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PubMed2006

Longitudinal analysis of haplotypes and polymorphisms of the APOA5 and APOC3 genes associated with variation in serum triglyceride levels: the Bogalusa Heart Study.

Polymorphisms in the APOC3 and APOA5 genes, from the APOA1/APOC3/APOA4/APOA5 gene cluster on chromosome 11q23, have been associated with interindividual variation in plasma triglycerides. APOA5 polymorphisms implicated include 2 in the promoter region (-1131 T/C and -3 A/G) and 1 in exon 2 (+56 C/G). APOC3 polymorphisms implicated include 1 (SstI) in the 3' untranslated region and 1 (-2854 G/T) in the APOC3-APOA4 intergenic region. We analyzed the associations of haplotypes and multilocus genotypes of these polymorphisms on longitudinal serum triglyceride profiles in 360 African American and 823 white subjects from the Bogalusa Heart Study. Subjects were examined from 2 to 8 times (mean +/- SD, 5.4 +/- 1.3) between 1973 and 1996, at ages ranging from 4 to 38 years, with 1978 observations in African Americans and 4465 in whites. Serum triglycerides were significantly higher among whites across all ages. Allele frequencies differed significantly between African Americans and whites at all but the APOA5 +56 C/G locus. Linkage disequilibrium among the loci was higher in whites and haplotype diversity lower: 6 haplotypes had estimated frequencies of more than 1% in African Americans, 5 in whites. Individually, all polymorphisms except APOC3 -2854 G/T showed significant associations with triglyceride levels in the full sample. However, genotype models including all 5 loci showed significant triglyceride associations for only 3 (APOC3 SstI, APOA5 -1131 T/C, and APOA5 +56 C/G); significant interactions among them indicated their effects were not independent. Neither APOC3 -2854 G/T nor APOA5 -3 A/G had significant effects when the other 3 loci were in the models. The EM algorithm was used to estimate haplotype frequencies and assign haplotype probabilities to individuals, which is conditional on their genotypes; individuals' haplotype probability vectors were then used as predictors in multilevel mixed models of longitudinal triglyceride profiles. Of haplotypes comprising, in order, APOC3 SstI and -2854 G/T and APOA5 -1131 T/C, -3 A/G, and +56 C/G, 3 were significantly associated with higher triglycerides, even after adjusting for multiple tests: GGTAG (P = .002), GTTAG (P < .0001), and CGCGC (P = .0002). Each GGTAG haplotype carried would be expected to raise triglyceride levels (relative to those of GTTAC homozygotes) by approximately 19 mg/dL, each GTTAG haplotype by approximately 15 mg/dL, and each CGCGC haplotype by approximately 7 mg/dL. Haplotypes comprising the 3 loci implicated by genotype analyses (SstI, -1131 T/C, and +56 C/G) were also tested: haplotypes C_C_C and G_T_G significantly raised triglycerides, even after adjustment for multiple comparisons (P < .002 for both), with each copy of C_C_C expected to raise triglycerides by approximately 7 mg/dL and each copy of G_T_G by approximately 15 mg/dL. Overall, our findings support those of others in associating specific polymorphisms and haplotypes in the APOA1/C3/A4/A5 gene cluster with higher serum triglyceride levels. However, the degree to which polymorphisms in the APOC3 and APOA5 genes may be independently associated with triglyceride levels remains to be determined.

Adolescent↗
PubMed1998

Triglyceride as a risk factor for coronary artery disease.

The data for an independent association between triglyceride concentrations and risk for coronary artery disease (CAD) are equivocal, unlike the data for low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol, which show strong, consistent, and opposing correlations with CAD risk. There is some evidence for triglyceride as an independent risk factor in certain subgroups, for example, women 50-69 years of age (Framingham Heart Study) and in patients with noninsulin-dependent diabetes. However, the evidence is stronger for triglyceride as a synergistic CAD risk factor. For example, patients with the "lipid triad" of high LDL cholesterol, low HDL cholesterol, and high triglyceride accounted for most of the event reduction with lipid-lowering therapy in the Helsinki Heart Study. An important confounder of the correlation between triglyceride and CAD risk is the heterogeneity of triglyceride-rich lipoproteins: the larger triglyceride-rich particles are thought not to be associated with CAD risk, whereas the smaller (and denser) particles are believed to be atherogenic. At present, measurement of fasting triglyceride levels and triglyceride assessment in conjunction with LDL cholesterol and HDL cholesterol concentrations are the most practical methods of evaluating hypertriglyceridemia in CAD risk, although postprandial lipemia may prove a better indicator of atherogenicity. Management of hypertriglyceridemia should initially focus on nonpharmacologic therapy (i.e., diet, exercise, weight control, and alcohol reduction). In diabetic patients, meticulous glycemic control is also important. However, if this approach proves inadequate, there are several pharmacologic options. Fibrates may be effective in decreasing triglyceride and increasing HDL cholesterol. Nicotinic acid (niacin) has been shown to decrease triglyceride, increase HDL cholesterol, lower LDL cholesterol, and decrease lipoprotein(a); it also decreases fibrinogen. The statins appear to be effective in decreasing triglyceride and LDL cholesterol in hypertriglyceridemia; however, they do not normalize metabolism of apolipoprotein B, and HDL cholesterol may remain low. Therefore, combination with a fibrate or niacin may be appropriate. Attention to hypertriglyceridemia with respect to increased CAD risk represents an important step in assessing global risk for CAD development.

Biomarkers↗
PubMed2002

Estrogen treatment of prostate cancer increases triglycerides in lipoproteins as demonstrated by HPLC and immunoseparation techniques.

BACKGROUND: Estrogen administration is known to increase serum triglyceride concentrations. This study measured changes in lipoproteins of patients with prostate cancer treated with estrogen to determine whether the increased triglyceride concentrations are associated with atherogenic lipoprotein patterns. METHODS: Fifteen patients (52-87 years) with histologically diagnosed prostate cancer received diethylstilbestrol diphosphate (250 mg/day). Serum samples were collected before and after 1 and 2 weeks of treatment. Cholesterol and triglyceride profiles of major lipoproteins were determined by HPLC, remnant-like particle cholesterol and triglyceride concentrations by an immunoseparation technique, and apolipoproteins by immunologic methods. RESULTS: Estrogen treatment induced a 63.3% increase in total triglyceride concentrations, which occurred in all major lipoprotein classes with significant increases in HDL-triglycerides (130.4%), LDL-triglycerides (60.7%) and VLDL-triglycerides (56.2%). HDL-cholesterol increased significantly by 26.8%, while LDL-cholesterol decreased (15.6%). Remnant-like particle triglyceride concentrations also increased significantly by 77%, whereas remnant-like particle cholesterol concentrations remained unchanged. Apolipoproteins A-I and A-II increased; apolipoprotein E and Lp(a) decreased. CONCLUSIONS: The techniques used here conveniently demonstrated that short-term estrogen treatment in prostate cancer patients resulted in triglyceride enrichment of all major lipoprotein classes but did not induce changes in the lipoprotein profiles generally recognized as increasing risk for cardiovascular disease, except for the elevation of plasma triglyceride and remnant-like particle triglyceride.

Aged↗
PubMed1999

Differences in activity of hepatic microsomal triglyceride transfer protein among species.

Five sows, five cows, five hens, six guinea pigs, six rabbits, and six rats were used in a study to determine if hepatic microsomal triglyceride transfer protein activity differed among species that varied in site of fatty acid synthesis and rate of hepatic triglyceride export. No differences in plasma nonesterified fatty acids were seen among species. Plasma concentrations of glucose were highest in the hen, intermediate in the rat, guinea pig, and rabbit and lowest in the sow and cow. Liver triglyceride was low in all species with the only significant difference being between the hen and the guinea pig (4.7 and 1.1%, DM basis, respectively). No microsomal triglyceride transfer protein activity was found in muscle. The cow, rat, and guinea pig had the lowest levels and the hen and rabbit the highest levels of duodenal microsomal triglyceride transfer protein activity. Hepatic microsomal triglyceride transfer protein activity was significantly higher in the sow than the other species. Hepatic microsomal triglyceride transfer protein activity was 1.51, 1.63, 2.36, 2.72, 2.95, and 6.70 nmole triolein transferred/h/mg microsomal protein for the guinea pig, rabbit, cow, rat, hen, and sow, respectively. Microsomal triglyceride transfer protein activity in duodenal tissue was 18.0, 18.6, 19.2, 33.4, 113, and 161% of hepatic microsomal triglyceride transfer protein activity for the sow, cow, rat, guinea pig, hen, and rabbit, respectively. Hepatic microsomal triglyceride transfer protein activity scaled to liver weight and metabolic body size was 2.69, 3.36, 4.58, 5.83, 7.49, and 22.3 nmole triolein transferred in the liver/min/kg body weight0.75 for the rabbit, guinea pig, rat, hen, cow, and sow, respectively. There was little relationship between previously published rates for triglyceride export and hepatic microsomal triglyceride transfer protein activity measured in this experiment.

Abetalipoproteinemia↗
PubMed1970

The composition of triglycerides from liver, egg yolk and adipose tissue of the laying hen.

The composition of the triglycerides of liver, egg yolk and adipose tissue of laying hens fed on a standard diet were investigated by using argentation thin-layer chromatography to separate the triglycerides according to their degree of unsaturation. About 40% of liver triglycerides consisted of one saturated and two monoenoic fatty acids. Triglycerides containing linoleate were more abundant in adipose tissue than in either yolk or liver. Hydrolysis by pancreatic lipase of the tissue triglycerides and fractions obtained from these triglycerides showed that the triglycerides of adipose tissue had a less ordered arrangement of fatty acids at the 2-position than did either yolk or liver triglycerides. The labelling patterns of triglycerides formed in liver slices incubated in the presence of [1-(3)(14)C]glycerol indicated that triglycerides containing four or more double bonds are formed to a greater extent than are other triglyceride fractions. This is evidence for the concept that the type of triglyceride formed depends on the availability of fatty acids to the liver cells.

Adipose Tissue↗
PubMed1993

Plasma triglyceride level and mortality from coronary heart disease.

BACKGROUND: Whether the plasma triglyceride level is a risk factor for coronary heart disease has been controversial, and evaluation of the triglyceride level as a risk factor is fraught with methodologic difficulties. METHODS: We studied the association between plasma triglyceride levels and the 12-year incidence of death from coronary heart disease in 10 North American populations participating in the Lipid Research Clinics Follow-up Study, while adjusting for the potential confounding effects of other risk factors for cardiovascular disease, including the level of high-density lipoprotein (HDL) cholesterol. All analyses were sex-specific, and separate analyses were performed in high and low strata of HDL cholesterol, low-density lipoprotein (LDL) cholesterol, fasting plasma glucose, and age. RESULTS: The rates of coronary death in both men and women increased with the triglyceride level. In Cox proportional-hazards models adjusted for age, in which the natural log of the triglyceride levels was used to give a normal distribution, the relative risk per natural-log unit of triglyceride (e.g., a triglyceride level of 150 mg per deciliter vs. a level of 55 mg per deciliter) was 1.54 (95 percent confidence interval, 1.19 to 1.98; P < 0.001) in men and 1.88 (95 percent confidence interval, 1.19 to 2.98; P < 0.007) in women. After an adjustment for potential covariates, however, these relative risks were not statistically significant. Analyses based on lipoprotein cholesterol levels revealed a positive association between the triglyceride level and coronary mortality in the lower stratum of both HDL and LDL cholesterol, but not in the higher stratum. Conversely, the HDL cholesterol level was unrelated to coronary mortality in the lower stratum of LDL cholesterol, but was strongly inversely associated with coronary death in the higher stratum of LDL cholesterol. The relative risk of coronary death associated with triglyceride level was higher at younger ages. The associations between the triglyceride level and coronary mortality in the lower HDL cholesterol, LDL cholesterol, and age strata were small and were further reduced by an adjustment for the fasting plasma glucose level. CONCLUSIONS: Overall, the plasma triglyceride level showed no independent association with coronary mortality. However, in subgroups of subjects with lower HDL and LDL cholesterol levels and in younger subjects, defined a priori, an association between the triglyceride level and coronary mortality was observed, although this association was small and was not statistically significant after an adjustment for the plasma glucose level.

Adult↗
PubMed1984

Comparison of the effects of medium and long chain triglyceride containing liquid meals on gall bladder and small intestinal function in normal man.

We investigated the effects of medium (MCT) and long (LCT) chain triglyceride test meals on gall bladder contraction (using ultrasonography) and small intestinal bile acid concentrations and ileal flow rates (using intubation techniques) in normal individuals. Comparing the effects of ingesting medium chain triglyceride and long chain triglyceride meals, the gall bladder volume was reduced by 23.4 +/- 33.6% and 59.0 +/- 17.1% respectively (mean +/- SD, p less than 0.01, n = 13), the jejunal bile acid concentrations increased significantly only after the ingestion of long chain triglyceride (p less than 0.05, n = 5), while the volume of the postprandial jejunal contents was not significantly different (540 +/- 150, 522 +/- 169 ml, medium chain triglyceride vs long chain triglyceride, p = 0.2, n = 5). The postprandial colonic inflow was 48.5 +/- 12.5 and 123.4 +/- 35.2 ml/h (medium chain triglyceride vs long chain triglyceride, p less than 0.01, n = 5). Thus medium chain triglyceride, compared with long chain triglyceride, produces a smaller input of bile acids into the small intestine and a smaller volume of fluid delivered to the colon. These observations may be relevant to the beneficial effects of medium chain triglyceride substitution for long chain triglyceride in the treatment of diarrhoea in patients with small intestinal disease.

Adult↗
PubMed1990

Absorption of triglycerides in the absence of lipase.

Medium chain triglycerides are considered to be readily absorbed intact in the absence of pancreatic lipase, unlike long chain triglycerides. Commercial medium chain triglyceride oils comprise various medium chain fatty acids from 6 to 12 carbons in length resulting in triglyceride molecules of different sizes and molecular weights. The effect of molecular weight and hence fatty acid chain length on the efficiency of intact medium chain triglyceride absorption is unknown. Therefore, this study measured, using a single-pass marker perfusion technique, intestinal jejunum absorption of five medium chain and one long chain triglycerides in anesthetized Sprague-Dawley rats. The molecular weights of the five medium chain triglycerides were 470.7, 498.8, 526.8, 554.9, 639.0, and the long chain triglyceride, 885.4. Residual luminal pancreatic lipase was removed prior to lipid perfusion. This study demonstrated that medium chain triglycerides were absorbed in the absence of lipase whereas long chain triglyceride was not. There was no significant variation in the absorption of the five different medium chain triglycerides perfused. The molecular weight of the medium chain triglyceride did not affect its intact absorption by the small intestine.

Animals↗
PubMedDate not supplied

With medium-chain triglycerides, higher and faster oxygen radical production by stimulated polymorphonuclear leukocytes occurs.

BACKGROUND: Parenteral lipid emulsions are suspected of suppressing the immune function. However, study results are contradictory and mainly concern the conventional long-chain triglyceride emulsions. METHODS: Polymorphonuclear leukocytes were preincubated with parenteral lipid emulsions. The influence of the lipid emulsions on the production of oxygen radicals by these stimulated leukocytes was studied by measuring chemiluminescence. Three different parenteral lipid emulsions were tested: long-chain triglycerides, a physical mixture of medium- and long-chain triglycerides, and structured triglycerides. Structured triglycerides consist of triglycerides where the medium- and long-chain fatty acids are attached to the same glycerol molecule. RESULTS: Stimulated polymorphonuclear leukocytes preincubated with the physical mixture of medium- and long-chain triglycerides showed higher levels of oxygen radicals (p < .005) and faster production of oxygen radicals (p < .005) compared with polymorphonuclear leukocytes preincubated with long-chain triglycerides or structured triglycerides. Additional studies indicated that differences in results of various lipid emulsions were not caused by differences in emulsifier. The overall production of oxygen radicals was significantly lower after preincubation with the three lipid emulsions compared with controls without lipid emulsion. CONCLUSIONS: A physical mixture of medium- and long-chain triglycerides induced faster production of oxygen radicals, resulting in higher levels of oxygen radicals, compared with long-chain triglycerides or structured triglycerides. This can be detrimental in cases where oxygen radicals play either a pathogenic role or a beneficial one, such as when rapid phagocytosis and killing of bacteria is needed. The observed lower production of oxygen radicals by polymorphonuclear leukocytes in the presence of parenteral lipid emulsions may result in immunosuppression by these lipids.

Adult↗
PubMedDate not supplied

Parenteral structured triglyceride emulsion improves nitrogen balance and is cleared faster from the blood in moderately catabolic patients.

BACKGROUND: Most postoperative patients lose net protein mass, which reflects loss of muscle tissue and organ function. Perioperative parenteral nutrition may reduce the loss of protein, but in general, with conventional lipid emulsions a waste of protein still remains. METHODS: We compared the effects on nitrogen balance of an emulsion containing structured triglycerides, a new type of synthesized triglycerides, with an emulsion of a physical mixture of medium- and long-chain triglycerides as part of parenteral feeding in moderately catabolic patients. The first 5 days after placement of an aortic prosthesis patients received total parenteral nutrition (TPN) providing 0.2 g of nitrogen per kg body weight per day; energy requirement was calculated using Harris and Benedict's equation, adding 300 kcal per day for activity. Twelve patients were treated with the structured triglyceride emulsion and 13 patients with the emulsion of the physical mixture of medium- and long-chain triglycerides. The design was a randomized, double-blind parallel study. RESULTS: In the patients who completed the study, the mean cumulative nitrogen balance over the first 5 postoperative days was -8+/-2 g in 10 patients on the structured triglyceride emulsion and -21+/-4 g in 9 patients on the emulsion of the physical mixture of medium- and long-chain triglycerides; the mean difference was 13 g of nitrogen (95% confidence interval 4 to 22, p = .015) in favor of the structured triglyceride emulsion. On the first postoperative day serum triglyceride and plasma medium-chain free fatty acid levels increased less during infusion of the structured triglyceride emulsion than with the physical mixture emulsion. CONCLUSIONS: The parenteral structured triglyceride emulsion improves the nitrogen balance and is cleared faster from the blood, compared with the emulsion of the physical mixture of medium- and long-chain triglycerides, in moderately catabolic patients.

Aged↗
PubMedDate not supplied

Effects of free glycerol contained in intravenous fat emulsion on plasma triglyceride determination.

BACKGROUND: Plasma triglyceride analyses to evaluate the clearance of IV fat emulsion are necessary in patients receiving parenteral nutrition. Enzymatic kits for triglyceride analysis measure the glycerol that is hydrolyzed from triglyceride. This study investigates the effect of fat emulsion free glycerol on plasma triglyceride determination. METHODS: Venous blood from fasting volunteers (n = 10) was drawn into tubes containing EDTA and was centrifuged to separate the plasma. An IV fat emulsion containing 2.25% glycerol was added to plasma samples to create serial dilutions ranging from 0.049% to 0.245% final lipid concentration. Total triglyceride and free glycerol concentrations were determined in each dilution and control sample. The free glycerol concentration was subtracted from the total triglyceride concentration to yield a true triglyceride value. RESULTS: Increasing concentrations of fat emulsion added to donor plasma produced increases in total triglyceride and free glycerol concentrations. The increase in free glycerol concentration produced significant concentration-related differences between total and true triglyceride concentrations. CONCLUSIONS: The total triglyceride level overestimated the true triglyceride concentration due to fat emulsion free glycerol. To assure reliable triglyceride results in patients receiving fat emulsion, blanking for free glycerol should be considered.

Adult↗
PubMed1988

Effects of dietary retinoid and triglyceride on the lipid composition of rat liver stellate cells and stellate cell lipid droplets.

Hepatic stellate cells store the majority of the liver's retinoid (vitamin A) reserves as retinyl esters in stellate cell lipid droplets. A study was conducted to explore the effects of differences in dietary retinoid and triglyceride intake on the composition of the stellate cell lipid droplets. Weanling rats were placed on one of five diets that differed in retinoid or triglyceride contents. The dietary groups were: 1) control (2.4 mg retinol (as retinyl acetate)/kg diet and 20.5% of the calories supplied by triglyceride (as peanut oil]; 2) low retinol (0.6 mg retinol/kg diet and control triglyceride levels); 3) high retinol (24 mg retinol/kg diet and control triglyceride levels); 4) low triglyceride (2.4 mg retinol/kg diet and 5% of the calories supplied by triglyceride); and 5) high triglyceride (2.4 mg retinol/kg diet and 45% of the calories supplied by triglyceride). Stellate cells were isolated using the pronase-collagenase method and stellate cell lipid droplets were isolated by differential centrifugation. The levels of retinoids and other lipids were measured by high performance liquid chromatography. The stellate cells from control rats contained 113 micrograms total lipid/10(6) cells. Control stellate cell lipid droplets had the following mean percent lipid composition: 39.5% retinyl ester; 31.7% triglyceride; 15.4% cholesteryl ester; 4.7% cholesterol; 6.3% phospholipids; and 2.4% free fatty acids. Both the concentration of stellate cell lipids and the composition of stellate cell lipid droplets were markedly altered by changes in dietary retinoid. The low and high retinol groups contained, respectively, 82 and 566 micrograms total lipid/10(6) cells, with retinyl ester representing, respectively, 13.6% and 65.4% of the lipid present in the stellate cell lipid droplets. Low and high triglyceride groups were similar to controls in both stellate cell lipid content and the composition of the stellate cell lipid droplets. These findings indicate that the composition of stellate cell lipid droplets is strongly regulated by dietary retinoid status but not by dietary triglyceride intake.

Animals↗
PubMed1971

Utilization of exogenous free fatty acids for the production of very low density lipoprotein triglyceride by livers of carbohydrate-fed rats.

High carbohydrate diets enhance the hepatic output of very low density lipoprotein triglycerides. The fatty acids of these triglycerides could come from exogenous sources (i.e., diet or adipose tissue) or from de novo fatty acid synthesis in the liver. The role of exogenous free fatty acids was evaluated in rats fed Purina Chow or diets containing 10% fructose for up to 14 wk. In carbohydrate-fed rats, serum triglycerides were twice normal, and VLDL accounted for about 60% of the increases. Pre-beta-lipoprotein was increased and alpha- and beta-lipoprotein were decreased. Phospholipid and cholesterol levels were unchanged. Livers were perfused with glucose and free fatty acids. Perfusate free fatty acids rose from 180 to 1800 micro eq/liter as the infused acids increased from 0 to 992 micro eq/3 hr; simultaneously, net free fatty acid uptake rose from < 1 to 18 micro eq/g/hr and triglyceride output by the liver doubled. However, rates of secretion of triglyceride became constant, and triglyceride accumulated in liver at uptakes of free fatty acids > 13 micro eq/g/hr. More lauric and myristic acid appeared in the perfusate than was infused, suggesting the hepatic discharge of free fatty acids. Livers of fructose-fed rats secreted twice as much oleate-(14)C-labeled triglyceride as controls at all levels of free fatty acid uptake. The ratios of the specific activities of perfusate triglyceride to free oleate-(14)C were unaffected by diet and were about 0.6 and 1.0 at low and high triglyceride secretion rates, respectively. Thus, carbohydrate feeding did not result in altered uptakes of free fatty acids or preferential secretion of triglycerides containing endogenously synthesized fatty acid. Instead, the increased secretion of triglyceride was accomplished by enhanced formation of VLDL triglyceride from exogenous free fatty acids.

Animals↗
PubMed1983

Role of triglycerides in endothelial cell arachidonic acid metabolism.

Arachidonic acid was incorporated into triglycerides by cultured bovine endothelial cells in a time- and concentration-dependent manner. At 75 microM or higher, more arachidonic acid was incorporated into triglycerides than into phospholipids. The triglyceride content of the cells increased as much as 5.5-fold, cytoplasmic inclusions appeared, and arachidonic acid comprised 22% of the triglyceride fatty acids. Triglyceride turnover occurred during subsequent maintenance culture; there was a 60% decrease in the radioactive arachidonic acid contained in triglycerides and a 40% decrease in triglyceride content in 6 hr. Most of the radioactivity was released into the medium as free fatty acid. The turnover of arachidonic acid, but not oleic acid in cellular triglycerides, decreased when supplemental fatty acid was added to the maintenance medium. Incorporation and turnover of radioactive arachidonic acid in triglycerides also was observed in human skin fibroblasts, 3T3-L1 cells, and MDCK cells. Other fatty acids were incorporated into triglycerides by the endothelial cells; the amounts after a 16-hr incubation with 50 microM fatty acid were 20:3 greater than 20:4 greater than 18:1 greater than 18:2 greater than 22:6 greater than 16:0 greater than 20:5. These findings indicate that triglyceride formation and turnover can play a role in the fatty acid metabolism of endothelial cells and that arachidonic acid can be stored in endothelial cell triglycerides.

Animals↗
PubMedDate not supplied

The triglyceride issue revisited. Findings from the Helsinki Heart Study.

BACKGROUND: In clinical practice, high triglyceride level is recognized as an indicator of increased risk of coronary heart disease (CHD), while most epidemiological studies have shown that triglyceride level is not an independent risk factor for CHD. In an effort to explain this discrepancy we reanalyzed the Helsinki Heart Study data in the light of findings from recent clinical studies related to the insulin resistance syndrome. METHODS: The log-linear modeling technique was used to study the pattern of cross-sectional interdependence of triglyceride level, high-density lipoprotein cholesterol (HDL-C) level, low-density lipoprotein cholesterol level, blood pressure, and blood glucose level. The CHD risk associated with different combinations of levels of triglycerides, HDL-C, and blood pressure was assessed via Cox proportional hazards models. RESULTS: Triglycerides occupied a central role in the pattern of associations of the factors studied; in particular, the associations with HDL-C level, blood pressure, and blood glucose level were without threshold values. The prevalence of high triglyceride level plus low HDL-C level was strongly associated with blood pressure and blood glucose level, while the prevalence of low HDL-C level alone was not. Only the subgroup with both high triglyceride and low HDL-C levels showed a substantial CHD risk, while those with low HDL-C levels alone or high triglyceride levels alone showed a marginal risk. CONCLUSIONS: Our results suggest that triglycerides play a central mediating role in the occurrence of several CHD risk factors, especially those related to the insulin resistance syndrome. Because of these interdependencies, the question of an independent effect of triglycerides is not relevant, and when assessing CHD risk, triglycerides should be considered jointly with HDL-C.

Adult↗
PubMed1976

Response of serum cholesterol and triglycerides to hormone treatment and the relation of pretreatment values to mortality in patients with prostatic cancer.

Cholesterol and triglycerides were measured in plasma samples from patient with cancer of the prostate before and after 3 months treatment with either Premarin, Provera, Provera and diethylstilbestrol, or diethylstilbestrol alone. Cholesterol was also measured before and after one of three doses of diethylstilbestrol or placebo. Pretreatment cholesterol levels at 196 +/- 1.3 mg per 100 ml (X +/- SE, N = 1093) were significantly lower than these reported for similar age group noncancer controls. Significant increases occurred with some of the estrogen treatments. Pretreatment cholesterol levels showed a significant negative correlation with age in Stage III and IV patients of both studies and a positive correlation with hemoglobin in Stage III patients of both studies. Pretreatment triglyceride levels at 120 +/- 1.9 mg per 100 ml (X +/- SE, N = 1089) were similar to levels reported for noncancer controls of similar age. Estrogen treatment produced a significant increase in triglyceride levels. Serum triglycerides were significantly correlated with hemoglobin, weight, and cholesterol and negatively correlated with age, Analysis of covariance for both cholesterol and triglycerides showed highly significant treatment effects, but no stage effects and no stage-treatment interactions. It showed that the pretreatment value is of extreme importance for predicting or explaining the 3-month value. Death rates were calculated by level of pretreatment cholesterol or pretreatment triglycerides for all Stage II and IV patients, all treatments combined, and for Study 2 and Study 3 separately. No consistent trends were evident for cholesterol. Spearman correlation coefficients between category of initial triglyceride value and rank of death rate were computed to test for a quadratic effect. When the absolute values of the initial triglyceride values minus the overall mean were correlated with the death rate, a significant negative correlation was found for all causes of death and for deaths due to cardiovascular disease and prostatic cancer. These results indicate that the death rate is highest near the overal mean for initial triglyceride values and decreases as the initial values deviate above or below the mean. Initial triglyceride levels appear to have potential as indicators of risk of death in patients with prostatic cancer. The percentage of patients dead at 1 year by initial triglyceride levels, measured only in Study 3, revealed a pattern similar to that observed for the death rate, that is, the highest percentages were associated with values near the overall mean.

Cholesterol↗
PubMed1995

Triglyceride metabolism in human keratinocytes cultured at the air-liquid interface.

Although epidermis reconstructed in vitro histologically demonstrates the presence of fully differentiated tissue with cornified strata, it does not synthesize or release epidermal barrier lipids in the same proportions as does native skin, causing the barrier function to be impaired. Lipids, the content of which deviates the most, include triglycerides that are present in high amounts and stored as lipid droplets. Our recent studies have revealed that a high triglyceride content may be a reflection of a high synthetic rate and a low turnover. Therefore, the present study was undertaken to examine whether the triglyceride accumulation in the air-exposed cultures may be a result of insufficient supplementation of cells with oxygen, an excessive supplementation of cells with glucose, dysregulation of lipogenesis, or an impaired catabolism of triglycerides caused either by insufficient activity of triglyceride lipase and/or accumulation of free fatty acids due to insufficient activity of beta-oxidase. When keratinocytes were cultured at the air-liquid interface in medium containing a standard glucose concentration, both the lactate and triglyceride production was high. Lowering glucose content in the medium resulted in a decrease in both lactate production and triglyceride synthesis. However, even when grown at a low glucose concentration the triglyceride content remained higher than found in vivo and synthesized triglycerides were stored in the cells as a stable pool, suggesting that the catabolism of triglycerides was impaired. Since both lipase and beta-oxidase were found to be active in cultured keratinocytes, another factor or other factors are probably implicated in the regulation of triglyceride metabolism.

Carnitine↗
PubMed1995

Relationships between triglycerides, lipoproteins, glucose and coronary artery disease.

We examined the relationship of apolipoprotein B (apo B), glucose, triglycerides and other lipoprotein lipids to coronary artery disease (CAD). Using receiver-operating characteristic curves (ROC), we noticed that the triglyceride ROC curve crossed above other lipoprotein curves at a triglycerides level of approximately 1.4 g/l. We examined subgroups of < 1.4 g/l and > 1.4 g/l. ANOVA (F = 18.9, P < 0.0001) and stepwise logistic regression (P = 0.0002) indicated that triglycerides were the best predictor in the < 1.4 g/l group. The best markers in the > 1.4 g/l group were low density lipoprotein cholesterol and apo B. Glucose did not appear to significantly alter the predictive power of triglycerides. These data suggest that triglyceride appears to be an overall significant univariate marker for CAD because of its effect at lower concentrations. The strong relationship between CAD and triglycerides at low triglyceride levels may reflect increased levels of very low density lipoprotein metabolites in some individuals. We conclude that some triglyceride-rich particles are independently atherogenic, that glucose did not alter this relationship and that when the samples were split into those with high and low levels of triglycerides, triglycerides and apo B but not HDLC was a significant predictor of CAD.

Adult↗