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PubMed1995

Epididymal fat depot lipoprotein lipase activity is lower in animals with high endogenous fat preferences.

Adipose tissue lipoprotein lipase (LPL) is a key enzyme responsible for the clearance of circulating triglycerides and has been linked to certain pathologic states such as obesity. In order to investigate whether an animal's endogenous fat-preference is associated with differences in adipose tissue LPL, we measured enzyme activity in epididymal fat from high- and low-fat preferring rats. Utilizing a 24h ad libitum feeding paradigm, four groups of outbred adult male Sprague-Dawley rats were screened separately for their macronutrient preferences. Animals exhibiting high- or low-fat preferences were identified and placed back on standard chow. LPL activity was measured in epididymal fat under chow fed or fasted conditions. Epididymal fat LPL activity was significantly less in the high-fat-preferring animals relative to the low-fat-preferring, in both the standard chow-fed state (p = 0.014) and fasted (p = 0.0007) state. LPL activity in heart ventricle and brown adipose tissue was also measured from the same animals. Activity in heart ventricle and brown adipose tissue was significantly lower in the high-fat-preferring group as compared with the low-fat-preferring only following a 24h fast (p = 0.0012 for heart and p = 0.0085 for brown adipose, high- versus low-fat preferring). The data indicate that differences in tissue LPL activity exist between animals with inherent differences in fat preference. Future comparative studies between the two groups of fat-preferring animals could lead to important clues to the regulation of the LPL.

Animals↗
PubMed2003

Myocardial dysfunction and male mortality in peroxisome proliferator-activated receptor alpha knockout mice overexpressing lipoprotein lipase in muscle.

Free fatty acids (FFA) are liberated from triglyceride-rich lipoproteins by lipoprotein lipase (LPL) and are considered to be a principal energy source for the heart. The peroxisome proliferator-activated receptor alpha (PPARalpha) is a key regulator of FFA catabolism. To investigate its role in cardiac muscle metabolism, transgenic mice overexpressing LPL in skeletal and cardiac muscle were bred on a PPARalpha knockout background. Fifty-five percent of male animals lacking PPARalpha and overexpressing LPL died within 4 months after birth. In contrast, females of this genotype stayed alive. Deceased animals exhibited cardiopulmonary congestion but had no increase of neutral lipids in the heart. Changes in plasma glucose, FFA, lactate, and triglycerides did not clearly account for gender-specific differences in mortality; however, they indicated a critical role for PPARalpha during fasting. Analysis of cardiac function revealed that in isolated perfused hearts, left ventricular developed pressure (a measure of contractility) was markedly lower in PPARalpha knockout mice overexpressing LPL compared with controls. Glucose uptake of isolated perfused hearts was significantly higher in PPARalpha knockout mice with both normal or increased LPL expression. However, uptake of FFA was not different among genotypes. In contrast, fasted FFA levels were significantly lower in cardiac muscle of PPARalpha knockout mice with normal LPL expression (-26%) and PPARalpha knockout mice overexpressing LPL (-38%) compared with controls. Our results indicate a critical role for PPARalpha in myocardial pump function and suggest that mouse models combining different genetic effects such as PPARalpha knockout mice overexpressing muscle LPL may be useful to study cardiomyopathies.

Animals↗
PubMed1986

Interaction of lipoprotein lipase with phospholipid vesicles: effect on protein and lipid structure.

The interaction of lipoprotein lipase (LpL) and a nonhydrolyzable phosphatidylcholine, 1,2-ditetradecyl-rac-glycero-3-phosphocholine (C14-ether-PC), has been studied by several physical methods. Analysis of the circular dichroic spectrum of LpL gave the following fractional conformation: 35% alpha-helix, 30% beta-pleated sheet, and 45% remaining structure. No significant change in the circular dichroic spectrum of LpL was observed on addition of C14-ether-PC vesicles. The quenching of LpL fluorescence by acrylamide and iodide ion was decreased only slightly by addition of C14-ether-PC vesicles. Addition of LpL to sonicated C14-ether-PC vesicles containing entrapped carboxyfluorescein caused the release of less than 15% of the vesicle contents in 20 min, indicating that the enzyme did not disrupt the structure of the lipid. In contrast, greater than 80% of the vesicle contents were released with the addition of apolipoprotein A-I to an identical vesicle preparation. The temperature dependence of the fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene incorporated into C14-ether-PC vesicles was not significantly altered by the addition of LpL. When LpL is added to vesicles, the bilayer structure of the vesicles is not disrupted as observed by freeze-fracture electron microscopy. However, at low ionic strength (0.1-0.25 M NaCl) significant aggregation of intact vesicles is observed by light scattering and electron microscopy. Vesicle aggregation is prevented and reversed by 1 M NaCl and by heparin. These data demonstrate that LpL binds to the surface of a lipid interface, without dramatic changes in lipid bilayer or protein structure.

Animals↗
PubMed1993

Evidence for a role of insulin in the regulation of abdominal adipose tissue lipoprotein lipase response to exercise training in obese women.

Abdominal and femoral adipose tissue lipoprotein lipase (AT-LPL) activities were measured in ten obese premenopausal women (mean age 35 +/- 5 years) who took part in a six month endurance exercise training programme. The programme involved four to five 90 min training sessions per week at about 50 to 55% of maximal endurance power (VO2max). Before training, the ratio of insulin to glucose area measured during an oral glucose tolerance test (OGTT) was significantly correlated with fat mass (r = 0.72, P < 0.05) as well as with abdominal AT-LPL activity (r = 0.69, P < 0.05). The training programme induced a significant increase in VO2max (P < 0.05) whereas no significant change in the mean body composition was observed. Abdominal as well as femoral AT-LPL activities were significantly reduced after the exercise training programme (P < 0.05) whereas plasma post-heparin (PH) LPL activity was significantly increased by training (P < 0.05). No significant association was observed between changes in VO2max and in body composition parameters and changes in abdominal or femoral AT-LPL activities. However, changes in insulin sensitivity, as estimated by changes in the insulin area/glucose area ratio were positively correlated with changes in abdominal AT-LPL activity expressed on a per cell (r = 0.72, P < 0.05) or per surface area (r = 0.81, P < 0.01) basis. These results suggest that the reduction in AT-LPL activity in both fat depots following endurance training in obese women can occur despite the lack of significant decrease in body weight and average fat cell size.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed1996

Differential regulation of lipoprotein lipase in the macrophage J774.2 cell line by cytokines.

The regulation of macrophage lipoprotein lipase (LPL) by cytokines is of potentially crucial importance in the pathogenesis of atherosclerosis and in the responses to endotoxin challenge. However, the precise mechanisms by which different cytokines modulate the expression of macrophage LPL activity are poorly understood. The action of six cytokines and bacterial lipopolysaccharide (LPS) on LPL function using the murine J774.2 cell line as a model system has, therefore, been studied. Although exposure to LPS, interleukin 11 (IL-11), tumour necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma) and IL-1, over the physiological range of concentrations, resulted in a decrease in the heparin-releasable LPL activity, LPL-mRNA levels and LPL-protein content of the cells, stimulation with IL-6 and leukaemia inhibitory factor (LIF) had no effect. The maximum suppression of LPL activity and mRNA levels in the cells by IFN-gamma (60%) was lower than that produced by LPS, IL-11, TNF-alpha and IL-1 (78-97%). Each cytokine displayed a characteristic dose-dependent pattern for the suppression of LPL activity and mRNA levels with IL-11/TNF-alpha being more potent than IFN-gamma/IL-1. More than 80% of the decrease in the LPL activity, at all doses of IL-11, TNF-alpha, IFN-gamma and IL-1, was due to a corresponding reduction in the mRNA levels. The time course of responses to LPS, IL-11, TNF-alpha, IFN-gamma and IL-1 were similar, with the time required to achieve half maximal suppression of LPL activity being between 7 and 9.5 h in each case. These results indicate that LPL in J774.2 macrophages is regulated differentially by various cytokines and that the major control responsible for the reduction of LPL activity by IL-11, TNF-alpha, IFN-gamma and IL-1 is exerted at the level of mRNA metabolism (decreased transcription or RNA stability). The responses identified also displayed several differences to those described previously for adipocytes (e.g. 3T3-L1 cell line), thereby suggesting the existence of potential cell-specific mechanisms for the regulation of LPL by cytokines.

Animals↗
PubMed1988

Regulation of lipoprotein lipase immunoreactive mass in isolated human adipocytes.

Previous studies of human adipose tissue lipoprotein lipase (LPL) have focused on enzyme catalytic activity, and have not measured the LPL protein directly. To study the regulation of the LPL protein, an antibody against purified bovine LPL was used. To demonstrate the specificity of the antiserum, adipose homogenates were Western blotted, and adipocytes were radiolabeled and the cell homogenates immunoprecipitated, yielding a single specific band at 53 kD. Breakdown products of LPL were demonstrated at 35 and 20 kD by Western blotting. An ELISA for human adipose LPL was established, in which LPL was sandwiched between affinity-purified antibody and biotinylated affinity-purified antibody. The standard curves for bovine LPL and human adipose LPL were parallel, and LPL activity correlated strongly with LPL immunoreactive mass. Thus, the bovine LPL standard curve was used to estimate LPL immunoreactive mass from human adipose tissue. The regulation of LPL activity and immunoreactive mass were compared in cultured adipocytes in the presence an absence of insulinlike growth factor-I/somatomedin C (IGF-I), insulin, and fetal bovine serum. IGF-I and a high insulin concentration (70 nM) stimulated only the heparin-releasable (HR) component of LPL activity and immunoreactive mass, and neither IGF-I nor insulin affected LPL specific activity. In contrast, 10% fetal bovine serum stimulated HR activity, HR mass, and cellular extractable (EXT) immunoreactive mass, with no effect on EXT activity. This resulted in a decrease in EXT specific activity in response to serum. The effects of the locally produced nucleosides adenosine and inosine were studied in a similar manner. As with serum, adenosine stimulated HR activity, HR mass, and EXT immunoreactive mass, resulting in a decrease in EXT specific activity. Inosine stimulated an increase in HR activity and HR mass, but had no effect on EXT, and thus did not change LPL specific activity. Thus, a sensitive ELISA for adipose tissue LPL has been developed using a specific, well-characterized antibody. Regulation of human LPL immunoreactive mass was demonstrated in vitro by IGF-I, serum, high concentrations of insulin, adenosine, and inosine. This method will permit further investigations into the regulation of the LPL protein.

Adenosine↗
PubMed1986

Regulation of lipoprotein lipase synthesis by recombinant tumor necrosis factor--the primary regulatory role of the hormone in 3T3-L1 adipocytes.

Tumor necrosis factor (TNF), a protein homologous to cachectin, has been implicated in mediating cachexia. This effect at least in part has been suggested to occur through the influence of the hormone on adipose tissue metabolism. Using fully differentiated 3T3-L1 adipocytes as a model system, we have been investigating the effects of recombinant TNF (rTNF) on key features of adipocyte metabolism. Exposure of fully differentiated 3T3-L1 adipocytes to recombinant tumor necrosis factor resulted in a dose and time-dependent suppression of the activity of lipoprotein lipase. The loss in activity results from an effect on the synthesis of the enzyme, as determined by a decreased incorporation of [35S]methionine into immunoprecipitable lipoprotein lipase. No effect of rTNF on the half-life of the enzyme was observed. General protein synthesis, as judged by [35S]methionine incorporation into acid-insoluble protein, was minimally affected by exposure of the cells to rTNF; this was further confirmed by sodium dodecyl sulfate-polyacrylamide gel analysis of total cellular protein. As opposed to our previously reported results with crude preparations of TNF, no effect on either the ability of the adipocytes to synthesize and store or mobilize triacylglycerol was observed. Our results are consistent with the hypothesis that other hormones present in crude preparations of TNF acting either alone or synergistically with TNF play a major role in the further metabolic derangements associated with adipose tissue during cachexia.

Adipose Tissue↗
PubMed1980

Effect of acute vigorous exercise on lipoprotein lipase activity of adipose tissue and skeletal muscle in physically active men.

Ten well-trained men ran a distance of 20 km in the morning after overnight fasting. Lipoprotein lipase (LPL) activity was determined from heparin eluates of adipose tissue and skeletal muscle before and after the exercise. The mean LPL activity rose 2.1-fold in skeletal muscle (p < 0.01) and by 20 % in adipose tissue (p < 0.05) during the running. No significant change occurred in serum lipid or lipoprotein concentrations. The plasma insulin decreased and plasma glucagon increased during the exercise. The muscle LPL increment was significantly related to the fall of insulin/glucagon ratio. The results show that during exercise the skeletal muscle is adapted for increased uptake of circulating triglycerides which are either utilized immediately or used for restoration of muscle lipid stores after the end of exercise.

Adipose Tissue↗
PubMed1994

A novel amino acid substitution (His183-->Gln) in exon 5 of the lipoprotein lipase gene results in loss of catalytic activity: phenotypic expression of the mutant gene in a heterozygous state.

We have identified a hitherto unrecognized mutation of the lipoprotein lipase gene (LPL) in a Finnish family with Russian and Swiss ancestors. A single base pair substitution of a guanine for cytosine in codon 183 of exon 5 of the LPL gene results in a change of histidine to glutamine in the mature enzyme protein. Expression of a mutant cDNA construct in COS cells resulted in secretion of inactive LPL enzyme protein confirming the functional significance of the mutation. The proband, a 50-year-old female and her two daughters were all heterozygous for the His183-->Gln mutation. Clinically, the proband was characterized by variable and occasionally severe hypertriglyceridemia, obesity, hypertension, coronary heart disease and non-insulin-dependent diabetes mellitus. The daughters, aged 24 and 19 years, were also obese but had milder hypertriglyceridemia. In conclusion, we have identified a novel LPL mutation that results in the synthesis of an inactive enzyme protein. Although the assessment of a causative link between the mutation and hyperlipidemia awaits further studies, our data suggest that heterozygosity for a functional defect of LPL should be considered in patients presenting with the metabolic dyslipidemic syndrome, "syndrome-X."

Amino Acids↗
PubMed1999

Identification of a silencing element in the chicken lipoprotein lipase gene promoter: characterization of the silencer-binding protein and delineation of its target nucleotide sequence.

Lipoprotein lipase (LPL) hydrolyzes triglycerides in chylomicrons and very low density lipoproteins (VLDL) and plays a central role in lipid metabolism. It is regulated tissue-specifically. By deletion analysis, a negative regulatory element was identified in the chicken LPL gene promoter at base pairs (bp) -263 to -241. This sequence contained two palindromic halves with a three nucleotide spacer. Either half was sufficient for full inhibitory function. A protein complex bound specifically to this element and a high correlation was found between binding of the complex and inhibition of transcription. Its molecular mass, evaluated by native gel electrophoresis and Ferguson plot analysis, was 120 kDa. UV cross-linking followed by SDS-PAGE revealed two protein subunits of 48 kDa and 44 kDa, respectively. This inhibitory protein complex may contribute to the tissue-specific regulation of LPL gene transcription. It was much more abundant in liver than in adipose tissue and heart. Our data showed that this negative element inhibited transcription even when placed at an upstream location (-666), but failed to function in the herpes simplex virus thymidine kinase promoter, indicating that it acted in conjunction with other element(s) in the chicken LPL gene to inhibit transcription.

Animals↗
PubMed1978

Metabolism of cholesterol-enriched chylomicrons. Catabolism of triglyceride by lipoprotein lipase of perfused heart and adipose tissues.

The chemical and biochemical properties of cholesterol-enriched and cholesterol-poor chylomicrons from rat lymph have been compared. The enriched particles, prepared from cholesterol-containing lipid dispersions, passed into the duodenum, had four to ten times the cholesteryl ester content of the control chylomicrons but had the same content of total "core" (cholesteryl ester + triglyceride) lipid. Both chylomicron species had the same protein composition, the same phospholipid composition, and the same composition of triglyceride fatty acids. The rate of hydrolysis of chylomicron triglyceride for enriched and control particles was determined using both soluble and membrane-supported lipoprotein lipase (LPL) species from heart and adipose tissues. The lipase that was functional in the isolated perfused heart showed no significant difference in initial catabolic rate with cholesterol-enriched and control chylomicrons. The same result was obtained with this isolated LPL species in vitro. The lipase that was functional in isolated perfused epididymal adipose tissue showed a slightly lower catabolic rate with cholesterol-enriched particles (84% of that obtained with control chylomicrons). The same result was obtained with isolated adipose tissue LPL. It is concluded that cholesteryl ester content of chylomicrons under these conditions neither affects their protein composition nor has a major effect on their rate of reaction with lipoprotein lipase.

Adipose Tissue↗
PubMed1982

Lipoprotein lipase and hepatic lipase deficiencies associated with impaired chylomicron clearance in D-(+) galactosamine hepatitis.

D-(+) galactosamine (GaIN) produces a reversible from of hepatic injury in the rat, accompanied by alterations in morphology and composition of plasma lipoproteins in the fasting state. Lipoprotein lipase (LPL) and hepatic lipase (HL) activities were measured in fasting control and GaIN rats 24 hr after GaIN injection and initiation of fasting. Significant (p less than 0.001) deficiencies of both enzymes were noted in GaIN animals as compared to controls with LPL activity decreasing to 37.6% and HL activity to 23.2% of control values in GaIN animals. Serial enzyme determinations performed in both GaIN and control animals after gastric fat loading revealed an early persistent HL deficiency (p less than 0.025) at 9 hr after GaIN injection and initiation of fasting which persisted after the fat loading at 15 hr, and a later appearing LPL deficiency (p less than 0.025) was noted at 24 hr after GaIN injection and at 9 hr after fat loading. Serial compositional studies of plasma lipoproteins in pooled specimens after a gastric fat load revealed a marked chylomicronemia in GaIN animals compared to controls which reached a maximum at 12 hr after fat loading. A slight increase in VLDL (very low density lipoprotein) triglyceride and total cholesterol (CH) and a late-appearing (16 hr after fat loading) LDL (low density lipoprotein) CH peak, consisting mostly of unesterified CH, were also noted in GaIN rats as compared to control animals. These data demonstrate a defect in chylomicron (CM) catabolism in GaIN hepatopathy in the rat which is probably secondary to the observed severe LPL and HL deficiencies, although other factors such as activator deficiency, plasma inhibitory substances, and a defective CM particle may be important.

Animals↗
PubMed2001

Effects of estradiol and progesterone on body composition, protein synthesis, and lipoprotein lipase in rats.

Prior studies suggest that estradiol and progesterone regulate body composition in growing female rats. Because these studies did not consider the confounding effect of changes in food intake, it remains unclear whether ovarian hormones regulate body composition independently of their effects on food intake. We utilized a pair-feeding paradigm to examine the effects of these hormones on body composition. In addition, skeletal muscle protein fractional synthesis rate and adipose tissue lipoprotein lipase activity were measured to examine pathways of substrate deposition into fat and fat-free tissue. Female Sprague-Dawley rats [pubertal: 7-8 wk old; 190 +/- 0.5 (SE) g] were separated into four groups: 1) sham-operated (S; n = 8), 2) ovariectomized plus placebo (OVX; n = 8), 3) ovariectomized plus estradiol (OVX+E; n = 8), and 4) ovariectomized plus progesterone (OVX+P; n = 8). All ovariectomized groups were pair-fed to the S group. Body composition was measured using total body electrical conductivity. The relative increase in fat-free mass was greater (P < 0.01) in the OVX group (31 +/- 2%) than in the S (17 +/- 2%), OVX+E (18 +/- 2%), and OVX+P (22 +/- 2%) groups. The fractional synthetic rates of gastrocnemius muscle protein paralleled changes in fat-free mass: OVX had a higher (P < 0.05) synthesis rate (21 +/- 3%/day) than S (12 +/- 2%/day), OVX+E (11 +/- 2%/day), and OVX+P (8 +/- 1%/day) groups. Body fat increased in the S group (31 +/- 7%; P < 0.01), whereas the OVX groups lost fat (OVX: -10 +/- 7%; OVX+E: -15 +/- 7%; OVX+P: -13 +/- 7%). No differences in lipoprotein lipase were found. Our results suggest that estradiol and progesterone may regulate the growth of fat and fat-free tissues in female rats. Moreover, ovarian hormones may influence skeletal muscle growth through their effects on skeletal muscle protein synthesis.

Adipose Tissue↗
PubMed1995

Corn oil, palm oil and butterfat fractions affect postprandial lipemia and lipoprotein lipase in meal-fed rats.

Our objective was to investigate the time course of postprandial lipemia and lipolytic activity in male Sprague-Dawley rats trained to eat meals containing butterfat fractions, palm oil or corn oil. Baseline and postprandial blood samples were obtained via a carotid cannula in rats fed the experimental diets for 4 wk. Rats fed saturated fats compared with corn oil showed a significantly greater peak increase in postprandial triacylglycerol concentrations. Corn oil ingestion resulted in significantly lower concentrations of cholesterol and triacylglycerol in plasma and significantly less triacylglycerol accumulation (millimoles per liter per 24 h) compared with ingestion of saturated fats. Postheparin plasma lipoprotein lipase activity and plasma insulin concentration were generally greater with ingestion of corn oil compared with palm oil or butterfat. Palm oil ingestion resulted in a biphasic plasma triacylglycerol response curve and greater postheparin plasma lipoprotein lipase activity compared with butterfat ingestion, suggesting differential effects of saturated fats on postprandial lipemia. Our results indicate that greater postprandial lipemia with ingestion of saturated fats compared with corn oil may be due in part to slower plasma triacylglycerol clearance.

Animals↗
PubMed1996

Temporal-regulation of serum lipids and stearoyl CoA desaturase and lipoprotein lipase mRNA in BALB/cHnn mice.

Databases for genes expressed in humans or cell cultures are being developed as a part of the Human Genome Project. Because genomes respond to nutritional and other environmental variables, quantitative analyses of mRNA abundance under defined nutritional and physiological states are required to understand normal metabolism and to clarify differences between normal and disease phenotypes. Reported here are comparisons of food intake, growthp5erum lipids and expression of mRNA for hepatic stearoyl CoA desaturase (Scd1) and heart lipoprotein lipase (Lpl) in female BALB/cHnn mice following food deprivation and refeeding at the end of 2 wk of feeding semipurified diets with 3, 10 or 20% corn oils. Body weights and utilization of dietary energy were similar for mice fed all three diets. There were no differences in serum lipid concentrations associated with the level of dietary fat during subsequent food deprivation and refeeding, but significant differences in serum triglycerides and total serum cholesterol were observed between food-deprived and fed mice. Heart lipoprotein lipase and hepatic Scd1 mRNA expression levels were affected significantly by concentration of corn oil and by time after eating. These and other studies examining gene regulation by dietary variables and nutrient availability are discussed in relation to development of diet-regulated gene databases for laboratory animals fed semipurified diets.

Animals↗
PubMed1998

Triglyceride turnover, lipoprotein lipase activity, and fat cell size in adipose tissue of rats during the first 2 weeks of pregnancy.

Understanding the biological function of the fat retained during pregnancy is important when estimating energy needs during reproduction. Women as well as rats are often considered to gain fat at specific anatomical sites during pregnancy and use this fat as a source of energy during lactation. However, mobilized body fat covers only a minor part of the energy needed by the lactating rat dam. In this paper, fat cell size, lipoprotein lipase activity, as well as triglyceride turnover in parametrial and subcutaneous adipose tissues were studied during the first 2 weeks of gestation and in virginal controls to further explore the metabolic and physiological basis for changes in body fat during reproduction in rats. Pregnancy increased the size of parametrial but not of subcutaneous adipocytes. The lipoprotein lipase activity in subcutaneous adipocytes was not increased by pregnancy. The accumulation in adipose tissue of 14C from orally administered 14C-oleic acid was higher in virginal than in pregnant rats. No effect of pregnancy on the rate of lipid turnover in parametrial or subcutaneous adipocytes was found. The findings are in accordance with the contention that body fat gained during rat pregnancy, to a large extent, is a consequence of a general growth of maternal tissues rather than the result of a stimulating effect of pregnancy on fat accumulation by adipocytes from specific body sites.

Adipocytes↗
PubMed1985

Essential role of post-heparin lipoprotein lipase activity and of plasma testosterone in coronary artery disease.

89 consecutive men for whom coronary angiography was requested because of suspected coronary artery disease were investigated with respect to plasma lipids, lipoproteins, post-heparin lipoprotein lipase (LPL), and some hormones that influence LPL. The severity of coronary-artery disease was expressed by the coronary score (CS). Coronary-artery disease correlated with total plasma cholesterol, low-density lipoproteins, high-density lipoprotein cholesterol (HDL-chol), and HDL2. In addition, there was a strong negative correlation (r = -0.479, p less than 0.001) between CS and LPL, as well as positive correlations between CS and plasma triglycerides (p less than 0.01) and very low-density lipoproteins (VLDL, p less than 0.01). The impairment of LPL activity correlated with increased VLDL and decreased HDL-chol. The extent of coronary-artery disease is thus strongly influenced by an LPL deficit. LPL activity correlated with plasma testosterone, and there is evidence that low plasma testosterone may be partly responsible for the low LPL and HDL-chol.

Cholesterol↗
PubMed1999

Effect of gemfibrozil on triacylglycerol synthesis and secretion by liver and lipoprotein lipase activity in adipose tissue of rats.

The role of gemfibrozil, a hypotriglyceridemic drug, in synthesis, secretion and catabolism of triacylglycerols (TG) in rats was assessed. Chow diet-fed Sprague-Dawley rats were given various doses of gemfibrozil (10, 30 and 100 mg/kg body weight) for 2 weeks. Rats receiving the drug at the lowest dose significantly lowered the concentration of serum TG and apolipoprotein (apo) B in comparison with control rats. Synthesis of fatty acids from [14C]acetate and esterification of [14C]oleate to TG by the liver were not suppressed by the drug. Secretion rates of TG and apo B, measured by the Triton method, were suppressed at the highest dose. Lipoprotein lipase activity of the acetone powder prepared from adipose tissue was not influenced by the drug. These results indicate that the primary cause of hypotriglyceridemic action of gemfibrozil is not due to suppressing synthesis and secretion of TG by the liver or enhancing lipoprotein lipase activity in adipose tissues.

Acetates↗