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Feeding hydrogenated fatty acids and triglycerides to lactating dairy cows.

Effects of feeding hydrogenated tallow fatty acids and triglycerides to lactating dairy cows were studied using five primiparous Holstein cows in a 5 x 5 Latin square design. A control diet with no supplemental fat and diets containing either hydrogenated tallow fatty acids or triglycerides at 2 and 5% levels were fed for ad libitum intake. Diets were isonitrogenous but not isocaloric. Each treatment period consisted of 28 d; the last 14 d were used for data collection. Fat-supplemented diets had no effects on DM intake, milk fat percentage, milk protein percentage, and BW compared with the control diet. Energy intake and milk yields were higher for cows fed fat-supplemented diets. Adding fatty acids to diets increased milk fat percentage above that in milk from cows fed triglyceride diets. Apparent digestibilities of DM and OM were lowered by the addition of fat, mainly in response to fatty acid additions. Feeding fatty acids reduced ash digestibility compared with feeding triglycerides, and NDF digestibility also tended to be lower for cows fed fatty acid diets. Fat addition to diets reduced fatty acid digestibility; digestibility of added fat averaged 37.7%. Although of similar saturation, the triglyceride supplement was more ruminally inert than the fatty acid supplement. Esterification and degree of saturation are features of importance when processing tallow for use in ruminant diets.

Animals↗

Essential fatty acids in tissue phospholipids and triglycerides of the zinc-deficient rat.

This study addressed the possibility that zinc deficiency has different effects on the fatty acid composition of triglyceride compared to total phospholipid. Male weanling Sprague-Dawley rats were maintained for 6 weeks on a semisynthetic diet deficient in zinc (3 mg/kg zinc). Control rats (40 mg/kg zinc) were pair-fed. Lipid fractionation and fatty acid analysis were by thin-layer and gas chromatography, respectively. In zinc-deficient rats, the percentage of linoleic acid was increased or that of arachidonic acid was decreased in total phospholipids of plasma, liver, and testis, and in skin total lipids. Saturated and monounsaturated fatty acids were increased in the triglyceride of liver but decreased in the triglyceride of epididymal fat of zinc deficient rats. Essential fatty acids, as a proportion of total fatty acids, were decreased in triglyceride of liver but increased in triglyceride of epididymal fat of zinc-deficient rats. Our fatty acid data from tissue total phospholipids therefore support the concept that linoleic acid desaturation is impaired in zinc deficiency.

Adipose Tissue↗

Plasma triglyceride and glucose clearance in broiler-type and white Leghorn chickens with different degrees of adiposity.

Broiler-type and White Leghorn chicks were given diets containing 30.5, 26.2, or 22.3% protein with and without addition of 5% corn oil during an 8- to 9-week conditioning period. The absolute weight of the abdominal fat pad was greater in the broiler-type birds on all dietary treatments. As a percentage of body weight the abdominal fat pads were similar in broiler-type and White Leghorn birds only when the diet contained 30.5% of protein without added oil. Following a 16-hr fast, plasma glucose was higher in the broiler-type than in the White Leghorn birds, whereas plasma triglyceride concentrations were higher in White Leghorns. In birds refed a high-fat meal, plasma glucose showed little change except in the broiler chickens previously fed the 30.5% protein diet without added oil. In these birds plasma glucose declined over a 5-hr period to reach a mean value of 130 mg/100 ml. Plasma triglyceride concentrations in both breeds were markedly elevated within 45 min of refeeding with a high-fat meal, but the peak concentrations were higher in the White Leghorns than in the broiler-type birds. Previous consumption of the high-oil diet increased postprandial triglyceride concentration in the plasma of the broiler-type but reduced it in the White Leghorn chickens. The difference in response of the chickens of the different genetic stocks is attributed to differences in the development of the activities of the systems associated with 1) fatty acid absorption and movement of triglycerides from the intestinal mucosa to the circulation and 2) clearance of plasma triglycerides to the adipocytes as a result of lipoprotein lipase activity.

Adipose Tissue↗

Serum leptin and triglyceride levels in patients on treatment with atypical antipsychotics.

BACKGROUND: Weight gain is a common adverse effect associated with the use of most antipsychotic drugs. Leptin has been reported to be associated with antipsychotic-induced weight gain. Previous studies have demonstrated a relationship between the atypical antipsychotics clozapine and olanzapine and serum leptin levels. We planned to comparatively investigate the effects of the atypical antipsychotics quetiapine, olanzapine, risperidone, and clozapine on leptin and triglyceride levels and weight gain. METHOD: The study population comprised 56 patients with DSM-IV schizophrenia, who were divided into 4 treatment groups: quetiapine (N = 14), olanzapine (N = 14), risperidone (N = 14), or clozapine (N = 14) monotherapy, and a control group of 11 patients receiving no psychopharmacologic treatment. The patients were evaluated at baseline and at the sixth week according to the Positive and Negative Syndrome Scale (PANSS), body mass index (BMI), weight, and fasting serum leptin and triglyceride levels. Data were gathered in 2001 and 2002. RESULTS: Olanzapine and clozapine caused a marked increase in weight and serum triglyceride and leptin levels, though increases in these variables were modest in the patients receiving quetiapine and minimal in those receiving risperidone. There were positive correlations between serum leptin levels and BMI and triglyceride levels. Clinical efficacy, as indicated by decrease in total PANSS scores, was associated with leptin levels in all atypical antipsychotic groups. CONCLUSION: Our results suggest that leptin may be associated with olanzapine- and clozapine-induced weight gain and that quetiapine appears to have modest influence and risperidone appears to have minimal influence on leptin and triglyceride levels and weight gain compared with olanzapine and clozapine.

Adult↗

Genetic effects for plasma factor VII levels independent of and in common with triglycerides.

BACKGROUND: Coagulation factor VII has been demonstrated as a potential risk factor for cardiovascular disease. Both genes and non-genetic factors are related to plasma levels of factor VII. However, the extent to which genetic effects influence variability in plasma factor VII levels is unknown. Further, increased levels of plasma factor VII are associated with serum triglycerides, yet the reason for this association is not fully understood. METHODS AND RESULTS: Quantitative genetic analyses were applied to evaluate the relative importance of genetic and different environmental influences on plasma factor VII levels and to test the significance of genetic and environmental factors in common to factor VII and triglycerides in 215 pairs of middle-aged and elderly twins, of whom 104 were reared apart and 120 were women. Genetic influences were found to account for 57% of the individual differences in plasma factor VII levels, whereas shared-rearing and residual-familial environmental factors were not significant. Furthermore, a significant genetic correlation of 0.38 was found between factor VII and triglycerides, but the environmental correlation between these two measures was not significant. Genetic factors in common to factor VII and triglycerides explain about 7% of the total variance for factor VII. CONCLUSION: The present study suggests that there are substantial genetic influences on plasma factor VII levels. Furthermore, genetic effects explain the phenotypic association between factor VII and triglycerides.

Aged↗

[Serum triglycerides as a risk factor for atherosclerosis].

The importance of plasma triglycerides as a risk factor for the development of coronary artery disease (CAD) has been controversial for many years. In univariate analysis plasma triglycerides predict CAD in several studies, but this effect is attenuated when high-density lipoprotein (HDL) cholesterol is included in the analysis. The controversy can be explained by the complexity of lipoprotein metabolism. Plasma triglycerides serve as markers for metabolic and clinical conditions associated with increased CAD risk. Several recent studies shed new light on the significance of triglycerides for the development of CAD, depending on their level in plasma: there appears to be an optimal concentration < 1.1 mmol/l, an intermediate range with increased risk at values 1.1-4 mmol/l, above which level the risk decreases. Very high levels of triglycerides confer increased risk of pancreatitis.

Biomarkers↗

Lowering triglyceride values in an occupational setting.

Within a multiphasic screening program it was possible to establish an effective industrial counseling program for individuals identified as potential cardiovascular risks by their serum triglyceride values. A significant reduction of serum triglyceride values was obtained even where minimal supervision was used to modify aspects of an employee's life style. A counseled group of 109 male employees, 40 years and older, with serum triglyceride levels of 200 mg. or higher per 100 ml., was matched by location and age with a control group of 135 noncounseled individuals with similarly elevated triglyceride levels. Individuals in both groups showing significant percentage reduction were those whose serum levels began above 250 mg. per 100 ml. The employees who lowered their triglyceride values most significantly were those that had dieted and were periodically counseled and checked by a physician.

Adult↗

Acute and chronic effects of a 24-hour intravenous triglyceride emulsion challenge on plasma lecithin: cholesterol acyltransferase, phospholipid transfer protein, and cholesteryl ester transfer protein activities.

Lecithin:cholesterol acyltransferase (LCAT), phospholipid transfer protein (PLTP), and cholesteryl ester transfer protein (CETP) are key factors in remodeling of high density lipoproteins (HDL) and triglyceride-rich lipoproteins. We examined the effect of a large, 24 h intravenous fat load on plasma lipids and free fatty acids (FFA) as well as on plasma LCAT, PLTP, and CETP activity levels in 8 healthy men. The effect of concomitant insulin infusion was also studied, with 1 week between the study days. During Lipofundin(R) infusion, plasma triglycerides and FFA strongly increased after 8 and 24 h (P < 0.001), whereas HDL cholesterol decreased (P < 0.01). The increase in triglycerides was mitigated with concomitant insulin infusion (P < 0.05 from without insulin). Plasma LCAT activity increased by 17.7 +/- 7.7% after 8 h (P < 0.001) and by 26.1 +/- 11. 1% after 24 h (P < 0.001), PLTP activity increased by 19.7 +/- 15.6% after 24 h (P < 0.001), but CETP activity remained unchanged. Concomitant insulin infusion blunted the increase in plasma LCAT activity (P < 0.05 from without insulin), but not that in PLTP activity. One week after the first fat load, plasma non-HDL cholesterol (P < 0.02), and triglycerides (P = 0.05) were increased, whereas HDL cholesterol was decreased (P < 0.02). Plasma CETP and PLTP activity levels were increased by 34.8 +/- 30.4% (P < 0.02) and by 15.9 +/- 6.4% (P < 0.02), respectively, but LCAT activity was then unaltered. In summary, plasma LCAT, PLTP, and CETP activity levels are stimulated by a large intravenous fat load, but the time course of their responses and the effects of insulin coadministration are different. Changes in plasma LCAT and PLTP activities may be implicated in HDL and triglyceride-rich lipoprotein remodeling under the present experimental conditions.

Carrier Proteins↗

Triglyceride-lowering effect of omega-3 LC-polyunsaturated fatty acids--a review.

There is increasing evidence that serum triglycerides are a significant and independent risk factor for CVD. The aim of this report is to review recent literature pertinent to the triglyceride-lowering effect of omega-3 long chain polyunsaturated fatty acids (LC-PUFA). Animal data are not considered because they are difficult to extrapolate to the human situation. A large body of evidence derived from epidemiological studies and clinical trials has consistently demonstrated that this effect is dose-dependent and can be achieved by diet. The smallest amount of omega-3 LC-PUFA needed to significantly lower serum triglycerides appears to be approximately 1 g/day as provided by a fish diet. Use of fish oil administering as little as 0.21 g EPA and 0.12 g DHA per day significantly lowered serum triglycerides in hyperlipidemics. In normolipidemics, a daily intake of 0.17 g EPA and 0.11 g DHA, given as a fish oil supplement, induced a non-significant reduction of 22%. These findings must be considered as preliminary and warrant further research. Intake of omega-3 LC-PUFA is frequently reported to modestly increase LDL cholesterol. However, in normo- or slightly hyperlipidemic individuals who received omega-3 LC-PUFA for 4 months or longer, changes of LDL cholesterol were not significantly different from a placebo group. Both EPA and DHA lower serum triglycerides, but they may have a differential effect on lipoproteins. Intake of omega-3 LC-PUFA in the amount mentioned above is safe.

Cardiovascular Diseases↗

Remnant lipoproteins are related to intima-media thickness of the carotid artery independently of LDL cholesterol and plasma triglycerides.

Remnants of triglyceride-rich lipoproteins (TRL) have been implicated in the early development of atherosclerosis. We tested this hypothesis by quantifying the plasma concentration of remnant-like particle cholesterol (RLP-C) in a cohort of healthy 50-year-old men in whom the common carotid artery intima-media thickness (CCA-IMT) was assessed by B-mode ultrasound as a surrogate marker for atherosclerosis. The subjects were given a fat-rich meal to study the generation of RLP-C during postprandial lipemia. Fasting plasma RLP-C and other major fasting plasma lipids and lipoproteins were determined twice, and the mean RLP-C concentration was strongly correlated with CCA-IMT (r = 0.32, P = 0.002). In addition, low density lipoprotein (LDL) cholesterol (r = 0.25, P = 0.01) and plasma triglycerides (r = 0.20, P = 0.05) were significantly related to CCA-IMT. Multivariate analyses showed a triglyceride-independent contribution of RLP-C to CCA-IMT. After fat intake, the median plasma RLP-C concentration was doubled after 3 h. The increase was strongly related to the postprandial generation of TRL apolipoprotein (apo)B-48, and large (S(f) 60;-400) TRL apoB-100. The association with CCA-IMT was somewhat stronger for the 3-h RLP-C level than for the fasting RLP-C concentration [r = 0.27, P < 0.01 (3 h) compared with r = 0.22, P < 0.05 (0 h)]. We conclude that the plasma concentration of RLP-C is related to CCA-IMT, independent of plasma triglycerides and LDL cholesterol, in a healthy middle-aged male population. - Karpe, F., S. Boquist, R. Tang, G. M. Bond, U. de Faire, and A. Hamsten. Remnant lipoproteins are related to intima-media thickness of the carotid artery independently of LDL cholesterol and plasma triglycerides. J. Lipid Res. 2001. 42: 17;-21.

Apolipoproteins↗

[Micronized fenofibrate, decreased triglyceride levels, total cholesterol and LDL fractions in serum].

Elevated serum level of triglycerides is a classic indication for fibrates. Micronized fenofibrate is hypolipemic drug with proven safety and efficacy in a view of triglycerides reduction, but according to few papers published so far on the subject is also effective in decreasing elevated total and LDL cholesterol. The aim of study was to confirm results obtained from these few previous studies. Forty seven persons with lipid disturbances (25 males and 22 females, age range 34-71 yrs. mean 48.0) entered the study. Thirty two patients had a history myocardial infarction and fifteen persons without clinical symptoms of heart diseases. All of them were treated with micronized fenofibrate 200 mg daily. Micronized fenofibrate decreased serum concentration of total cholesterol by 13.4% (p < 0.01), LDL cholesterol by 21.2% (p < 0.001) and triglycerides by 39.5% (p < 0.001) in whole group of patients. Most beneficial effects were obtained in persons with mixed hyperlipidemia: reduction of total cholesterol, triglycerides and LDL cholesterol serum levels was 22.4% (p < 0.01), 52.5% (p < 0.0001), 25.4% (p < 0.01), respectively. In individuals with hypercholesterolemia a reduction of total cholesterol by 11% (p < 0.05) and LDL cholesterol by 15.4% (p < 0.05) was observed. In the group with hypertriglyceridemia or mixed hyperlipidemia reduction of serum triglycerides concentration by 33.5% (p < 0.05) was achieved. No significant change in serum HDL cholesterol level in any group was observed. The treatment with micronized fenofibrate was well tolerated. Our study shows that this drug is safe and seems to be effective in some cases with increased serum total and LDL cholesterol level as well.

Adult↗

[Effects of Kupffer cells stimulated by triglyceride and very low-density lipoprotein on proliferation of rat hepatic stellate cells].

OBJECTIVE: To study the effects of Kupffer cell-conditioned medium (KCCM) derived from triglyceride and very low-density lipoprotein (VLDL) treatment on proliferation of rat hepatic stellate cells (HSC). METHODS: HSC and Kupffer cells were isolated from liver of Wistar rats by in situ perfusion with pronase and collagenase and density gradient centrifugation with Nycodenz and then cultured. KCCM was prepared and MTT colorimetric assay was used to detect HSC proliferation. RESULTS: HSC and Kupffer cells were isolated successfully with high purity. 12.5 mg/L of triglyceride and 25 - 100 mg/L of VLDL promoted HSC proliferation (P < 0.05 or 0.01); KCCM + triglyceride and KCCM + VLDL might promote HSC proliferation as compared with a control group (P < 0.01). There was no significant difference between KCCM + triglyceride and KCCM + VLDL (P > 0.05). CONCLUSION: The technique for isolation of HSC and Kupffer cells described here is simple and reliable. Triglyceride, VLDL and KCCM stimulated by them may promote HSC proliferation and be associated with fatty liver and hepatic fibrogenesis.

Animals↗

A new on-line dual enzymatic method for simultaneous quantification of cholesterol and triglycerides in lipoproteins by HPLC.

We describe an on-line dual detection method using HPLC for lipoprotein analysis that allows simultaneous determination of cholesterol and triglyceride profiles from a single injection of sample. Two different gel permeation columns, TSKgel LipopropakXL and Superose 6HR, were applied to the dual detection system, evaluating analytical performance of the proposed method and the columns by analyzing serum samples from human and nonhuman subjects. Both TSK and Superose columns produced good within-day imprecision values less than 4.7% for cholesterol and 4.2% for triglyceride determination. Linear regression analysis showed the results from the Superose column (y) correlated well with those from the TSK column (x): y = 0.969x + 5.44 (r = 0.990) for total cholesterol (mg/dl), y = 1.08x - 11.14 (r = 0.985) for total triglycerides (mg/dl), and y = 1.093x - 0.06 (r = 0.978) for the ratios of triglycerides to cholesterol (mg/mg). Furthermore, the cholesterol and triglyceride profiles elucidated the differences in the resolution ability of the columns, which have not been apparent from a single lipid profile. We conclude that the dual detection concept with proper choice of column and enzymic reagents specific to the objectives of the particular study can facilitate studies of lipoprotein metabolism.

Cholesterol↗

Triglycerides predict plasma fibronectin in children with type I diabetes mellitus rather than diabetes.

Fibronectins are adhesive proteins considered as markers of endothelial activation. Plasma fibronectin levels in diabetes mellitus (DM) have been found to be associated with atherosclerotic risk factors. This study was carried out to investigate plasma fibronectin and its relation with serum lipids, apolipoproteins AI, B100 and lp(a) in diabetic children. 35 children (19F/16M) with type I DM and 30 non-diabetic age and gender-matched controls were enrolled. Apolipoprotein and fibronectin concentrations were determined with nephelometric methods. Plasma fibronectin levels of the children with type I DM and the control group are not statistically different. HbA1c and triglycerides concentration are found to be significant predictors of plasma fibronectin in diabetic children, while effect of plasma cholesterol, apolipoprotein AI, B100 and lp(a) are insignificant. Diabetic children with triglycerides 1.13 mmol/l have elevated plasma fibronectin (median, 25th-75th percentiles; 29.6, 8.3-40.8 mg/dL) compared to the diabetic > or = 19.9, 8.6-30.7 mg/dL, p < 0.05) and non-diabetic children (16.6, 12.7-32.4 mg/dL, p < 0.01) with triglycerides < 1.13 mmol/L. On the other hand plasma fibronectin concentrations of diabetic and non-diabetic children with high triglycerides are not significantly different. In conclusion our data does not support the concept that plasma fibronectin is elevated in type I diabetes mellitus at least in children, but high plasma triglycerides secondary to diabetes or not is associated with higher FNp concentrations which may have implications on atherogenesis. Plasma cholesterol, apolipoproteins AI, B100 and lp(a) are not significant determinants of FNp in type I diabetic children.

Child↗

Triglyceride, high density lipoprotein, and coronary heart disease.

The National Institutes of Health Consensus Development Conference on Triglyceride, High Density Lipoprotein, and Coronary Heart Disease brought together experts in lipid metabolism, epidemiologists, and clinicians as well as other health care professionals and the public to address the following questions: (1) is the relationship of high triglyceride and/or low HDL cholesterol with coronary heart disease causal? (2) Will reduction of high triglyceride and/or elevation of HDL cholesterol help prevent coronary heart disease? (3) Under what circumstances should triglycerides and HDL cholesterol be measured? (4) Under what circumstances should active intervention to lower triglyceride and/or raise HDL cholesterol be considered in high risk individuals and the general population? (5) What can be accomplished by dietary, other hygienic, and drug treatments? (6) What are the significant questions for future research? Following two days of presentations by experts and discussion by the audience, a consensus panel weighed the evidence and prepared their consensus statement. Among their findings, the panel concluded that (1) existing data provide considerable support for a causal relationship between low HDL and CHD; however, with respect to TG data are mixed and the evidence on a causal relationship is incomplete; (2) initial TG and/or HDL levels modify benefit achieved by lowering low density lipoprotein cholesterol (LDL-C); however, evidence from clinical trials is insufficient to draw conclusions about specific benefits of TG and/or HDL altering therapy; (3) HDL-C measurement should be added to total cholesterol measurement when evaluating CHD risk in healthy individuals provided accuracy of measurement, appropriate counseling, and followup can be assured; (4) there is general agreement with the Adult Treatment Panel (ATP) guidelines that LDL-C is essential in cardiovascular risk assessment, as well as that persons with elevations of LDL-C greater than 150 mg/dl refractory to nondrug therapies may require drug treatment; (5) there is a strong consensus that hygienic approaches (diet, exercise, smoking cessation, weight loss) should be employed to lower TG and/or raise HDL; there is no consensus for the use of drug treatment in patients with borderline hypertriglyceridemia and low HDL-C levels in the presence of a desirable LDL-C level.

Causality↗

Dietary fat level as determinant of protein-sparing actions of structured triglycerides.

This study assessed the effects of total parenteral nutrition (TPN) containing long-chain triglycerides (LCTs), an equimolar physical mixture of LCT and medium-chain triglycerides (MCTs), and a structured triglyceride synthesized from equimolar amounts of MCT and LCT on energy and protein metabolism after thermal injury (25% body surface area full-thickness scald burn). Male Sprague-Dawley rats (245-271 g) received isovolemic diets intravenously that supplied 250 kcal.kg-1.day-1, 2 g amino acid nitrogen.kg-1.day-1, and 50% of nonprotein calories as lipid and 50% as dextrose for 3 days. Whole-body and tissue leucine kinetics were estimated by a 4-h continuous infusion of L-[1-14C]leucine on day 3. Nitrogen balance, plasma albumin, plasma glucose, energy expenditure, and whole-body and liver and rectus muscle protein kinetic parameters were determined. No significant differences were noted in any of the parameters measured. This study suggests that the unique protein-sparing actions usually associated with structured triglyceride administration are not seen when they are provided as 50% of nonprotein calories. In addition, the ratio of MCT to LCT in the starting mixture from which the structured triglycerides are synthesized may be an important determinant of the protein-sparing actions attributed to these lipids.

Animals↗

Poloxamer 407-mediated changes in plasma cholesterol and triglycerides following intraperitoneal injection to rats.

Poloxamer (Pluronic) nonionic surfactant vehicles are a series of chemically-related block copolymers finding widespread use in parenteral formulations as solubilizing and wetting agents for traditional, low-molecular weight organic drug molecules, as well as stabilizing agents for proteins and polypeptide drugs. We report the effects of poloxamer 407 (Pluronic F-127) on plasma cholesterol and triglyceride concentrations in rats. Poloxamer 407 injected into rats by intraperitoneal injection (dose = 1.5 gm/kg) resulted in sustained (greater than 96 hour) hypercholesterolemia and hypertriglyceridemia. A larger dose of poloxamer 407 was required to elevate plasma triglyceride relative to total cholesterol. Ingestion of commercial rat chow had a negligible effect on plasma cholesterol and triglycerides levels in control (no poloxamer injection) animals, but consumption of food by animals that received an intraperitoneal injection of poloxamer 407 (30% w/w) resulted in significantly (p < .05) greater elevations in plasma cholesterol and triglycerides than in fasted animals administered poloxamer 407. The route of poloxamer 407 administration, namely intramuscular vs. intraperitoneal injection, was observed to be a more important factor for poloxamer-induced elevations in plasma cholesterol than poloxamer-mediated elevations in plasma triglycerides. Our results also provide suggestive evidence that the mechanism responsible for the elevation of plasma cholesterol following intraperitoneal injection of a poloxamer 407 solution (30% w/w) to rats may be due to stimulation of 3-hydroxy-3-methylglutaryl-co-enzyme A (HMG-CoA) reductase activity in the liver by the poloxamer vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Anti-lipoprotein lipase antibody in systemic sclerosis: association with elevated serum triglyceride concentrations.

OBJECTIVE: The vascular damage systemic sclerosis (SSc) consists mainly of microvascular changes, but recently macrovascular changes with dyslipidemia were recognized. In systemic lupus erythematosus (SLE), autoantibody to lipoprotein lipase (LPL), a key enzyme that hydrolyzes triglycerides, suggested a role of autoimmunity for elevated serum triglyceride levels and atherosclerosis. We investigated the prevalence and levels of anti-LPL antibodies, their clinical correlation, and their functional significance in patients with SSc. METHODS: Serum samples from patients with diffuse cutaneous SSc (dSSc; n = 55), limited cutaneous SSc (lSSc; n = 75), SLE (n = 21), and dermatomyositis (DM; n = 21) and healthy controls (n = 41) were examined by ELISA. The presence of anti-LPL antibody was evaluated by immunoblotting analysis using purified LPL. To determine the functional relevance of anti-LPL antibody in vivo, we assessed whether anti-LPL autoantibody was able to inhibit LPL activity using the LPL activity kit. RESULTS: ELISA revealed that IgG or IgM anti-LPL antibodies were detected in 35% of SSc patients, while they were also positive in 67% of SLE patients and 43% of DM patients. The presence of IgG anti-LPL antibody was associated with elevated serum triglyceride levels, greater extent of skin fibrosis, and more frequent presence of lung fibrosis, heart involvement, and anti-topoisomerase I antibodies. The presence of anti-LPL autoantibody was confirmed by immunoblotting analysis. LPL activity was inhibited by IgG anti-LPL antibodies in sera from SSc patients with elevated serum triglyceride levels. CONCLUSION: Our results suggest that anti-LPL autoantibody contributes to elevated serum triglyceride levels by inhibiting LPL enzyme activity in patients with SSc.

Autoantibodies↗