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PubMed2001

Retinoid X receptor agonist elevation of serum triglycerides in rats by potentiation of retinoic acid receptor agonist induction or by action as single agents.

Hypertriglyceridemia is a major side-effect of retinoid therapy in humans. We previously reported that agonists for the retinoic acid receptors (RARs), but not the retinoid X receptors (RXRs), elevate serum triglycerides in male Fischer rats, and that, surprisingly, the RAR/RXR pan-agonists 9-cis-retinoic acid and AGN 191659 [(E)-5-[2-(5,6,7,8-tetrahydro-3,5,5,8,8-pentamethyl-2-naphthyl)propen-1-yl]-2-thiophenecarboxylic acid] induce 2- to 3-fold higher levels of serum triglycerides than the RAR-selective agonists alone. We have now demonstrated that hypertriglyceridemia induced by an RAR agonist, AGN 190121 [4-[4-(2',6',6'-trimethylcyclohex-1-enyl)-but-1-yne-3-enyl]benzoic acid], is substantially potentiated by the RXR-selective agonists AGN 191701 [(E) 2-[2-(5,6,7,8-tetrahydro-3,5,5,8,8-pentamethyl-2-naphthyl)propen-1-yl]-4-thiophene-carboxylic acid] and AGN 192849 [(3,5,5,8,8,-pentamethyl-5,6,7,8-tetrahydronaphthalen-2-yl) (5 carboxypyrid-2-yl)sulfide] in a dose-dependent manner. RXR-specific retinoids, as previously reported, had no independent effect on serum triglycerides when tested at 24 hr after final dosing, but did elicit a reversible hypertriglyceridemia at 2.5 and 5 hr. This induction of serum triglycerides could not be blocked by the potent RAR-specific antagonist AGN 193109 [4-[(5,6-dihydro-5,5-dimethyl-8-(4-methylphenyl)-2-naphthalenyl)-ethynyl] benzoic acid]. The RXR ligand-induced hypertriglyceridemia was independent of the effect of feeding or fasting. The relative potencies of RXR-specific retinoids for acute triglyceride elevation (AGN 194204 [3,7-dimethyl-6S,7S-methano-7-[1,1,4,4-tetramethyl-1,2,3,4-tetrahydronaphth-7-yl] 2(E),4(E) heptadienoic acid] > AGN 192849 approximately AGN 191701) approximately correlated with potencies in the activation of the RXR receptors. The RAR/RXR pan-agonist effect included >50% inhibition of total heparin-releasable lipase activity in serum, consistent with inhibition of lipase-mediated triglyceride disposal. These data also indicate that RAR and RXR ligands can act synergistically to induce hypertriglyceridemia through distinct mechanisms of action.

Animals↗
PubMed1999

3-Hydroxy-3-methylglutaryl CoA reductase inhibitors reduce serum triglyceride levels through modulation of apolipoprotein C-III and lipoprotein lipase.

Statins are hypolipidemic drugs which not only improve cholesterol but also triglyceride levels. Whereas their cholesterol-reducing effect involves inhibition of de novo biosynthesis of cellular cholesterol through competitive inhibition of its rate-limiting enzyme 3-hydroxy-3-methylglutaryl CoA reductase, the mechanism by which they lower triglycerides remains unknown and forms the subject of the current study. Treatment of normal rats for 4 days with simvastatin decreased serum triglycerides significantly, whereas it increased high density lipoprotein cholesterol moderately. The decrease in triglyceride concentrations after simvastatin was caused by a reduction in the amount of very low density lipoprotein particles which were of an unchanged lipid composition. Simvastatin administration increased the lipoprotein lipase mRNA and activity in adipose tissue and heart. This effect on lipoprotein lipase was accompanied by decreased mRNA as well as plasma levels of the lipoprotein lipase inhibitor apolipoprotein C-III. These results suggest that the triglyceride-lowering effect of statins involves a stimulation of lipoprotein lipase-mediated clearance of triglyceride-rich lipoproteins.

Animals↗
PubMed2002

Hypertriglyceridemia is associated with an elevated blood viscosity Rosenson: triglycerides and blood viscosity.

Elevated blood viscosity is a predictor of cardiovascular disease. The major determinants of blood viscosity are hematocrit and plasma viscosity. Plasma triglycerides elevate plasma viscosity; however, the contribution of plasma triglycerides to blood viscosity after adjustment for other major covariates has not been reported. This cross-sectional study of 257 adult subjects evaluated the associations between fasting plasma lipids, fibrinogen, total serum protein, hematocrit and blood viscosity. Blood viscosity was measured at 37 degrees C with a coaxial cylinder microviscometer at shear rates of 100 and 1 s(-1). Blood viscosity values are reported both as uncorrected measurements and measurements corrected to a hematocrit of 45% by a regression equation. Uncorrected blood viscosity at a shear rate of 100 s(-1) was significantly associated with triglycerides, fibrinogen, high density lipoprotein (HDL) cholesterol, total serum protein, and hematocrit using stepwise multivariate regression analysis. When corrected blood viscosity at 100 s(-1) was the dependent variable, there were statistically significant associations with triglycerides, HDL cholesterol, and total serum protein. Corrected blood viscosity at 1 s(-1) was significantly associated with triglycerides, fibrinogen, total serum protein, and an indicator variable for diabetes mellitus. This study supports an additional mechanism whereby triglycerides may contribute to cardiovascular risk.

Adult↗
PubMed1997

Serum HDL cholesterol values are associated with apoB-containing lipoprotein metabolism and triglyceride-body fat interrelation in young Japanese men.

Serum levels of total cholesterol, high density lipoprotein (HDL) cholesterol, triglyceride, apolipoprotein (apo) AI, ApoB, ApoE and body fat were measured in 226 fasting male Japanese college students aged 18 to 20 years. They were normolipidemic (total cholesterol: 169 +/- 31 mg/dl, triglyceride: 56 +/- 25 mg/dl) and their HDL cholesterol concentrations were high (61 +/- 13 mg/dl). An HDL cholesterol value < 35 mg/dl was observed in only one student (0.4%). In contrast, 112 men (49.6%) had an HDL cholesterol level > or = 60 mg/dl. Even in this normolipidemic group, as compared with students in a top HDL cholesterol tertile (HDL cholesterol; 75 +/- 9 mg/dl), students in a lower HDL cholesterol tertile (HDL cholesterol; 48 +/- 5 mg/dl) had significantly increased serum levels of LDL cholesterol (103 +/- 30 vs. 91 +/- 26 mg/dl), triglyceride (68 +/- 30 vs. 45 +/- 16 mg/dl) and apoB (83 +/- 20 vs 73 +/- 17 mg/dl). In addition, they had greater body mass index (23.2 +/- 3.6 vs. 20.6 +/- 2.5 kg/m2) and greater percent body fat (20.2 +/- 6.2 vs. 16.2 +/- 4.2%) determined using a bioelectrical impedance analyzer. HDL cholesterol levels were much more strongly related to triglyceride (r = -0.37) than was apoAI (r = -0.13). In stepwise multiple regression analysis in 184 nonsmokers, apoE, apoB and fat mass explained 21% of apoAI variability. Triglyceride in addition to these three parameters explained 41% of HDL cholesterol variability. These results suggest that serum levels of HDL cholesterol are associated with metabolism of apoB-containing lipoproteins as well as triglyceride-body fat interrelationship.

Adipose Tissue↗
PubMed1999

Effect of apo E phenotype on plasma postprandial triglyceride levels in young male adults with and without a familial history of myocardial infarction: the EARS II study. European Atherosclerosis Research Study.

The goal of the present study was to assess whether the effect of the apolipoprotein E polymorphism on postprandial lipemia explained part of the risk attributable to familial history of coronary heart disease. Cases (n = 407) were students, aged between 18 and 28 years, whose fathers had a proven myocardial infarction before the age of 55 years. Age-matched controls (n = 415) were recruited from the corresponding student registers. Blood was obtained after an overnight fast and at 2, 3, 4 and 6 h after ingestion of a fatty meal for triglyceride measurements. Apolipoprotein E phenotype was associated with postprandial triglyceride variability in both cases and controls. However, the apolipoprotein E-dependent triglyceride response was not significantly heterogeneous between cases and controls. In the pooled data, postprandial triglyceride levels were higher in carriers of the E2 and, to a lesser extent, of the E4 isoform, than in E3/3 homozygotes, independently of fasting triglyceride levels. At 6 h, triglyceride levels were increased by 21.2% (P < 0.01) in E2 carriers and 11.5% (P = 0.053) in E4 carriers by comparison to E3/3 subjects. These effects were not significantly different between regions. In conclusion, the effects of the apolipoprotein E polymorphism on postprandial triglyceridemia are similar across regions of Europe, and homogeneous in healthy young subjects with and without a family history of early myocardial infarction. This suggests that the influence of apolipoprotein E on myocardial infarction risk may be acting through mechanisms other than through effects on postprandial triglyceridemia.

Adolescent↗
PubMed1988

Separation of triglyceride groups by reversed-phase thin-layer chromatography on silanized Kieselguhr.

The resolution of triglyceride mixtures on a Kieselguhr G layer silanized with dimethyldichlorosilane and the mobile phase acetone-acetonitrile-water under different chromatographic conditions has been investigated. The influence of the water content on the separation has been studied. Each triglyceride mixture needs a mobile phase with a definite polarity, which depends on the partition numbers of the triglyceride components. Since a linear correlation between the partition number and the water content was observed, prediction of the mobile phase composition for any triglyceride mixture is possible, provided the partition numbers of the components are known. The chromatographic conditions found can be applied for resolution of triglyceride groups with partition numbers ranging from 30 to 52, in different triglyceride mixtures.

Chemical Phenomena↗
PubMed1976

Changes in plasma triglyceride metabolism during withdrawal of bile.

The relationship between bile acid turnover and plasma triglyceride metabolism was examined in a group of seven moderately overweight and hypertriglyceridemic men. Bile acid synthesis was stimulated by the continuous aspiration of duodenal contents so that 150% of the bile acid pool was removed in 18 hr. In comparison with the average concentration of very low density lipoprotein triglyceride (VLDL-TG) during a preceding 8-10 hr control period, bile withdrawal led to an increase in VLDL-TG of 34%, 43%, 32%, 14%, 26%, 14%, and 8% (mean +24%) in the seven men. In control studies performed on another day the mean change over a similar period of time, but without bile withdrawal, was +1% (p less than 0.01). The kinetics of VLDL triglyceride were studied in some of the subjects by analyzing the triglyceride specific radioactivity curves following injections of radiolabelled glycerol. In control studies of 26 hr duration the curves were resolved into two apparent exponential functions, the second part of the curve appearing between 15 and 18 hr after pulse-labeling. During bile withdrawal, the second apparent exponential developed sooner, within 4 hr of beginning the aspiration and coincided with the rise in triglyceride concentration. The fractional rate of the second exponential was at least as fast during bile withdrawal as during the control period despite the increase in VLDL-TG pool size, suggesting that the turnover of triglyceride was higher at a time when bile acid production was being stimulated.

Adult↗
PubMed2003

Serum cholesterol and triglycerides: potential role in mortality prediction.

The present study was performed in order to evaluate the diagnostic usefulness of serial cholesterol and triglycerides measurements in patients with severe burns. One of the main objective was to find out if these parameters are clinically relevant to determine the morbidity of a burn patient and thereby the patient's outcome. In 220 patients with thermal injuries, cholesterol and triglyceride concentrations were measured daily. Blood samples were drawn immediately upon admission and thereafter daily until patient's discharge or death. For both parameters, a characteristic course was noted: in the group of non-survivors, a decrease of cholesterol prior to death was noted, while survivors, increased prior to discharge. The time courses of both groups (survivors-non-survivors) differed statistically significantly (P=0.0068). An increase in triglycerides was observed in all non-survivors prior to death, but in the group of survivors triglycerides remained more or less unchanged. These time courses also had statistically significant differences (P=0.0004). In our 220 patients, changes in cholesterol (P<0.0001, hazard ratio 1.02) and triglycerides (P=0.0008, hazard ratio 1.01) had comparable capability to predict the severity of a burn trauma and thereby its outcome than the established parameters in the treatment of burns (total body surface area burned, age, inhalation). We consider the serial measurements of cholesterol and triglycerides as clinically relevant to assess the morbidity of a patient and thereby to estimate the patient's outcome. We think that these serial measurements provide useful information for the clinician treating patients with severe burns.

Biomarkers↗
PubMed2001

On the anti-atherogenic effect of the antioxidant BHT in cholesterol-fed rabbits: inverse relation between serum triglycerides and atheromatous lesions.

We have shown that inclusion of the antioxidant butylated hydroxytoluene (BHT) in the diet protects against development of atherosclerotic lesions in cholesterol-fed rabbits. In parallel, BHT treatment results in increased plasma triglyceride levels. The present study explores the relationship between the triglyceride-inducing and protective effects of BHT in two different studies. The combined material contains 22 rabbits fed cholesterol and 18 rabbits fed cholesterol in combination with 1% BHT. In the BHT group there was an inverse relationship between triglyceride exposure/cholesterol exposure and extent of lesions with r=0.74 (P=0.0005). Our results show that increased triglyceride exposure parallels the anti-atherogenic effect of BHT. There was no significant correlation between atheromatosis and serum BHT levels. beta-very low density lipoprotein (beta-VLDL) from cholesterol and BHT animals was triglyceride-enriched and smaller compared to beta-VLDL from cholesterol-fed animals, but there was no significant association between the anti-atherogenic effect of BHT and particle size or apolipoprotein pattern of LDL or beta-VLDL. LDL isolated from rabbits treated with cholesterol and BHT was less sensitive to oxidative modification than LDL isolated from rabbits treated with cholesterol only. In conclusion, our results demonstrate that the degree of triglyceride exposure may be an important modulator of the anti-atherogenic effect of an antioxidant.

Animals↗
PubMed2000

GC-FID- and acyl carbon number-based determination of characteristic groupings of complex triglyceride (Benefat S and other) mixtures.

Techniques for the gas and liquid chromatographic separation of complex mixtures of triglycerides have evolved over the past two decades, as reviewed in detail by Huang et al. (J. Agric. Food Chem. 1995, 43, 1834-1844; J. Agric. Food Chem. 1997, 45, 1770-1778). A novel method for the quantitative partitioning of complex mixtures of triglycerides into functionally related groups is developed and applied to a low-calorie triglyceride mixture [namely, Benefat S or Salatrim plus mid-chain (C(6,8,10,12)) fatty acids]. The method is based on a nonlinear calibration of retention times (RTs) of a suite of standard triglycerides on their acyl carbon numbers [(ACNs), the sum of all the acyl carbon atoms in a given triglyceride] to estimate all of the intermediate ACNs (from 6 to 66). With the calibrated ACN scale and identifications of some components of a complex mixture's composition, ACN-based partitions were established and a Benefat S-triglyceride chromatogram was partitioned into seven functionally related groups. This method is provisional in the sense that it would typically be employed when the identifications of many components of a complex, homologous series were unknown, yet functionally related groups needed to be quantified. This method has proven to be particularly useful in the intercalibration of research laboratories with production facility laboratories during complex ( approximately 50-90 compounds) and large-scale ( approximately 20 ton) syntheses because of the high reproducibility of the ACN-based partitioning of complex chromatograms. This carbon number and statistically based method can be generally applicable to other complex mixtures of organic compounds and is readily adaptable to laboratory intercalibration efforts.

Chromatography, Gas↗
PubMed2000

Obesity resistance and multiple mechanisms of triglyceride synthesis in mice lacking Dgat.

Triglycerides (or triacylglycerols) represent the major form of stored energy in eukaryotes. Triglyceride synthesis has been assumed to occur primarily through acyl CoA:diacylglycerol transferase (Dgat), a microsomal enzyme that catalyses the final and only committed step in the glycerol phosphate pathway. Therefore, Dgat has been considered necessary for adipose tissue formation and essential for survival. Here we show that Dgat-deficient (Dgat-/-) mice are viable and can still synthesize triglycerides. Moreover, these mice are lean and resistant to diet-induced obesity. The obesity resistance involves increased energy expenditure and increased activity. Dgat deficiency also alters triglyceride metabolism in other tissues, including the mammary gland, where lactation is defective in Dgat-/- females. Our findings indicate that multiple mechanisms exist for triglyceride synthesis and suggest that the selective inhibition of Dgat-mediated triglyceride synthesis may be useful for treating obesity.

Absorption↗
PubMed1976

Quantitative analysis of metabolism of hepatic triglyceride in ethanol-treated rats.

An acute intraperitoneal injection of ethanol (0.7 or 2.1g/kg body wt.) causes the reversible, dose-dependent accumulation of hepatic triglyceride in rats. By using a pulse of [14C]palmitate injected into a tail vein, it was found that ethanol (2.1g/kg)had no effect on the flux of unesterified fatty acid of serum (4.3mumol/min per 100g body wt.). However, either dose increased the fraction of the total flux going to liver from 0.16 to0.27 as rapidly as could be measured (30s), and it remained elevated until all ethanol had been cleared from the blood. The fraction of the total radioactivity in lipids of liver that was in triglyceride increased linearly for 1 h from 30 to 50% and there was a simultaneous decrease in phospholipid from 60 to 40%. The rate of synthesis of hepatic triglyceride derived directly from unesterified fatty acid of serum was calculated by using the flux rate of unesterified fatty acid in serum, the fractional hepatic uptake of this flux, and the percentage of liver fatty acid esterified to triglyceride. This contribution is related to the total synthetic rate of hepatic triglyceride (rate of accumulation+rate of release) to determine quantitatively how much of the developing fatty liver is attributable to increased uptake of unesterfied fatty acid of serum. At the higher dose of ethanol, about half of the accumulating triglyceride is derived from this source, whereas with the lower dose of ethanol it can account for all of the build-up.

Animals↗
PubMed1976

Post-heparin plasma lipoprotein lipase and hepatic lipase in normal subjects and in patients with hypertriglyceridaemia: correlations to sex, age and various parameters of triglyceride metabolism.

1. A selective immunochemical method was used to measure post-heparin plasma lipoprotein lipase and hepatic lipase activity in eighty-two normal subjects and in twenty patients with type IIb, IV or V hypertriglyceridaemia. In twenty-six normal subjects the activity of post-heparin plasma lipases was compared with the kinetic parameters of endogenous plasma triglyceride metabolism. 2. The activity of post-heparin lipoprotein lipase was significantly higher in normal females than in males, whereas the activity of hepatic lipase showed an opposite sex ratio. The activity of lipoprotein lipase decreased with age both in males and females, whereas no significant age variation was observed in the activity of hepatic lipase. 3. In normal subjects a highly significant negative correlation was present in both sexes between the activity of post-heparin plasma lipoprotein lipase and fasting serum triglyceride concentration, but not between the activity of post-heparin hepatic lipase and serum triglycerides. 4. The fractional removal rate of endogenous triglycerides was positively correlated to the activity of lipoprotein lipase but not to the activity of hepatic lipase. No relationship was found between the activities of post-heparin plasma lipases and the absolute turnover of serum triglycerides. 5. The mean activity of post-heparin plasma lipo-protein lipase was significantly lower in subjects with hyperprebetalipoproteinaemia than in normal individuals. However, many hypertriglyceridaemic patients had lipoprotein lipase within the normal range and there was no correlation between serum triglyceride concentration and the activity of post-heparin lipases. 6. All three patients with fasting chylomicronaemia had low post-heparin lipoprotein lipase activity. Several subjects with high post-heparin plasma hepatic lipase activity were present in the group with hyperprebetalipoproteinaemia, but the mean value of the hepatic lipase was not significantly different from normal.

Adult↗
PubMed1999

Growth hormone (GH) status is an independent determinant of serum levels of cholesterol and triglycerides in healthy adults.

OBJECTIVE: Both severe growth hormone (GH) deficiency in hypopituitary adults and physiological ageing are associated with an increase in fat mass, dyslipidaemia, and an increased incidence of cardiovascular disease. Ageing is also associated with a physiological decrease in spontaneous as well as stimulated GH secretion. We wished to evaluate the effects of endogenous GH status on circulating lipoproteins. DESIGN: A cross-sectional study. SUBJECTS: Forty-two healthy nonobese adults of both sexes (20 M + 22 F) aged 27-59 years. MEASUREMENTS: Twenty-four hour GH secretion, arginine-stimulated GH secretion, and fasting values of lipoproteins and triglycerides. Body composition was measured by CT-scan and whole body DXA-scan. VO2-max was measured on an ergometer bicycle. RESULTS: GH secretion decreased with age and was lower in males. Older subjects had more total body fat, subcutaneous abdominal fat, and intra-abdominal fat than younger ones, and their VO2-max was decreased. Men had more intra-abdominal and subcutaneous abdominal fat but less total body fat than women. There was no sex difference in VO2-max. Total cholesterol (TC) and LDL-C (mmol/l) were higher in older than in the younger subjects (TC: 5.32 (95% CI = 0.49) vs. 4. 17 (95% CI = 0.28), P < 0.001; LDL-C: 3.66 (95% CI = 0.52) vs. 2.54 (95% CI = 0.37), P = 0.001) without sex differences. HDL-C did not show any difference with age or between sexes. Triglycerides (mmol/l) were higher in older subjects and in males (older: 1.36 (95% CI = 0.19) vs. younger: 1.02 (95% CI = 0.20), P = 0.015; M: 1. 34 (95% CI = 0.24) vs. F: 1.03 (95% CI = 0.16), P = 0.03). There was no age-difference in lipoprotein (a), but concentrations were higher in women (M: 4.35 (2.95-8.30) vs. F: 19.40 (4.10-32.80), P = 0.03). TC, LDL-C, and triglycerides correlated positively with age and indices of adiposity, and inversely with VO2-max. TC, LDL-C, and triglycerides also correlated significantly and negatively with arginine-stimulated GH secretion (peak GH) (TC vs. peak GH (r = - 0. 395, P = 0.01); LDL-C vs. peak GH (r = - 0.365, P = 0.017); triglycerides vs. peak GH (r = - 0.386, P = 0.01)). Multiple linear regression analysis showed GH status to be an independent predictor of both TC, LDL-C, and triglycerides. CONCLUSION: We hypothesize that GH may exert direct effects on lipid metabolism.

Adult↗
PubMed1998

Release of peptide YY and inhibition of gastric acid secretion by long-chain and medium-chain triglycerides but not by sucrose polyester in men.

METHODS: In the present study, we have investigated the effects of intraduodenal perfusion of long-chain and medium-chain triglycerides and of sucrose polyester on the release of peptide YY in healthy men. RESULTS: Perfusion of medium-chain triglycerides (180 mmol fatty acids) increased the plasma concentration of peptide YY from 7.9 pmol L(-1) (SEM 0.2, n=8) to 10.7 pmol L(-1) (SEM 0.5, n=8), whereas perfusion of long-chain triglycerides (180 mmol fatty acids) had a significantly greater effect, increasing peptide YY concentration from 8 6 pmol L(-1) (SEM 0.2, n=8) to 18.9 pmol L(-1) (SEM 2.4, n=8, P < 0.008). A smaller quantity of long-chain triglycerides (90 mmol fatty acids) increased plasma concentration of peptide YY from 7.4 pmol L(-1) (SEM 0.4, n=8) to 13.3 pmol L(-1) (SEM 1.5, n=8), whereas sucrose polyester (90 mmol fatty acids) did not change peptide YY concentration. In a previous study, we investigated gastrin-stimulated gastric acid output in response to these treatments. The correlation between increases in peptide YY in response to all treatments and the decrease in acid output was r=0.72 (n=48, P < 0.0001). These results show that both long-chain and medium-chain triglycerides, but not sucrose polyester, stimulate the release of peptide YY. CONCLUSION: We speculate that peptide YY may play an important role in the inhibition of gastrin-stimulated gastric acid secretion by long-chain and medium-chain triglycerides.

Adult↗
PubMed2002

Saturated triglycerides and fatty acids activate neutrophils depending on carbon chain-length.

BACKGROUND: Unsaturated fatty acids are known as neutrophil activators. In the present study we investigated whether saturated triglycerides and fatty acids may also contribute to the previously observed activation of neutrophils by nutritional lipid emulsions. Furthermore we tested the hypothesis that carbon-chain length is of importance in this respect. MATERIALS AND METHODS: Neutrophils (1 x 10(6) mL(-1)) were isolated from the blood of nine volunteers. Chemiluminescence was used to evaluate neutrophil activation, characterized by the production of oxygen radicals by neutrophils during incubation with 1 mmol L(-1) saturated fatty acid (6-20 carbon) or triglycerides (6-12 carbon fatty acid), dissolved in aqueous medium by preparing micelles with dipalmitoyl phosphatidylcholine (DPPC). Results were expressed as means +/- SEMs of the overall luminescence signal relative to the signal of cells incubated in medium. RESULTS: Similar to a positive control, the polyunsaturated fatty acid arachidonic acid (C20 : 4), the triglycerides tricaproin (TC6 : 0), tricaprylin (TC8 : 0) and trilaurin (TC12 : 0) as well as the fatty acids lauric acid (C12 : 0), palmitic acid (C16 : 0), stearic acid (C18 : 0) and arachidic acid (C20 : 0) all induced oxygen radical production in neutrophils, while the medium-chain triglyceride tricaprin (TC10 : 0) and fatty acids caproic acid (C6 : 0), caprylic acid (C8 : 0) and capric acid (C10 : 0) exerted no clear effects, similar to negative controls (DPPC and glycerol). CONCLUSIONS: Besides their (poly)-unsaturated counterparts, saturated triglycerides and fatty acids also activate neutrophils. Carbon chain-length is pivotal in the interaction of fatty acids and triglycerides and cells of the immune system.

Adult↗
PubMed2002

Cholesterol and triglyceride concentration as risk factors for myocardial infarction and death in women, with special reference to influence of age.

OBJECTIVE: To evaluate the importance of serum cholesterol and triglyceride concentrations as predictors of myocardial infarction and death in women of different ages. DESIGN: Prospective observational study, initiated in 1968-69. Setting. Gothenburg, Sweden, with about 430 000 inhabitants. SUBJECTS: A population-based sample of 1462 women aged 38, 46, 50, 54 and 60 years at start of the study, followed up for 24 years. Main outcome measures. Within each age group, myocardial infarction and death were predicted by serum cholesterol and triglyceride concentrations and smoking in a multivariate model. RESULTS: In the total population only serum triglyceride concentration was a strong independent risk factor for both end-points studied. Serum triglyceride concentration measured in 38- and 46-year-old women had no predictive value with respect to 24-year incidence of myocardial infarction or death. In 50-, 54- and 60-year-old women, high serum triglyceride concentration consistently predicted myocardial infarction and total mortality. Serum cholesterol concentration, on the other hand, showed evidence of direct association for 24-year all-cause mortality in the younger premenopausal group. Serum cholesterol had no predictive value for myocardial infarction or mortality in the peri- and postmenopausal ages. CONCLUSIONS: There appears to be age-specificity in association between serum lipids and these end-points in women, serum cholesterol concentration being more important for younger women and serum triglyceride concentration more important for postmenopausal women as risk factors, observations which need further attention.

Adult↗
PubMed2002

Relationship of regional adiposity to insulin resistance and serum triglyceride levels in nonobese Japanese type 2 diabetic patients.

The aim of this study was to investigate the relationships between insulin resistance and regional abdominal fat area, body mass index (BMI), and serum lipid profile in nonobese Japanese type 2 diabetic patients. A total of 63 nonobese Japanese type 2 diabetic patients aged 45 to 83 years were examined. The duration of diabetes was 8.4 +/- 0.8 years. BMI, glycosylated hemoglobin (HbA(1c)) levels, and fasting concentrations of plasma glucose, serum lipids (total cholesterol, high-density lipoprotein [HDL] cholesterol, and triglycerides), and serum insulin were measured. The low-density lipoprotein (LDL) cholesterol level was calculated using the Friedewald formula (LDL cholesterol = total cholesterol - HDL cholesterol - 1/5 triglycerides). Insulin resistance was estimated by the homeostasis model assessment (HOMA-IR). Computed tomography (CT) was used to measure cross-sectional abdominal subcutaneous and visceral fat areas in all the patients. Adipose tissue areas were determined at the umbilical level. Subcutaneous and visceral abdominal fat areas were 136.5 +/- 6.0 and 86.0 +/- 4.1 cm(2), respectively. Univariate regression analysis showed that insulin resistance was positively correlated with subcutaneous (r =.544, P <.001) and visceral (r =.408, P =.001) fat areas, BMI (r =.324, P =.009), HbA(1c) (r =.254, P =.001), serum triglycerides (r =.419, P <.001), and serum LDL cholesterol (r =.290, P =.019) levels and was negatively correlated with serum HDL cholesterol level (r =.254, P =.041). Multiple regression analyses showed that insulin resistance was independently predicted by the areas of subcutaneous (F = 6.76, P <.001) and visceral (F = 4.61, P <.001) abdominal fat and serum triglycerides (F = 8.88, P <.001) level, which explained 36.9% of the variability of insulin resistance. Moreover, the present study demonstrated that whereas BMI was positively correlated with visceral (r =.510, P <.001) and subcutaneous (r =.553, P <.001) fat areas, serum triglyceride level was positively associated with visceral (r =.302, P =.015), but not with subcutaneous (r =.222, P =.074) fat area. From these results, it can be suggested that (1) both subcutaneous and visceral abdominal fat areas are independently associated with insulin resistance and (2) visceral fat area, but not the subcutaneous one, is associated with serum triglyceride levels in our nonobese Japanese type 2 diabetic patients.

Adipose Tissue↗