL receptor, VLDL receptor binds apolipoprotein (apo) E2/2 VLDL particles as well as apoE3/3 VLDL, and the expression is not down-regulated by intracellular lipoproteins. Recently, various functions of the VLDL receptor have been reported in lipoprotein metabolism, metabolic syndrome/atherosclerosis, cardiac fatty acid metabolism, neuronal migration and angiogenesis/tumor growth. Gene therapy of VLDL receptor into the liver showed a benefit effect for lipoprotein metabolism in both LDL receptor knockout and apoE mutant mice. Beyond its function as a peripheral lipoprotein receptor, possibilities of its physiological function have been extended to include signal transduction, angiogenesis and tumor growth.

Animals↗
PubMed2001

Ex vivo measurement of lipoprotein lipase-dependent very low density lipoprotein (VLDL)-triglyceride hydrolysis in human VLDL: an alternative to the postheparin assay of lipoprotein lipase activity?

The plasma lipolysis of triglyceride (TG)-rich lipoproteins is mainly due to the activity of lipoprotein lipase (LPL). Albeit important for our analysis of certain physiopathological situations, the determination of the magnitude of LPL-dependent lipolysis is not easy to perform. This essentially results from the binding of LPL to the luminal surface of vascular endothelium. The measurements of the whole putative LPL activity have been achieved after injection of heparin, a procedure that releases LPL from endothelium. However, the physiopathological relevance of this postheparin lipolysis assay (PHLA) remains questionable because it has never been demonstrated that the bulk of endothelium-bound LPL was active. It has been recently shown that a small part of LPL is associated to circulating lipoproteins in nonheparinized plasma, raising the possibility that the lipolysis mediated by this circulating LPL might reflect the overall LPL-dependent TG hydrolysis in plasma. To address this question, we developed a new lipolysis assay in which the very low density lipoprotein (VLDL)-bound LPL-dependent VLDL-TG hydrolysis (LVTH) was directly determined through the measurement of nonesterified fatty acid (NEFA) release during in vitro incubations. LVTH measurements were performed in control subjects, in type 2 diabetics, and in either heterozygous or homozygous LPL-deficient patients. In the latter group, LVTH values were extremely low. Those of heterozygous patients and of diabetics were similarly decreased by about 40% with respect to control group. Plasma TG concentrations exhibited an inverse relationship with LVTH level. In a subgroup of subjects, LVTH and PHLA were positively correlated and the inverse correlation of LVTH with plasma or VLDL-TG concentration was stronger than that obtained with PHLA. To further study the validity of this new assay, we measured LVTH in nine subjects who were studied for their catabolism of VLDL labeled with stable isotope. No relation was observed between the direct hepatic removal of VLDL and LVTH, whereas the latter was strikingly correlated with the rate of conversion of VLDL to intermediary density lipoprotein. Collective consideration of these findings strongly suggests that LVTH is a physiologically relevant index which could advantageously replace the measurements of PHLA in numerous physiopathological situations.

Adult↗
PubMed2002

Very low density lipoprotein (VLDL) receptor-deficient mice have reduced lipoprotein lipase activity. Possible causes of hypertriglyceridemia and reduced body mass with VLDL receptor deficiency.

Although very low density lipoprotein (VLDL) receptor (VLDLr) knockout mice have been reported to have no lipoprotein abnormalities, they develop less adipose tissue than control mice when fed a high calorie diet. Mice that are deficient in adipose tissue expression of lipoprotein lipase (LpL) also have less fat, but only when crossed with ob/ob mice. We hypothesized that the VLDLr, a protein that will bind and transport LpL, is required for optimal LpL actions in vivo and that hypertriglyceridemia due to VLDLr deficiency is exacerbated by either LpL deficiency or VLDL overproduction. Fasted VLDLr knockout (VLDLr0) mice were more hypertriglyceridemic than controls (2-fold greater triglyceride levels). The hypertriglyceridemia due to VLDLr0 was even more evident when VLDLr0 mice were crossed with heterozygous LpL-deficient (LpL1) and human apolipoprotein B (apoB) transgenic mice. This was due to an increase in apoB48-containing VLDL. [(3)H]VLDL turnover studies showed that VLDL-triglyceride clearance in VLDLr0/LpL1 mice was impaired by 50% compared with LpL1 mice. VLDLr0/LpL1 mice had less LpL activity in postheparin plasma, heart, and skeletal muscle. Infection of mice with an adenovirus-expressing receptor-associated protein, an inhibitor of the VLDLr, reduced LpL activity in wild type but not VLDLr0 mice. Therefore, the VLDLr is required for normal LpL regulation in vivo, and the disruption of VLDLr results in hypertriglyceridemia associated with decreased LpL activity.

Adipose Tissue↗
PubMed1984

Effect of human high density lipoproteins, anti-apolipoproteins CII and CIII, and hydrolysis of very low density lipoprotein (VLDL) cholesterol ester on VLDL catabolism in vitro.

Lipolysis of human very low density lipoproteins (VLDL) by lipoprotein lipase (LPL) was inhibited in the presence of high density lipoproteins (HDL), anti-apolipoprotein (apo) CII, and by increasing the VLDL free cholesterol content but not with anti-apo CIII or lipoprotein-free plasma. The experiments lend direct evidence that the composition of VLDL and their milieu are important determinants of lipolysis by LPL. Apo CIII may not be critical in LPL mediated VLDL catabolism.

Antibodies↗
PubMed1983

Plasma very low density lipoprotein (VLDL) in cholesterol-fed rabbits: chylomicron remnants or liver lipoproteins?

When iodinated hypercholesterolemic plasma very low density lipoprotein (VLDL), chylomicrons or chylomicron remnants were injected intravenously, the apoB of chylomicrons and chylomicron remnants was removed more rapidly than apoB of hypercholesterolemic VLDL. In perfused livers from normal or cholesterol-fed rabbits, chylomicron remnants were removed 69% and 125% more rapidly, respectively, than hypercholesterolemic VLDL. Chylomicron remnants were removed equally well by perfused livers from normal and cholesterol-fed rabbits, but hypercholesterolemic plasma VLDL was removed more slowly by perfused livers of cholesterol-fed than by those of normal rabbits. Chylomicron remnant removal by livers from normal and cholesterol-fed rabbits was inhibited by high levels of hypercholesterolemic plasma VLDL in the perfusate. Twenty-four hours after a single dose of retinyl ester was fed to cholesterol-fed rabbits, less than 1% of the absorbed retinol remained in the plasma as retinyl ester. Thus, increases in plasma VLDL cholesterol levels in cholesterol-fed rabbits cannot be accounted for by the accumulation of chylomicron remnants. Apparently, a cholesterol-rich VLDL, probably of hepatic origin, accumulates in the postabsorptive plasma of the cholesterol-fed rabbit.

Animals↗
PubMed1999

[Lowering of resistance to oxidation of VLDL lipoproteins and some subfractions of LDL lipoproteins in patients with non-insulin-dependent diabetes mellitus].

AIM: To investigate composition of very low density lipoproteins (VLDLP) and some subfractions of low density lipoproteins (LDLP), and their resistance to oxidation in patients with non-insulin-dependent diabetes mellitus (NIDDM) varying in severity compared to healthy subjects. MATERIALS AND METHODS: 26 NIDDM patients and 16 healthy controls. VLDLP and subfractions of LDLP were isolated by ultracentrifugation. The lipoproteins were assayed for protein, cholesterol, initial products of lipid peroxidation (LPO). After autooxidation of lipoproteins, fluorimetry examined the degree of the oxidant modification. RESULTS: The initial level of LPO products was elevated in VLDLP and light subfractions of LDLP in severe and moderate NIDDM patients. Even in mild NIDDM, resistance to oxidation of dense LDLP subfractions was low and continued to decrease with aggravation of the disease. High ratio cholesterol/ protein occurred in VLDLP and subfractions of LDLP from patient with severe NIDDM. CONCLUSION: It is shown that subnormal resistance to oxidation of LDLP dense subfractions even in mild NIDDM is an informative diagnostic criterion of risk factor to develop atherosclerosis.

Adult↗
PubMed1981

Membrane receptors for very low density lipoprotein (VLDL) inhibitor of lymphocyte proliferation.

Physiologic concentrations of human plasma very low density lipoproteins inhibit the DNA synthesis of lymphocytes stimulated by allogeneic cells or lectins. In this report we have compared the effects of isolated lipoproteins [very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL)] and lipoprotein-depleted plasma (LDP) on DNA synthesis by phytohemagglutinin-stimulated human lymphocytes. The relative potency for the inhibition of lymphocyte proliferation was VLDL greater than LDL greater than HDL greater than LDP. Fifty percent inhibition of DNA synthesis was observed at a VLDL protein concentration of 1.5--2.0 microgram/ml. We have further demonstrated the presence of specific receptors for VLDL on human lymphocytes. Native VLDL was more effective than LDL in competing for 125I-VLDL binding sites. Subsequent to binding to lymphocytes, 125I-VLDL was internalized and degraded to acid-soluble products. Based on a Scatchard analysis of VLDL binding at 4 degrees C, the number of VLDL receptors per lymphocyte was estimated at 28,000 +/- 1300. Based on an estimated mean binding affinity for the VLDL receptor complex at half saturation of approximately 8.8 X 10(7) liter/mole, it is estimated that 91% of lymphocyte VLDL receptors are occupied at physiologic VLDL concentrations in blood. Although the immune regulatory role of plasma lipoproteins is uncertain, we suggest tha VLDL and LDL-In may maintain circulating blood lymphocytes in a nonproliferative state via their respective cell receptor mechanisms.

Cholesterol↗
PubMed1981

Rat hematopoietic cell receptors for very low density lipoprotein (VLDL) growth inhibitor.

Physiologic concentrations of rat plasma very low density lipoproteins (VLDL) have profound inhibitory effects in tissue culture on the proliferation of hormonally stimulated bone marrow granulocytic and erythrocytic cells and mitogen-stimulated spleen cells. In this study we have evaluated the in vitro uptake and binding of 125I-VLDL by rat marrow cells and spleen lymphocytes. To this end, VLDL were isolated from rat plasma by sequential ultracentrifugation flotation and radioiodinated using iodine monochloride. Biological activity of 125I-VLDL was ascertained by demonstrating that 125I-VLDL and native VLDL had comparable proliferative inhibitory effects when added to erythropoietin-stimulated marrow cells and PHA-stimulated lymphocytes. After 1 h exposure of marrow to VLDL, exhaustive cell washing did not reverse the lipoprotein growth inhibitory effect. The cell uptake of VLDL was evaluated by adding 125I-VLDL to marrow or spleen cells. Uptake of 125I-VLDL by rat cells showed a preference for binding of VLDL as compared to chylomicrons, LDL, or HDL. Based on Scatchard plot analysis of 125I-VLDL binding at 37 degrees C, the approximate number of saturable VLDL receptors available per marrow or spleen cell during a 3 h incubation was 34,000 and 63,000, respectively. We conclude that rat marrow cells and lymphocytes have specific receptors for plasma VLDL and that receptor binding of VLDL is an initial step in its growth inhibitory effect. The physiologic role of plasma lipoprotein cell growth inhibitors will remain speculative, however, until the in vivo distribution of the biologically active lipoprotein moiety to extravascular sites of hematopoiesis has been determined.

Animals↗
PubMed1976

Turnover and aortic uptake of very low density lipoproteins (VLDL) from hypercholesteremic rabbits as a model for testing antiatherosclerotic compounds.

VLDL from hypercholesteremic (HC) rabbits display features which are suggestive of inherent atherogenicity. The lipid composition, compared to that of control VLDL, shows an enrichment of cholesterol esters, which have a very high 18:1/18:2 ratio in their fatty acids, and an increased sphingomyelin content, with decreased PC/Sph ratio. This lipid composition is very similar to that of the atherosclerotic plaqua. Apoprotein peptides of HC VLDL show a predominance of arg-rich proteins, similar to human conditions (Type III hyperlipoproteinemia and hypothyroidism) characterized by early and severe atherosclerosis. Turnover of 125I-labelled HC VLDL is significantly slower than that of control VLDL, both when the lipoprotein is injected into the donor animals and into controls. Conversion of HC VLDL into lipoproteins of higher density is also very small, as compared to control VLDL. Uptake of radioactivity into the aortic wall after injection is about doubled, as compared to control VLDL, when HC rabbits receive HC VLDL. This experimental model suggests that structural modifications of the HC VLDL make them poorly metabolizable, and possible more akin to the recently described arterial lipoprotein complexing factor (ALCF). Metformin was selected as the test compound, because it has been shown to decrease aortic and liver lipid accumulation in cholesterol fed rabbits, while only slightly affecting plasma cholesterol levels. VLDL from rabbits fed cholesterol and metformin (HC+Met), while still enriched in cholesterol esters, have a higher protein content, less sphingomyelin and more phosphatidylethanolamine and phosphatidylinositol than HC VLDL, while fatty acid composition of cholesterol esters does not differ. Turnover of HC+Met VLDL is extremely rapid, with a t1/2 even shorter than that of control VLDL.

Animals↗
PubMed1998

The intracellular triacylglycerol/fatty acid cycle: a comparison of its activity in hepatocytes which secrete exclusively apolipoprotein (apo) B100 very-low-density lipoprotein (VLDL) and in those which secrete predominantly apoB48 VLDL.

Hamster hepatocytes, like human hepatocytes, secrete triacylglycerol (TAG) as very-low-density lipoprotein (VLDL) in association with apolipoprotein (apo) B100, whereas in the rat, TAG is secreted predominantly in association with apoB48. Nevertheless, in hepatocytes from both species, a minimum of between 60% and 70% [69. 1+/-1.4% (hamster), 60.6+/-2.5% (rat)] of the VLDL TAG was secreted following lipolysis and re-esterification of intracellular TAG. The fractional rates of hepatocellular TAG turnover (lipolysis and re-esterification) were similar in both species [1.83+/-0.28 pools/24 h (hamster), 1.39+/-0.23 pools/24 h (rat)]. Comparison of the relative changes in the 3H and 14C specific radioactivities of the VLDL and cellular TAG, pre-labelled with [3H]glycerol and [4C]oleate, suggested that fatty acids released by lipolysis either were recruited directly into a VLDL assembly pool or were recycled to the cellular pool following re-esterification. Recycling in the hamster was somewhat greater than in the rat (66.1+/-5.7% versus 53. 7+/-4.8% of TAG lipolysed respectively). Similarly, a larger proportion of newly synthesized TAG was retained within the cell, rather than secreted as VLDL, in the hamster compared with the rat (37.9+/-2.8% versus 20+/-3.8%, P<0.01). These factors may have contributed to the somewhat lower rate of VLDL TAG secretion in the hamster hepatocytes compared with those from the rat (43.3+/-4.2 versus 96.4+/-3.4 microg/24 h per mg of cell protein). Rat hepatocytes were more sensitive to inhibition of VLDL secretion by insulin than were those from hamster. In neither case did insulin affect total or fractional TAG turnover. The results suggest that assembly of both apoB100 VLDL and apoB48 VLDL is associated with efficient intracellular TAG lipolysis.

Animals↗
PubMed1992

Alterations in the levels and lipid composition of plasma lipoproteins (VLDL, LDL and HDL) in Brazilian patients with hepatosplenic schistosomiasis mansoni.

1. The plasma concentrations of low- and high-density lipoproteins (LDL and HDL) were significantly reduced in Brazilian patients with compensated hepatosplenic schistosomiasis mansoni (SM) when compared with healthy individuals, but very low-density lipoprotein (VLDL) levels were unchanged. 2. All three classes of lipoproteins isolated from SM plasma had an increased content of triacylglycerol and unesterified cholesterol and decreased cholesteryl ester and phospholipid. 3. The individual phospholipid composition of patient VLDL, LDL, HDL was also altered; the amount of phosphatidylcholine was increased and that of lysophosphatidylcholine decreased. 4. The saturated and monounsaturated fatty acyl content of cholesteryl esters in patient lipoproteins was also significantly increased, and diunsaturated and polyunsaturated fatty acyl content was decreased. 5. When isolated lipoproteins were examined as negatively stained preparations by electron microscopy, the morphology of SM patient LDL was normal but the HDL fraction was abnormal and showed marked heterogeneity of size with the presence of occasional discoidal particles which resembled "nascent" HDL.

Adult↗
PubMed1997

Lipoprotein abnormalities in type 2 diabetic patients. Increased distribution of triglycerides (TG) in very low density lipoprotein (VLDL) and decreased apolipoprotein E/VLDL-TG ratio are risk for ischemic heart disease.

Plasma lipoproteins and clinical characteristics of type 2 diabetic patients with (n = 50) and without (n = 108) ischemic heart disease (IHD) were compared. The patients with IHD were older (64 +/- 9 vs 59 +/- 9 years, mean +/- SD, p < 0.01) and had a longer duration of diabetes (14 +/- 9 vs 11 +/- 8 years, p < 0.05). Lipids, lipoproteins and apolipoproteins were comparable in the two groups. The percent distribution of triglycerides (TG) in the very low density lipoprotein (VLDL) fraction was significantly higher (55 +/- 16 vs 50 +/- 17%, p < 0.05). The level of low density lipoprotein (LDL) (33 +/- 14 vs 39 +/- 15%, p < 0.05) and the apo E/VLDL-TG ratio (0.085 +/- 0.045 vs 0.120 +/- 0.097, p < 0.01), however, was significantly lower in patients with IHD than in those without IHD. Multiple regression analysis also indicated that age, duration of diabetes, percent distribution of TG in VLDL, percent distribution of TG in LDL and the apo E/VLDL-TG ratio were significantly related to the presence of IHD. Hypertriglyceridemia, particularly when characterized by abnormalities of TG distribution, may play an important role in the development of IHD in type 2 diabetic patients.

Aged↗
PubMed1977

Female steroid hormones and lipoprotein synthesis in the cockerel: effects of progesterone and nafoxidine on the estrogenic stimulation of very low density lipoproteins (VLDL) synthesis.

Since progesterone is known to modulate the effects of estradiol in a number of organ systems, we have studied the effects of the two hormones on very low density lipoproteins (VLDL) synthesis in the cockerel. We have also examined the effect of an estrogen antagonist, nafoxidine-HCl, on the process. When three week-old cockerels were treated with a single injection of estradiol (1 mg) or estradiol (1 mg) + progesterone (2 mg), plasma VLDL increased within 5 h, reached a peak at 48 h and returned to baseline values at 68 h. There was no significant difference between estradiol or estradiol + progesterone treated animals. Liver slices were prepared from similarly treated animals and incubated in vitro with L-[3H]lysine for 2 h. Following homogenization and centrifugation at 105,000 X g, newly synthesized VLDL were quantitiated in the supernatant fluid by immunoprecipitation with a monospecific antibody. Radioactivity incorporated into VLDL was found to increase from low baseline levels to a peak at about 17 h after treatment. There was, again, no significant difference between estradiol and estradiol + progesterone-treated animals. Estrogen priming or progesterone pretreatment also did not significantly alter the VLDL biosynthetic response in liver slices to estradiol alone or in combination with progesterone. When the estrogen-antagonist nafoxidine-HCl (5 mg) was administered simultaneously with estradiol (1 mg), it totally inhibited the VLDL biosynthetic response in liver slices in vitro. The interaction of estradio, progesterone and nafoxidine-HCl on the hepatic synthesis of VLDL should serve as a valuable model for the study of VLDL synthesis and its regulation as well as the mode of action of the sex steroid hormones in the liver.

Animals↗