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PubMed1993

Activities of lipoprotein lipase and hepatic triglyceride lipase in postheparin plasma of patients with low concentrations of HDL cholesterol.

Previous investigations have shown that abnormalities in the postheparin plasma levels of the lipolytic enzymes, lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL), are correlated with variations in plasma high-density lipoprotein cholesterol (HDL-C) levels. The present study was performed to determine correlations between the postheparin plasma activities of these two enzymes and HDL levels in a sizable number of subjects with low HDL-C levels. Two types of low-HDL subjects were investigated: 159 male subjects with low HDL-C (< 40 mg/dL) and normal triglyceride (< 250 mg/dL) levels (the low-HDL group) and 80 male subjects with low HDL-C (< 40 mg/dL) and elevated triglyceride (> or = 250 mg/dL) levels (the low-HDL/high-TG group). Postheparin plasma activities of LPL and HTGL were determined in these two groups, and these levels were compared with those obtained from 51 normolipidemic (normal-HDL) male subjects. Postheparin LPL activities were significantly lower in the low-HDL and low-HDL/high-TG groups (mean +/- SD, 9.9 +/- 2.9 and 10.4 +/- 3.0 mmol/h per liter, respectively; P < .001 for both) compared with the normal-HDL group (12.5 +/- 3.7 mmol/h per liter). Conversely, postheparin HTGL activities were significantly higher in the low-HDL and low-HDL/high-TG groups (39.3 +/- 16.2 and 44.4 +/- 16.7 mmol/h per liter, respectively; P < .001 for both) compared with the normal-HDL group (29.7 +/- 11.3 mmol/h per liter). Consequently, mean LPL/HTGL ratios were markedly lower in the two low-HDL groups compared with the normal-HDL group.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2003

Lipoprotein lipase (LPL) gene variation and progression of carotid artery plaque.

BACKGROUND AND PURPOSE: Coding single nucleotide polymorphisms (cSNPs) in the lipoprotein lipase (LPL) gene have been associated with lipoprotein phenotypes and vascular disease risk. We studied the association between LPL cSNPs and a novel noninvasive measure of disease, namely, cross-sectional carotid plaque area (CPA) on B-mode ultrasound. METHODS: Four hundred fifty-two patients from an atherosclerosis prevention clinic had determinations of baseline and total CPA. Traditional atherosclerosis risk factors were recorded, and the LPL D9N, N291S, and S447X cSNPs were genotyped. Multiple regression analysis was used to identify determinants of CPA. RESULTS: Minor allele frequencies for LPL D9N, N291S, and S447X were 2.8%, 0.9%, and 4.4%, respectively. There were no significant between-genotype differences in treated fasting lipids. The LPL D9N genotype was a significant predictor of both baseline CPA (P=0.008) and plaque progression from baseline to 1 year later (P=0.001). Heterozygotes for the N9 allele had higher mean baseline CPA and plaque progression than did LPL D9/D9 homozygotes. CONCLUSIONS: LPL D9N genotype may be a determinant of atherosclerosis as estimated by static baseline CPA and by progression of CPA.

Adult↗
PubMed1998

Expression of type III hyperlipoproteinemia in patients homozygous for apolipoprotein E-2 is modulated by lipoprotein lipase and postprandial hyperinsulinemia.

Type III hyperlipoproteinemia (HLP) is a multifactorial disorder associated with homozygosity for the apolipoprotein (apo) E-2 allele. Factors which may promote the development of HLP include lipoprotein lipase (LPL) and hyperinsulinemia. These factors were investigated in eight patients with type III HLP and in nine normolipidemic controls. In vitro the interaction of apoE with LPL was analyzed in cell binding assays. All type III HLP patients showed delayed triglyceride (TG) clearance and remnant lipoprotein accumulation in an oral fat tolerance test. Normolipidemic apoE-2/2 controls revealed normal TG clearance comparable to apoE3/3 controls. HLP patients showed lower LPL activity and mass than controls. Analysis of the LPL gene revealed an Asn 291-->Ser mutation in three patients and a -93 T-G substitution combined with an Asp 9-->Asn mutation in one control subject. In addition to LPL abnormalities, postprandial hyperinsulinemia was observed in five out of eight patients. In vitro LPL compensated the defective function of apoE-2 in mediating remnant lipoprotein binding to cells. In summary, seven out of eight patients with type III HLP showed LPL abnormalities and/or postprandial hyperinsulinemia. Together with the in vitro data these findings support a coordinate effect of apoE and LPL for the manifestation of type III HLP. Hyperinsulinemia appears to be an additional factor important for disease expression.

Adult↗
PubMed2000

Two novel mutations in the lipoprotein lipase gene in a family with marked hypertriglyceridemia in heterozygous carriers. Potential interaction with the polymorphic marker D1S104 on chromosome 1q21-q23.

Two novel mutations in the lipoprotein lipase (LPL) gene are described in an Austrian family: a splice site mutation in intron 1 (3 bp deletion of nucleotides -2 to -4) which results in skipping of exon 2, and a missense mutation in exon 5 which causes an asparagine for histidine substitution in codon 183 and complete loss of enzyme activity. A 5-year-old boy who exhibited all the clinical features of primary hyperchylomicronemia was a compound heterozygote for these two mutations. Nine other family members were investigated: seven were heterozygotes for the splice site mutation, one was a heterozygote for the missense mutation, and one had two wild-type alleles of the LPL gene. LPL activity in the post-heparin plasma of the heterozygotes was reduced to 49;-79% of the mean observed in normal individuals. Two of the heterozygotes had extremely high plasma triglyceride levels; in three of the other heterozygotes the plasma triglycerides were also elevated. As plasma triglycerides in carriers of one defective LPL allele can be normal or elevated, the heterozygotes of this family have been studied for a possible additional cause of the expression of hypertriglyceridemia in these subjects. Body mass index, insulin resistance, mutations in other candidate genes (Asn291Ser and Asp9Asn in the LPL gene, apoE isoforms, polymorphisms in the apoA-II gene and in the apoAI-CIII-AIV gene cluster, and in the IRS-1 gene) could be ruled out as possible factors contributing to the expression of hypertriglyceridemia in this family. A linkage analysis using the allelic marker D1S104 on chromosome 1q21;-q23 suggested that a gene in this region could play a role in the expression of hypertriglyceridemia in the heterozygous carriers of this family, but the evidence was not sufficiently strong to prove this assumption. Nevertheless, this polymorphic marker seems to be a good candidate for further studies.

Adult↗
PubMed1977

Supplementation with vitamin E in hyperlipidemic patients treated with diet and clofibrate. Effects on serum lipoprotein concentrations, plasma fatty acid composition and adipose tissue lipoprotein lipase activity.

Twelve hyperlipidemic patients on long term treatment with a lipid lowering diet enriched in polyunsaturated fatty acids and with clofibrate were supplemented with vitamin E (400 mg/day). The effect on serum lipoprotein concentration, plasma lipid fatty acid composition, and adipose tissue lipoprotein lipase activity was studied. No additional lipid-lowering effect was registered during a treatment period of 4 months. A slight increase in total serum cholesterol concentration and in high density lipoprotein concentration was probably attributable to seasonal variations in serum lipoprotein concentrations. No major changes of fatty acid composition in plasma cholesteryl esters or triglycerides were recorded. However, an increased relative amount of arachidonic acid and a reduced amount of palmitic acid in the plasma phospholipids after 2 months was possibly caused by the vitamin E therapy.

Adipose Tissue↗
PubMed2001

Adipose tissue fatty acid composition in humans with lipoprotein lipase deficiency.

BACKGROUND: Lipid stores in human adipose tissue are maintained primarily by incorporating lipid from circulating chylomicrons and very low density lipoproteins. Adipose tissue lipoprotein lipase (LPL) hydrolyzes triglyceride from these lipoprotein particles to facilitate their entry into adipocytes for storage. Subjects deficient in LPL still have normal adiposity, and this may result from increased adipocyte lipogenesis or from uptake of circulating lipid through alternate mechanisms. The objective of this study was to determine whether fatty acid composition of adipose tissue from LPL-deficient subjects reflects maintenance of lipid stores through increased lipogenesis or through alternate mechanisms of lipoprotein uptake. METHODS: Adipose tissue samples from LPL-deficient subjects who consume fat-restricted diets and normal subjects were analyzed for fatty acid composition by gas-liquid chromatography. RESULTS: Compared with that of normal subjects, adipose tissue from LPL-deficient subjects showed an increase in 16:1 and decreases in 18:0, 18:2, and 18:3 fatty acids, whereas other nonessential fatty acid levels were not statistically different. CONCLUSIONS: The reduction in essential fatty acids and increase in nonessential fatty acids in adipose tissue of those with LPL deficiency, taken together with recent data from animal studies, suggest that lipid stores in these subjects are maintained primarily through enhanced adipocyte lipogenesis.

Adipose Tissue↗
PubMedDate not supplied

Cholesteryl ester transfer protein TaqI B and lipoprotein lipase Ser447Ter gene polymorphisms are not associated with ischaemic stroke in Greek patients.

Cholesteryl ester transfer protein (CETP) and lipoprotein lipase (LPL) are both key players in plasma lipoprotein homeostasis and, as such, genetically induced alterations in their respective activities may affect susceptibility to cerebrovascular diseases. In this study, we examined the distribution of two common polymorphisms, namely CETP TaqI B and LPL Ser447Ter in a cohort of Greek clinically diagnosed late-onset ischaemic stroke patients (n = 98) and an ethnicity-, age- and sex-matched control group with no manifestations of vascular disease (n = 100). Our study revealed no statistically significant differences with respect to the distribution of either polymorphism, examined separately or in combination, between the two groups.

Aged↗
PubMedDate not supplied

Lipoprotein alterations and plasma lipoprotein lipase reduction in familial hemophagocytic lymphohistiocytosis.

Serum lipid abnormalities are common in familial hemophagocytic lymphohistocytosis (FHL), a disorder also characterized by fever, hepatosplenomegaly, pancytopenia and a prominent lymphohistiocytic accumulation in the mononuclear phagocyte system. The lipoprotein pattern in nine children with FHL was studied with a quantitative method measuring cholesterol and triglycerides in each major class of lipoproteins. Triglycerides were markedly elevated during active FHL in serum, very low density lipoproteins, and low density lipoproteins. Cholesterol was increased in very low density lipoproteins whereas both triglycerides and cholesterol were extremely low in high density lipoproteins. These lipoprotein abnormalities, reversible on successful therapy, are compatible with a depressed lipolytic activity. Post-heparin levels of lipoprotein lipase and hepatic lipase in plasma were studied in four children and found to be markedly low during active FHL. We suggest that inflammatory cytokines, which may strongly suppress lipoprotein lipase activity, can be important mediators in the pathophysiology of FHL and that they may participate in the development of the lipid abnormalities.

Child, Preschool↗
PubMed2004

Moderate hyperalphalipoproteinaemia in a Brazilian population is related to lipoprotein lipase activity, apolipoprotein A-I concentration, age and body mass index.

We investigated 95 Brazilian adults, aged 21-79 years, who were divided into two groups defined as having high-density lipoprotein (HDL)-cholesterol concentrations above [hyperalphalipoproteinaemia (HALP); n=48] or below (controls; n=47) the 90th percentile of a local population. The activities of lipid transfer proteins and enzymes involved in the plasma reverse cholesterol transport and the prevalence of factors that modulate HDL metabolism (alcohol consumption, ponderosity, physical exercise, menopause and use of hormone replacement treatment in women and smoking) were measured, as well as the prevalence of cardiovascular disease and of its various risk factors. The two groups showed no differences in their frequencies of cardiovascular disease. The HDL2/HDL3-cholesterol and triacylglycerol (triglyceride) ratios and the activities of the phospholipid transfer protein (PLTP) and cholesteryl ester transfer protein (CETP) were similar in both groups. Lipoprotein lipase (LPL) and hepatic lipase (HL) activities were 35% higher (P=0.0002) and 40% lower (P=0.0006) respectively, in HALP compared with control subjects. In a multivariate analysis, HDL-cholesterol and its subfractions were influenced by LPL, apolipoprotein A-I, age (negative relationship) and body mass index (negative relationship). Use of alcohol and ponderosity, as well as the interaction of these factors, explained the LPL activity. HL activity was modulated by smoking, and hormone-replacement therapy influenced the apolipoprotein A-I concentration. CETP activity was influenced by race and PLTP by age. The unique phenotype found in this Brazilian HALP population, namely low HL and high LPL activities, could be determined mostly by genetic components, on which future work will focus.

Adult↗
PubMed1989

Inhibition of lipoprotein lipase by the receptor-binding domain of apolipoprotein E.

A synthetic peptide (residues 139-153) corresponding to the receptor-binding domain of apolipoprotein E (ApoE) was tested for lipoprotein lipase (LPL) inhibitory properties. In systems using both natural and synthetic substrates, inhibition of LPL was observed. Using the synthetic substrate, 50% inhibition was observed at 50 microM while high concentrations completely inhibited LPL activity. These studies suggest an additional functional role for the receptor-binding domain of ApoE-modulation of LPL activity.

Animals↗
PubMed2002

Single-nucleotide polymorphisms in the lipoprotein lipase gene associated with coronary heart disease in Chinese.

Coronary heart disease is a complex disease reflecting the interaction of multiple genes with the environment (e.g. diet, life style). Lipoprotein lipase (LPL) plays an important role in lipid metabolism and the pathogenesis of coronary atherosclerosis. Recent associations between single-nucleotide polymorphisms in the LPL gene and heart disease have been reported, but little is known in Chinese. The LPL gene spans >26 kb, with an mRNA of 3549 bp. In the present study, we screened 5155 bp (565 bp of 5' flanking region, nine exons and donor- and acceptor-splice sites, and some intronic bases) in 160 Chinese patients with confirmed coronary heart disease and 150 age- and gender-matched controls. Thirteen of the sixteen single-nucleotide polymorphisms that we found have not been previously reported. In males, significant (P<0.05) differences between the coronary heart disease patients and controls were found for five single-nucleotide polymorphisms: -421G>A (5' flanking region); +13,577C>A (intron 2); +16,052G>A, R192Q (exon 5); +16,173C>G and +16,177T>C (intron 5). In females, significant differences between the patients with coronary heart disease and controls were found for only the -421G>A and +16,052G>A (R192Q) mutations. Among the coronary heart disease males, significant (P<0.05) associations were found between the low-HDL high-triglyceride (LHDL/HTG) phenotype and the non-LHDL/HTG trait for the 5' flanking-421G, the intron 2+13,577C, and the exon 5+16,052G mutations, with odds-ratios (ORs)[confidence intervals] of 3.90[1.12-13.66], 3.38[1.22-9.40], and 3.22[1.04-10.01], respectively; no corresponding associations were found in females. There were 69, 51, 57 and 41 unphased haplotype patterns in male coronary heart disease, male control, female coronary heart disease and female control groups, respectively; the computer program PM-Plus found the heterogeneity model by far the best fit (P<0.0001 in males, >0.01 in females). These data show that some single-nucleotide polymorphisms in the LPL gene among Chinese are associated with abnormal lipid and lipoprotein profiles and predisposition to coronary heart disease, a genetically heterogeneous complex disease, and that they are gender-specific.

Adult↗
PubMed2006

The angiotensin II receptor antagonist valsartan enhances lipoprotein lipase mass in preheparin serum in type 2 diabetes with hypertension.

Recent studies suggest that blockade of angiotensin type 1 (AT1) receptor may have some effect on glucose and lipoprotein metabolism. Serum level of preheparin lipoprotein lipase (LPL) reflects LPL production mainly in adipocytes and is believed to be related to insulin sensitivity. We studied the effect of a selective AT1 antagonist, valsartan, on glucose, lipid metabolism and the preheparin LPL mass in 55 patients with type 2 diabetes and hypertension. Patients were randomized into a group administered valsartan 80 mg/day for 12 weeks or a group not administered valsartan (control). Blood pressure decreased significantly. HbA1c and TG levels decreased and HDL-C level increased, but these changes tended to be significantly different. TC and LDL-C levels were not significant changes. Preheparin LPL mass increased after valsartan administration compared with control (P = 0.0307), and migration ratio of LDL (LDL-Rm), which correlated negatively with LDL particle size, decreased compared with control (P < 0.0001). DeltaLDL-Rm correlated inversely with Delta preheparin LPL mass (r = -0.459). Among subjects treated with valsartan, greater improvement in preheparin LPL mass and blood pressure was observed in the subgroup with preheparin LPL mass <40 ng/ml. The results of this study suggest that valsartan may enhance LPL production in adipocytes, resulting in enlarged LDL particle size.

Aged↗
PubMed2001

Effects of 2 G on adiposity, leptin, lipoprotein lipase, and uncoupling protein-1 in lean and obese Zucker rats.

Male Zucker rats were exposed to 2 G for 8 wk to test the hypothesis that the leptin regulatory pathway contributes to recovery from effects of 2 G on feeding, growth, and nutrient partitioning. After initial hypophagia, body mass-independent food intake of the lean rats exposed to 2 G surpassed that of the lean rats maintained at 1 G, but food intake of the obese rats exposed to 2 G remained low. After 8 wk at 2 G, body mass and carcass fat were less in both genotypes. Leptin and percent fat were lower in lean rats exposed to 2 G vs. 1 G but did not differ in obese rats exposed to 2 G vs. 1 G. Although exposure to 2 G did not alter uncoupling protein-1 levels, it did elicit white fat pad-specific changes in lipoprotein lipase activity in obese but not lean rats. We conclude that 2 G affects both genotypes but that the lean Zucker rats recover their food intake and growth rate and retain "normal" lipoprotein lipase activity to a greater degree than do the obese rats, emphasizing the importance of a functional leptin regulatory pathway in this acclimation.

Adipose Tissue, Brown↗
PubMed2002

Overexpression of muscle lipoprotein lipase and insulin sensitivity.

PURPOSE OF REVIEW: The number of people affected with obesity and type 2 diabetes has reached epidemic proportions worldwide. Insulin resistance, a common feature of both conditions, has come under intense investigation. This review focuses on our current understanding of the insulin signaling cascade and potential mechanisms of regulation. RECENT FINDINGS: Recent studies have concentrated on inhibition of insulin-stimulated glucose uptake by free fatty acids as the primary cause of insulin resistance, particularly in muscle, a major site of insulin-stimulated glucose disposal. Mouse models of muscle-specific lipoprotein lipase overexpression permit closer examination of the consequences of lipid oversupply to muscle. Such mice exhibit whole-body and muscle insulin resistance, accompanied by increased accumulation of intramyocellular triglyceride and other fatty acid metabolites (i.e. long-chain acyl coenzyme A, diacylglycerol, and ceramide). These molecules may impede glucose transport by interfering with insulin signal transduction. The mechanisms for the inhibitory effect of free fatty acids on insulin-stimulated glucose transport are complex, and multiple pathways may be involved. Although key molecules have been identified, no single, clearly defined pathway has been established. SUMMARY: The mouse model of muscle-specific lipoprotein lipase overexpression allows closer examination of increased free fatty acid delivery to the muscle and of effects on insulin sensitivity. Further study of this model may provide additional insight into the role that lipids play in the development of insulin resistance, and may possibly help to identify novel approaches to prevention or treatment.

Animals↗
PubMed2000

The hypolipidemic action of bezafibrate therapy in hypertriglyceridemia is mediated by upregulation of lipoprotein lipase: no effects on VLDL substrate affinity to lipolysis or LDL receptor binding.

Fibrates are regarded as drugs of choice in hypertriglyceridemia (HTG). Downregulation of apolipoprotein (apo) C-III gene expression and upregulation of lipoprotein lipase (LPL) gene expression have been suggested to explain the hypolipidemic action of fibrates. This study was designed to study the effects of bezafibrate therapy on very low density lipoprotein (VLDL) susceptibility to lipolysis, VLDL binding to the low density lipoprotein (LDL) receptor and postheparin LPL activities in patients with HTG. VLDL lipolysis was studied with heparan sulfate proteoglycan-bound LPL. Binding affinity of VLDL to the LDL receptor was determined in J774 cells with 125I-labeled control LDL. Eighteen HTG patients were randomized to receive, in a double-blind placebo-controlled cross-over fashion, 400 mg bezafibrate once daily for 6 weeks. In response to bezafibrate therapy, plasma triglyceride and apoC-III levels decreased by 69 and 42%, respectively. HTG VLDL was lipolyzed less efficiently compared to control VLDL, and lipolysis did not improve by bezafibrate therapy. VLDL binding affinity to the LDL receptor was comparable between the control group and HTG group, and did not change upon bezafibrate therapy. However, the post-heparin LPL activity in the HTG patients increased from 153 to 192 U/l (P = 0.025). A strong inverse relation was observed between the change in LPL activities and the change in triglyceride levels (r = -0.62, P = 0.006). In conclusion, the hypolipidemic action of bezafibrate therapy in HTG may be attributed to increased LPL activity, whereas VLDL susceptibility to lipolysis and LDL receptor binding are not affected.

Adult↗
PubMed1987

Effect of atherogenic diet on lipoprotein lipase activity in cynomolgus monkeys.

Cynomolgus monkeys (Macaca fascicularis) fed monkey chow (n = 10) had a mean +/- SD post-heparin plasma lipoprotein lipase (LPL) activity level (14.7 +/- 5.5 units/ml) similar to that found in human beings (15.7 +/- 3.9 units/ml). However, the hepatic triglyceride lipase (H-TGL) in these monkeys was extremely low (0.5 +/- 0.3 units/ml) when compared with that in human beings (10.9 +/- 4.3 units/ml). The consumption of isocaloric atherogenic diets (0.2 mg cholesterol/Cal) with either saturated (P/S = 0.34) or polyunsaturated (P/S = 2.2) fat led to increased LPL activity levels (27.6 +/- 6.5 and 28.8 +/- 16.1 units/ml, respectively) and the accumulation of plasma low density lipoprotein cholesterol (LDL-C). The results indicate that cholesterol-containing atherogenic diets with either primarily saturated or polyunsaturated fat have similar potential for the increase of LPL activity. However, it is not clear whether the high dietary cholesterol content represents an obligatory component for the increase of LPL. We speculate that the high level of LPL in cynomolgus monkeys when fed a cholesterol-rich, high fat diet could be a contributing factor to the accumulation of excessive plasma LDL-C.

Animals↗