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PubMed1977

The effects of prolonged fasting on plasma triglyceride kinetics in man.

Studies were undertaken to examine triglyceride turnover in obese humans on isocaloric balanced diets and during prolonged (3-5 wk) fasting. The data were related to plasma concentrations of insulin (IRI), glucagon (IRG), and free fatty acids (FFA) and to blood ketone concentrations. The triglyceride turnover rates were also related to the plasma triglyceride concentration. This relationship was the same in the obese on isocaloric balanced diets as that we have previously observed in lean humans on similar diets. The relationship between triglyceride turnover and concentration changed during prolonged fasting in a way that suggested that triglyceride removal was impaired. This viewpoint is consistent with the known effects of fasting on adipose tissue lipoprotein lipase activity. In another group of fasted obese, refed with a hypocaloric diet, the relationship returned toward normal. In addition to the impaired triglyceride removal, prolonged fasting resulted in a decrease in triglyceride production. This decrease occurred despite an increase in plasma FFA. After 3-5 wk of fasting the IRI was about 50% of the initial value, while the IRG was the same as the initial value. While triglyceride production fell during fasting, the blood ketone concentration rose. Others have seen similar changes in ketones and triglycerides in livers perfused with medium in which the ratio of insulin to glucagon fell. The rate of triglyceride production was not related to body weight. However, regardless of nutritional state, it was positively related to the basal plasma insulin levels. These data indicate that, in man as in animal preparations, insulin may regulate hepatic triglyceride production.

Diet, Reducing↗
PubMed1984

Structured medium-chain and long-chain triglyceride emulsions are superior to physical mixtures in sparing body protein in the burned rat.

The present study was undertaken to compare the effectiveness of a physical mixture of long-chain and medium-chain triglycerides with an emulsion consisting of chemically synthesized triglycerides composed of medium-chain and long-chain fatty acids in similar proportions. Sprague-Dawley rats received a 25% body surface area full-thickness scald burn on the dorsum. For the next three days, all rats received 300 kcal/kg/day as 160 kcal/kg/day glucose, 50 kcal/kg/day amino acid, and an additional 90 kcal/kg/day lipid emulsion as either long-chain triglyceride, medium-chain triglyceride, a 1:1 physical mix of medium-chain and long-chain triglycerides or a chemically structured triglyceride made up of 60% medium-chain fatty acid and a 40% safflower oil. Rats receiving the chemically structured lipid emulsion showed the greatest gain in body weight, the greatest positive nitrogen balance, and the highest serum albumin concentration, outstripping rats receiving the long-chain triglyceride, medium-chain triglyceride, and even the physical mixture long-chain and medium-chain triglycerides (P less than 0.01). A 30% increase in oxygen consumption and 35% increase in energy expenditure in rats given the medium-chain triglyceride emulsion alone (P less than 0.01) was observed. This study confirms that the metabolism of chemically structured triglycerides composed of medium-chain and long-chain fatty acids markedly differs from similar physical mixtures. For these reasons, the new structured lipid emulsions may prove advantageous in feeding the severely injured patient.

Amino Acids↗
PubMed2004

Relationship of adiposity to the population distribution of plasma triglyceride concentrations in vigorously active men and women.

Although it is known that triglyceride concentrations increase with adiposity, whether the same increase applies for different percentiles of the triglyceride distribution has not been reported. Therefore, physician-supplied triglyceride concentrations from 7288 male and 2326 female runners were divided into strata according to the body mass index (BMI) and circumferences of the waist, hip and chest. The percentiles of the triglyceride distribution within each stratum were used to determine the cross-sectional regression slope between adiposity and triglyceride levels at each triglyceride percentile. Compared to the 5th percentile of the triglyceride distribution, the rise in men's triglycerides at the 95th percentile per unit of adiposity was 14-fold greater for BMI, 7.8-fold greater for waist circumference, 3.6-fold greater for hip circumference, and 4.4-fold greater for chest circumference. The rise in women's triglyceride concentrations at the 95th percentile was 8-fold greater than at the 5th percentile for each kg/m(2) increase in BMI. These results suggest that the metabolic effects of adiposity on plasma triglycerides depend upon whether the concentrations are high or low. This contradicts statistical assumptions upon which prior studies of adiposity have based their analyses. We speculate that the reported greater increases in triglycerides per unit of adiposity in whites than blacks, in men than women, and in low-density lipoprotein (LDL) pattern B than A are all consistent with the relationships we observe. It remains to be verified whether these relationship also apply to less active populations.

Adipose Tissue↗
PubMed2001

Squalene synthase inhibitors reduce plasma triglyceride through a low-density lipoprotein receptor-independent mechanism.

Inhibitors of squalene synthase are considered to be candidate drugs to reduce both plasma cholesterol and triglyceride. However, little is known about the mechanism of squalene synthase inhibitor-specific effect on plasma triglyceride. In this study, we confirmed the triglyceride-lowering effect of ER-27856, a potent squalene synthase inhibitor prodrug, in rhesus monkeys. To determine the role of low-density lipoprotein (LDL) receptor in the triglyceride-lowering effect of squalene synthase inhibitors, we intravenously administered ER-28448, the active form of ER-27856, to Watanabe heritable hyperlipidemic (WHHL) rabbits for 4 days. In heterozygotes, ER-28448 reduced plasma cholesterol and triglyceride by 52% and 37%, respectively. In homozygous rabbits, in contrast, ER-28448 lowered plasma triglyceride by 40% but did not lower plasma cholesterol. Orally administered ER-27856 reduced plasma triglyceride in homozygous animals but atorvastatin and bezafibrate did not. In hepatocytes isolated from homozygous WHHL rabbits, squalene synthase inhibitors but not atorvastatin reduced triglyceride biosynthesis. These data demonstrate that squalene synthase inhibitors reduced plasma triglyceride through an LDL receptor-independent mechanism, which was distinct from that of the triglyceride-lowering action of atorvastatin or bezafibrate. The reduction of hepatic triglyceride biosynthesis may play an important role in the hypotrigyceridemic action of squalene synthase inhibitors.

Animals↗
PubMed1998

Important contribution of lipoprotein particle number to plasma triglyceride concentration in type 2 diabetes.

The aim of the present study was to determine the contributions of particle size versus number to differences in plasma triglyceride-rich lipoprotein concentrations in patients with type 2 diabetes. Fasting plasma was obtained from 174 consecutive eligible men and women with type 2 diabetes (with or without insulin treatment, mean age 57.0 + 6.3 years) who were undergoing coronary angiography. The triglyceride-rich (Sf 12-400) lipoproteins (TRL) were subfractionated into the Sf 12-60 and Sf 60-400 subfractions. Particle numbers, estimated by measuring apolipoprotein B by electroimmunoassay, in each of these lipoprotein fractions were related to enzymatically determined triglyceride levels in the triglyceride-rich lipoproteins. Approximately 87% of the triglyceride-rich lipoprotein particles were in the Sf 12-60 fraction and 13% in the Sf 60-400 fraction. Multiple linear regression indicated that 69% (i.e. r2=0.69) of the variance in the triglyceride levels could by explained by differences in TRL particle number and 17% (i. e. r2=0.17) by the differences in particle triglyceride content. These observations are similar in each gender and in those with or without insulin treatment. In conclusion, in type 2 diabetes, the vast majority of triglyceride-rich lipoproteins are smaller particles which are in the Sf 12-60 fraction. Differences in particle number, rather than triglyceride content, account for approximately 70% of the differences in triglyceride levels observed between individuals. Previous demonstrations, in those without diabetes, of an association between small triglyceride-rich lipoproteins with coronary artery disease suggest the importance of these findings to the increased atherosclerosis in diabetes.

Adult↗
PubMed2001

Triglyceride-rich lipoprotein cholesterol exceeds low-density lipoprotein cholesterol in hypertriglyceridemia patients.

The atherogenicity of triglyceride-rich lipoprotein has been revealed. This study was performed to explore the clinical importance of triglyceride-rich lipoprotein by measuring its cholesterol content and comparing it with other lipoprotein fractions. Blood samples were obtained from 103 patients whose fasting plasma triglyceride concentration exceeded 300 mg/dl. The cholesterol monitor using the technique of high-performance liquid chromatography was used for the measurement of their plasma cholesterol concentrations and the determination of cholesterol distribution among lipoprotein fractions. This monitor showed 4 peaks: large-triglyceride-rich lipoprotein, small-triglyceride-rich lipoprotein, low-density lipoprotein, and high-density lipoprotein. Total cholesterol increased with increasing triglyceride. The increment of total cholesterol was nearly equal to that of small-triglyceride-rich lipoprotein cholesterol. Small-triglyceride-rich lipoprotein cholesterol exceeded low-density lipoprotein cholesterol where plasma triglyceride concentration was over 500 mg/dl. In conclusion, triglyceride-rich lipoprotein may be clinically important for hypertriglyceridemic patients as a source of cholesteryl ester in arteriosclerotic plaques, and increased triglyceride-rich lipoprotein cholesterol may be used as a basis for hypertriglyceridemia atherogenicity. Our study suggests that hypertriglyceridemia should be treated to prevent arteriosclerotic disease.

Apolipoproteins E↗
PubMed1999

Microphase separation in low density lipoproteins. Evidence for a fluid triglyceride core below the lipid melting transition.

The structural organization of the neutral lipid core in human low density lipoproteins (LDL) was investigated in physicochemically defined, distinct human LDL subspecies in the density range of 1. 0244-1.0435 g/ml by evaluation of the core lipid transition temperature, chemical composition, and the behavior of spin-labeled core lipids. Calorimetric studies were performed on more than 60 LDL preparations, and the transition temperature, which varied between 19 and 32 degreesC, was correlated to the chemical composition and revealed a discontinuity at a critical cholesteryl ester to triglyceride ratio of approximately 7:1. For electron spin resonance studies, several LDL preparations were probed with spin-labeled cholesteryl esters and triglycerides, respectively. In LDL with a high triglyceride content, both labels exhibited similar mobility behavior. In contrast, in LDL with only small concentrations of triglycerides, the behavior of labeled cholesteryl esters and labeled triglycerides differed distinctly. The cholesteryl esters were strongly immobilized below the transition temperature, whereas the triglycerides remained fluid throughout the measured temperatures. These results suggest that the critical cholesteryl ester to triglyceride mass ratio of 7:1 corresponds to two concentric compartments with a radial ratio of 2:1, where the liquid triglycerides occupy the core, and the cholesteryl esters form the frozen shell. At higher triglyceride contents, the triglyceride molecules insert into the cholesteryl ester shell and depress the peak transition temperature of the LDL core, whereas at lower triglyceride contents, excess cholesteryl esters are dissolved in the core.

Calorimetry, Differential Scanning↗
PubMed1978

Effect of age and sex on triglyceride metabolism in the rat.

The effect of age and sex on triglyceride metabolism were investigated in 3-mo- and 1-year-old rats. Although 3-mo-old female rats produce as much triglyceride as comparably aged male rats, their plasma triglyceride levels are lower. This suggests that 3-mo-old female rats remove triglycerides from plasma more efficiently than do similar aged male rats, and this is supported by the observation that the t1/2 of very low density lipoprotein triglyceride removal is somewhat faster in female rats of this age (p less than 0.1 greater than 0.5). As rats grow to 1 year of age, the ability of both sexes to remove triglycerides from plasma deteriorates, resulting in a rise in plasma triglyceride levels. The decrease in efficiency of triglyceride removal from plasma in female rats is coupled with an increase in triglyceride production rate, leading to an even greater increase in triglyceride levels. These results indicate that both age and sex modify triglyceride metabolism in the rat.

Age Factors↗
PubMed1994

Effect of long-term administration of probucol on triglyceride turnover in rats.

BACKGROUND: Our previous observation revealed that probucol, a well known cholesterol-lowering drug, can improve impaired catabolism of plasma triglyceride in streptozotocin-diabetic rats without reducing plasma glucose. The present study was conducted using Triton WR1339 and endogenously radiolabeled lipoproteins in order to examine the mechanisms whereby the drug can stimulate triglyceride removal from the circulation in rats independent of glucose metabolism. METHODS: The short- and long-term effects of probucol on triglyceride turnover were examined in rats. Male Wistar rats received a diet containing probucol (1%) for 2 weeks and 4 months. Triglyceride turnover was estimated in rats using Triton WR1339. RESULTS: After 2 weeks of probucol administration, triglyceride and cholesterol concentrations in plasma and in the very-low-density lipoprotein (VLDL) fraction were suppressed slightly but significantly in the probucol-administered rats compared with standard chow-fed control rats. However, triglyceride secretion rates were similar in the two groups. Probucol-administered rats showed markedly suppressed triglyceride concentration in plasma and the VLDL fraction compared with chow-fed control rats after 4 months of administration. However, triglyceride secretion rate was significantly increased in rats given probucol. The radioisotope experiment revealed that probucol-administered rats can remove VLDLs (lipoproteins either from probucol-administered or control rats) from their system faster than normal rats and that probucol-containing VLDL can be removed from the circulation of both groups of rats more rapidly than normal VLDL. Therefore, probucol-administered rats as well as probucol-containing VLDL (lipoprotein from probucol-administered rats) are responsible for accelerated catabolism of VLDL-triglyceride. CONCLUSION: No significant differences in the lipid composition of newly-secreted VLDL particles between control rats and those given probucol were noted after Triton injection. The precise mechanism behind increased triglyceride secretion rate in rats after long-term administration of probucol is not known. However, we concluded from the present data that long-term administration of probucol results in markedly accelerated VLDL-triglyceride turnover without affecting lipid composition of newly secreted VLDL particles in normal rats.

Animals↗
PubMed2006

Decrease in triglyceride level by bezafibrate is related to reduction of recurrent coronary events: a Bezafibrate Infarction Prevention substudy.

BACKGROUND: Fibrates were reported to be effective in reducing recurrent coronary events in coronary heart disease patients with elevated triglycerides. It is not known whether this effect is related to the extent of triglyceride reduction. METHODS: Participants comprised 3090 coronary heart disease patients enrolled in the Bezafibrate Infarction Prevention study, which showed a nonsignificant reduction (9.4%; P=0.26) in fatal or nonfatal myocardial infarction and sudden death during a mean follow-up time of 6.2 years. RESULTS: Significant reduction in triglyceride serum level was evident only among patients allocated to bezafibrate, ranging between 0.06 mmol/l (5 mg/dl) in the lowest decile of baseline triglycerides level and 0.68 mmol/l (60 mg/dl) in the highest baseline decile. The extent of triglyceride reduction with bezafibrate was significantly associated with the reduction of risk; relative risk reduction of 55% (hazards ratio: 0.45; 95% confidence interval: 0.24-0.84) was observed among patients with baseline triglycerides>or=2.26 mmol/l who reduced triglyceride level to >0.50 mmol/l (>44.3 mg/dl). In contrast, the risk of recurrent events among patients treated with bezafibrate and achieving less triglyceride reduction or failing to reduce triglyceride level was not significantly different from that of patients treated with placebo. CONCLUSION: Bezafibrate treatment was associated with significant risk reduction among coronary heart disease patients with elevated triglyceride levels that substantially reduced their triglyceride level with treatment.

Aged↗
PubMedDate not supplied

Plasma triglyceride and coronary heart disease.

Although the literature on epidemiological associations between plasma triglyceride and CHD is not completely consistent, trends do emerge from the studies described here. First, the majority of observational studies demonstrate a significant univariate relation, although the results of case-control and cross-sectional studies are more uniform than those from prospective study designs. In many but not all studies, triglyceride remains a significant predictor of CHD in multivariate statistical analyses after controlling for TC or LDL-C. Perhaps the least consistent result is that the triglyceride association does not persist in some analyses controlling for HDL-C, while in other studies, the association remains significant. Although most studies have been conducted in men, the studies providing data on women, normocholesterolemic subjects, and diabetic subjects have generally found triglyceride to be, at the very least, a univariate risk factor. The results of intervention trials differ considerably, but no such study to date has been specifically designed to evaluate triglyceride-lowering effects on primary prevention of CHD. Important statistical properties must be taken into consideration in evaluating triglyceride as a risk factor for CHD. The large variability of triglyceride measurements and the correlation of triglyceride values with other lipid measures appears to result in the underestimation of the association between triglyceride and disease in multivariate analyses. Finally, individual genetic susceptibility may play an important role in the relation between plasma triglyceride levels and CHD. For example, risk of CHD clearly varies among the well-established familial forms of hypertriglyceridemia. A predominance of small, dense, LDL particles (LDL subclass pattern B) also appears to be a genetic trait associated with both increased risk of MI and increases in plasma triglyceride levels.

Coronary Disease↗
PubMed2003

CP-346086: an MTP inhibitor that lowers plasma cholesterol and triglycerides in experimental animals and in humans.

A microsomal triglyceride transfer protein (MTP) inhibitor, CP-346086, was identified that inhibited both human and rodent MTP activity [concentration giving half-maximal inhibition (IC50) 2.0 nM]. In Hep-G2 cells, CP-346086 inhibited apolipoprotein B (apoB) and triglyceride secretion (IC50 2.6 nM) without affecting apoA-I secretion or lipid synthesis. When administered orally to rats or mice, CP-346086 lowered plasma triglycerides [dose giving 30% triglyceride lowering (ED30) 1.3 mg/kg] 2 h after a single dose. Coadministration with Tyloxapol demonstrated that triglyceride lowering was due to inhibition of hepatic and intestinal triglyceride secretion. A 2 week treatment with CP-346086 lowered total, VLDL, and LDL cholesterol and triglycerides dose dependently with 23%, 33%, 75%, and 62% reductions at 10 mg/kg/day. In these animals, MTP inhibition resulted in increased liver and intestinal triglycerides when CP-346086 was administered with food. When dosed away from meals, however, only hepatic triglycerides were increased. When administered as a single oral dose to healthy human volunteers, CP-346086 reduced plasma triglycerides and VLDL cholesterol dose dependently with ED50s of 10 mg and 3 mg, and maximal inhibition (100 mg) of 66% and 87% when measured 4 h after treatment. After a 2 week treatment (30 mg/day), CP-346086 reduced total and LDL cholesterol and triglycerides by 47%, 72%, and 75%, relative to either individual baselines or placebo, with little change in HDL cholesterol. Together, these data support further evaluation of CP-346086 in hyperlipidemia.

Animals↗
PubMed2001

Biologic role of fetal lung fibroblast triglycerides as antioxidants.

The pulmonary response to hyperoxia is highly variable, depending on such seemingly disparate biologic factors as gestational age, sex, hormonal milieu, and nutritional status. Descriptively, the magnitude and direction of these biologic differences in response to hyperoxia correlate with the triglyceride content of developing fetal rat lung fibroblasts (FRLFs). Mechanistically, these same factors affect the triglyceride content of FRLFs, e.g. d 21 FRLFs contain more triglyceride than d 18 FRLFs; female FRLFs contain more triglyceride than male FRLFs (d 20); dexamethasone increases FRLF triglyceride content, dihydrotestosterone decreases it; nutritionally, exposure of FRLFs to graded amounts of serum triglyceride (0%, 2%, 10%, 20%) results in increased intracellular FRLF triglyceride content. To test the hypothesis that these biologic differences in intracellular triglyceride content may account for differences in the cytoprotection of lung fibroblasts against oxidant injury, fibroblast cultures representing each of these biologic groups were challenged with graded doses of the reactive oxygen species hydrogen peroxide (0.1-1.0 mM for 5 min). The number of surviving cells and their antioxidant status, as measured by lipid peroxidation and glutathione content of the surviving cells, were determined. We found that in response to hydrogen peroxide 1) d 21 FRLFs were more resistant than d 18 FRLFs; 2) female FRLFs were more resistant than male FRLFs; 3) dexamethasone-treated FRLFs were more resistant than dihydrotestosterone-treated fibroblasts; 4) fibroblasts fed increasing amounts of serum triglycerides were increasingly resistant to hydrogen peroxide; 5) cell survival in different serum triglyceride- and hormone-treated groups was not related to the antioxidant status as measured by glutathione content. These data are consistent with the hypothesized role of FRLF triglycerides as antioxidants.

Animals↗
PubMed2005

The effect of cholesteryl ester transfer protein -629C->A promoter polymorphism on high-density lipoprotein cholesterol is dependent on serum triglycerides.

CONTEXT: The -629C-->A cholesteryl ester transfer protein (CETP) promoter polymorphism is a determinant of HDL cholesterol (HDL-C). The effect of the closely linked CETP TaqIB polymorphism on HDL-C has been suggested to be modified by obesity and hyperinsulinemia. OBJECTIVE: Because the CETP-mediated cholesteryl ester transfer out of HDL is stimulated by high triglycerides, we hypothesized that triglycerides modify the effect of the CETP -629C-->A promoter polymorphism on HDL-C. DESIGN: In 7083 nondiabetic subjects of the PREVEND population, the -629C-->A promoter polymorphism, HDL-C, serum triglycerides, waist circumference, and insulin resistance (HOMA(ir)) were determined. Serum apolipoprotein A-I was available in 6948 subjects. The TaqIB polymorphism was also assessed. SETTING: The study is set in the general community. RESULTS: HDL-C and serum apolipoprotein A-I were on average 0.14 mmol/liter and 0.05 g/liter higher in -629AA (22.9%) compared to -629CC (26.8%) homozygotes (P < 0.001 for both). This genotype effect on HDL-C was on average 0.15 mmol/liter in the lowest triglyceride tertile but only 0.08 mmol/liter in the highest tertile (P < 0.01). Multiple regression analysis showed that HDL-C was determined by the CETP promoter variant (P < 0.001), gender (P < 0.001), triglycerides (P < 0.001), and interactions between triglycerides and genotype (P < 0.05), between triglycerides and gender (P < 0.05), and between genotype and gender (P < 0.05), independently from waist, HOMA(ir), alcohol use, age, and use of lipid-lowering drugs. The TaqIB polymorphism also interacted with triglycerides on HDL-C. The -629C-->A promoter polymorphism did not interact with obesity and HOMA(ir) on HDL-C. CONCLUSIONS: The HDL-C-raising effect of the CETP -629A allele is diminished with higher triglycerides, which may be explained by a predominant effect of triglyceride-rich lipoproteins over circulating CETP itself on cholesteryl ester transfer out of HDL with rising triglycerides.

Adult↗
PubMed2005

Rosiglitazone improves postprandial triglyceride and free fatty acid metabolism in type 2 diabetes.

OBJECTIVE: Increased postprandial lipemia is part of diabetic dyslipidemia and is associated with accelerated atherosclerosis. We investigated the effects of the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone on postprandial lipemia in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: A randomized, 8-week, crossover, placebo-controlled, double-blind trial was performed in which rosiglitazone at 4 mg was administrated twice daily in 19 patients with type 2 diabetes. Standardized 6-h oral fat-loading tests were performed after each treatment period. Postprandial curves were calculated as the total area under the curve (AUC) and the incremental area under the curve (dAUC). RESULTS: Rosiglitazone did not change fasting plasma triglycerides compared with placebo (1.97 +/- 0.22 vs. 1.88 +/- 0.20 mmol/l, respectively) but decreased postprandial triglyceride levels, leading to significantly lower triglyceride dAUC (-37%, P < 0.05), without changing total triglyceride AUC. Significant postprandial triglyceride reductions in the chylomicron fraction (Svedberg flotation rate [Sf] >400) were achieved with rosiglitazone, which resulted in a significant lower triglyceride AUC (-22%) in this fraction. The postprandial triglyceride increase in VLDL1 (Sf 60-400) was also lower after rosiglitazone (-27%), but this did not result in a significant lower triglyceride AUC. In VLDL2 (Sf 20-60), there were no significant differences in triglyceride AUC and triglyceride dAUC between rosiglitazone and placebo. Rosiglitazone decreased free fatty acid (FFA) AUC (-12%) and FFA dAUC (-18%) compared with placebo. CONCLUSIONS: Rosiglitazone improves the metabolism of large triglyceride-rich lipoproteins and decreases postprandial FFA concentrations in type 2 diabetes. This may have clinical implications, as these effects may contribute to cardiovascular risk reduction.

Adult↗
PubMed1989

Milk fatty acid composition and plasma energy metabolite concentrations in lactating cows fed medium-chain triglycerides.

Six lactating Holstein cows were used in a replicated 3 x 3 Latin square design to determine the effects of medium-chain triglyceride supplementation on milk fatty acid composition and plasma energy metabolites. Treatments were no supplemental triglyceride, 500 ml of odd-carbon, medium-chain triglyceride (fatty acid composition: 100% pelargonic acid), or 500 ml of even-carbon, medium-chain triglyceride (fatty acid composition: 65% caproic acid, 35% capric acid) added daily to a total mixed ration. Medium-chain triglyceride supplementation did not affect ruminal molar proportions of acetate or propionate but slightly increased the molar proportion of butyrate. Even-carbon and odd-carbon, medium-chain triglycerides reduced DM intake by 1.7 and 1.3 kg/d, respectively, but did not affect milk yield or milk protein percentage. Cows that did not receive supplemental triglyceride produced milk with 3.29% fat. Milk fat concentration was increased by even-carbon, medium-chain triglyceride supplementation relative to odd-carbon, medium-chain triglyceride supplementation (3.44 vs. 2.99%). Although changes in milk fatty acid composition were observed, they were minor and mostly unexplained. Feeding even-carbon, medium-chain triglycerides caused slight increases in plasma glucose and nonesterified fatty acid concentrations, but plasma beta-hydroxybutyrate concentration was not affected by treatments. Odd-carbon, medium-chain triglyceride supplementation (500 ml/d) does not appear to be antiketogenic.

Analysis of Variance↗
PubMed1999

Prevalence of high plasma triglyceride combined with low HDL-C levels and its association with smoking, hypertension, obesity, diabetes, sedentariness and LDL-C levels in the Canadian population. Canadian Heart Health Surveys Research Group.

OBJECTIVE: To report the associations of plasma triglyceride, high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) with nonlipid coronary artery disease risk factors. In particular, the associations for persons with high triglyceride and low HDL-C levels were examined. DESIGN: A stratified random probability sample of 29,855 men and women aged 18 to 74 years from the Canadian Heart Health Surveys (1986 to 1992) in 10 provinces. Blood samples were obtained from 18,555 participants who had fasted for 8 h or more. Plasma lipids were determined at the J Alick Little Lipid Research Laboratory, Toronto, Ontario, with standardization of the Centers for Disease Control Lipid Standardization Program, Atlanta. OUTCOME MEASURES: Fasting plasma total cholesterol, triglyceride, LDL-C and HDL-C levels. MAIN RESULTS: The prevalence of men with triglyceride levels above 1.7 mmol/L and HDL-C levels below 0.9 mmol/L was 10%, compared with 3% for men with triglyceride levels below 1.7 mmol/L and HDL-C levels below 0.9 mmol/L. The prevalence of women with triglyceride levels above 1.7 mmol/L and HDL-C levels below 0.9 mmol/L was 3% compared with a prevalence of less than 1% for women with triglyceride levels below 1.7 mmol/L and HDL-C levels below 0.9 mmol/L. Even when plasma LDL-C was low at less than 3.4 mmol/L, there was an age trend for increasing prevalences of the combination of triglyceride levels 2.3 mmol/L or greater and HDL-C levels less than 0.9 mmol/L in both sexes. The prevalence of a triglyceride levels 2.3 mmol/L or greater combined with an HDL-C level below 0.9 mmol/L was increased in groups who were cigarette smokers, diabetic, hypertensive, obese or sedentary, or who had higher LDL-C levels in both sexes, and the increase was even greater in the presence of two or more of these other risk factors. CONCLUSIONS: Among men or women with low HDL-C and high triglyceride levels, smoking, diabetes, sedentariness, hypertension and obesity were much more prevalent than among those at low risk with high HDL-C and low triglyceride levels.

Adolescent↗
PubMed1999

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 triglyceride, very low-density lipoprotein (VLDL), and Kupffer cell-conditioned medium (KCCM) derived from triglyceride and VLDL treatment on proliferation of rat hepatic stellate cells (HSC). METHODS: HSC and Kupffer cells were isolated and cultured from liver of Wistar rats by in situ perfusion with proteinase and collagenase, and density gradient centrifugation with Nycodenz; HSC and Kupffer cells were identified by immunohistochemistry, endocytosis, and ultrastructure, etc. Kupffer cells were incubated with triglyceride (25 micrograms/ml) and VLDL (25 micrograms/ml) for 24 hours, KCCM were prepared, and MTT colorimetric assay was detected for HSC proliferation. RESULTS: HSC proliferation was 0.1894 +/- 0.0316 (12.5 micrograms/ml), 0.1637 +/- 0.0243 (25 micrograms/ml), 0.1450 +/- 0.0264 (50 micrograms/ml), 0.1212 +/- 0.0275 (100 micrograms/ml), 0.1226 +/- 0.0138 (200 micrograms/ml) and 0.0990 +/- 0.0163 (400 micrograms/ml) in the presence of triglyceride and was 0.1583 +/- 0.0314 (6.25 micrograms/ml), 0.1642 +/- 0.0269 (12.5 micrograms/ml), 0.1834 +/- 0.0498 (25 micrograms/ml), 0.1964 +/- 0.0287 (50 micrograms/ml) and 0.2202 +/- 0.0284 (100 micrograms/ml) in presence of VLDL, respectively. Compared with the control, HSC proliferation at 400 micrograms/ml of triglyceride was lower (P < 0.01), but at 12.5 micrograms/ml of triglyceride and 25, 50, 100 micrograms/ml of VLDL higher (P < 0.05 or 0.01); HSC proliferation was 0.1569 +/- 0.0144, 0.1924 +/- 0.0113 and 0.1871 +/- 0.0116 in the presence of KCCM, KCCM + triglyceride and KCCM + VLDL, respectively. Compared with the control and KCCM, KCCM + triglyceride and KCCM + VLDL might promote HSC proliferation (P < 0.01); there was no statistical significance between KCCM + triglyceride and KCCM + VLDL (P > 0.05); KCCM was greater in HSC proliferation than the control, but there was no significant change (P > 0.05). CONCLUSIONS: Triglyceride, VLDL, and KCCM stimulated by triglyceride and VLDL might promote HSC proliferation and be associated with fatty liver and hepatic fibrogenesis.

Animals↗