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PubMed1991

Relationship between serum pseudocholinesterase and triglycerides in experimentally induced diabetes mellitus in rats.

This study was designed to understand the reasons for the increase in serum pseudocholinesterase activity in diabetes mellitus. Streptozotocin-induced diabetic rats were used for the study. Serum pseudocholinesterase activity increased with the induction of diabetes (381.5 units/l +/- 11.8) compared to the non-diabetic rats (243.1 units/l +/- 7.2). Serum triglycerides, total low density lipoprotein and glycerol also increased concurrently with the development of diabetes. Insulin treatment of the diabetic rats normalized serum glucose concomitant with the reduction of pseudocholinesterase activity, triglycerides, total low density lipoprotein and glycerol. Heparin injection appeared to activate lipoprotein lipase in the diabetic rats by showing a marked fall in serum triglyceride and total low density lipoprotein levels but not in pseudocholinesterase activity. Administration of tetraisopropylpyrophosphoramide a specific pseudocholinesterase inhibitor, inhibited serum and adipose tissue pseudocholinesterase activity by greater than 80% and liver greater than 50%. Concurrent with the inhibition of pseudocholinesterase activity serum triglyceride, low density lipoprotein and glycerol decreased significantly. In normal rats treatment with tetraisopropylpyrophosphoramide also reduced serum lipoproteins markedly, while glycerol only showed a marginal decrease. Glycerol was used as a marker of adipose tissue lipolysis and total low density lipoprotein which is defined as lipoproteins of density less than 1.063 (LDL + VLDL).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effects of Acipimox on the metabolism of free fatty acids and very low lipoprotein triglyceride.

The mechanism of triglyceride lowering by Acipimox, a nicotine acid analogue, was examined in a group of five moderately hypertriglyceridemic male rhesus monkeys. Two experiments were designed to examine the effect of the drug on lipid and glucose metabolism in nondiabetic, insulin-resistant animals. A single dose of Acipimox (8 mg/kg) given with a meal lowered the plasma free fatty acids (FFA) significantly at 4 h (0.102 +/- 0.008 vs 0.154 +/- 0.020 g/l; mean +/- SEM; P < 0.03); however, FFA concentrations returned to control levels at 6 h. Chronic administration of Acipimox (16 mg/kg q. i. d.) for 2 months produced a 31% reduction in triglyceride concentration (P < 0.05) and a significant decrease in low density lipoprotein (LDL)-cholesterol (P < 0.04), without changes in insulin action as measured by the hyperinsulinemic euglycemic clamp. Fasting FFA concentrations were not significantly altered by chronic treatment (0.163 +/- 0.013 versus 0.140 +/- 0.034 g/l). Fatty acid metabolic studies indicated increases in FFA transport (203.7 +/- 59.1 versus 136.1 +/- 26.6 microEq/min; P < 0.05), while FFA fractional clearance rate (FCR) was unchanged. Very low density lipoprotein triglyceride (VLDL-Tg) metabolic experiments, using [3H]glycerol, showed increases in production and FCR with the drug. Increased VLDL-Tg clearance, in spite of increased production of VLDL, appears to be the mechanism by which triglycerides are lowered upon chronic Acipimox administration.

Animals↗
PubMed1988

Plasma-triglycerides and exercise: a delicate balance.

Alimentary lipemia was studied in 12 healthy young men with and without exercise. Three sets of experiments were performed. While continuous exercise of 90 min duration significantly reduced postprandial triglycerides by 26% (study I), this effect could not be observed when exercise was interrupted for 5 min after each 25 min (study II). Plasma free fatty acid concentrations, in the latter experiment, were significantly higher (by 311%) than during rest. When, in a third experiment continuous exercise was compared with intermittent physical activity, the latter condition significantly increased postprandial triglyceridemia, most probably due to precipitous rises of free fatty acids on each interruption of ergometry. It is concluded that in the third experiment the balance between triglyceride removal and triglyceride synthesis was shifted toward the latter. Whether exercise lowers, leaves unaltered, or raises plasma triglyceride levels may depend on subtle changes of experimental design.

Adult↗
PubMedDate not supplied

Enhanced lipolysis of myocardial triglycerides during low-flow ischemia and anoxia in the isolated rat heart.

We studied lipolysis in the isolated rat heart, measured as glycerol release during anoxia, low-flow ischemia and subsequent reperfusion. It was found that the rate of lipolysis was enhanced during ischemia/anoxia while the lipase activities in tissue extracts involved in the myocardial lipolysis and the amount of triglycerides were not affected. This indicates the dominant occurrence of a lipolysis-reesterification principle in ischemic and anoxic tissue. A common observation of ischemia/anoxia is an increase in the tissue NADH/NAD+ ratio. Therefore we investigated the effect of lactate and malate, both of which enhance the tissue redox state on myocardial lipolysis. Perfusion in the presence of lactate (10 mM) and malate (10 mM) both stimulated myocardial lipolysis by about five times. This suggests that the rate of reesterification of product fatty acids to triglycerides, which is determined by the NADH/NAD+ ratio, because of the increased formation of glycerol 3-phosphate from dihydroxy acetone phosphate, plays an important role in the regulation of lipolysis. The existence of triglyceride-fatty acid-triglyceride cycle is discussed.

Animals↗
PubMed1975

[The triglycerides with medium chains].

Medium chain triglycerides (MCT) (fatty acids with 6-12 C) are absorbed more quickly than long chain triglycerides. Medium chain fatty acids are not incorporated into hepatic triglycerides, but oxidized. If MCT are given alone, they stimulate ketogenesis. Nevertheless MCT are of great interest in the diet of numerous affections of the digestive tract. When long chain triglycerides are not tolerated, MCT can replace them with efficiency.

Animals↗
PubMedDate not supplied

Oxidized LDL autoantibodies are related to apolipoprotein E phenotype, independently of postprandial change in plasma triglycerides and LDL size, among patients with angiographically verified coronary artery disease and healthy controls.

OBJECTIVE: Oxidized low-density lipoprotein (LDL) autoantibodies (oxLDLab), apolipoprotein E (apoE) phenotype, postprandial triglyceride changes and LDL size are suggested to be risk factors for coronary artery disease (CAD). Our aim was to study the interaction between these new risk factors among patients with CAD and healthy controls. METHODS: oxLDLab from 31 men with angiographically verified CAD and 31 healthy men were analyzed by enzyme-linked immunosorbent assay. Isoelectric focusing and immunoblotting were used for apoE phenotyping. Triglyceride level was measured after 12 h of fasting and 3, 5 and 7 h after a high-fat meal. Nondenaturing gradient gel electrophoresis was used to separate LDL particles according to size. RESULTS: oxLD- Lab levels increased according to apoE phenotype in the following order: E2 < E3 < E4 (p = 0.004, ANOVA). The postprandial response of triglycerides, the size of LDL particles and the concentration of LDL and high-density lipoprotein (HDL) cholesterol did not differ between apoE phenotypes, and the use of these variables as covariates did not change the statistically significant difference in oxLDLab levels between apoE phenotypes (p = 0.01, ANCOVA). oxLDLab levels did not differ between the patient and control groups. CONCLUSION: We found an association between apoE allele epsilon2 and decreased levels of oxLDLab, which was independent of the postprandial response of triglycerides, the size of LDL particles and plasma LDL and HDL cholesterol levels. The mechanism by which apoE affects oxidation of LDL remains unknown.

Adult↗
PubMed1975

Stimulatory effect of glucose upon triglyceride synthesis from acetate, decanoate, and palmitate by mammary gland slices from lactating mice.

Slices prepared from the mammary glands of lactating mice incorporate only small amounts of (1--14C) acetate, (1--14C) decanoate, or (1--14C) palmitate into lipids. However, when glucose is added to the incubation medium, fatty acid incorporation is stimulated-13-fold from acetate, 17-fold from decanoate, and 2-fold from palmitate. Over 90% of the -14C activity in the lipid fraction is in triglycerides. Analysis of fatty acids in the triglycerides showed that almost all of the decanoate and the palmate were incorporated as intact molecules, while acetate yielded acids of varying chain lengths. The glucose stimulation of triglyceride synthesis is not solely due to its effect upon chain elongation but also could involve glyceride-glycerol availability, as well as other unknown factors. However, from measurements of the amounts of glycerol 3-phosphate in the tissue incubated in the presence of palmitate, it would appear that glyceride-glycerol availability is not rate limiting in triglyceride synthesis.

Acetates↗
PubMed1975

Specificity of digestive lipases in hydrolysis of wax esters and triglycerides studied in anchovy and other selected fish.

The physiological specificity of fat digestion in several species of marine fish was studied by incubating a variety of synthetic and natural lipid substrates in fish intestinal fluid. Wax ester and triglyceride hydrolyses were studied in vivo and in vitro. In vivo feeding studies showed triglyceride hydrolysis and reesterification in the gut occurred 4 times faster than wax ester metabolism. In vitro comparisons of wax and triglyceride lipolysis always showed triglycerides to be hydrolyzed faster than wax esters; however, wide variation in the ratio occurred among different batches of intestinal juice. Ca. 50% of the 2 monoglycerides formed in the lipolytic sequence were hydrolyzed. Esters of lipase resistent fatty acids (20:4 and 20:5) were cleaved faster than normal fatty acid esters (18:2 and 18:3). Two of the species studied, the northern anchovy, Engraulis mordax and the jack mackerel, Trachurus symmetricus, empty lipase(s) into their gall bladders and produce-phospholipid free bile.

Animals↗
PubMed1977

Hypercholesterolemia and triglyceride secretion rates in monkeys fed different dietary fats.

The influence of hypercholesterolemia on the triglyceride secretion rate was studied in both squirrel and cebus monkeys fed coconut oil, corn oil, or safflower oil. The triglyceride secretion rate (TGSR) was determined in vivo following the administration of Triton WR1339, which blocks the clearance of very low density lipoprotein (VLDL). Thus, the increase observed in circulating triglyceride after Triton administration presumably reflecte hepatic triglyceride (VLDL) secretion in the fasted state. The VLDL-TGSR was lowest in hypercholesterolemic monkeys and highest in those fed unsaturated fat diets and having a low serum cholesterol. In all instances, TGSR was inversely correlated with the plasma cholesterol concentration. While a definitive explanation for these observations must await further investigation, the possibility that circulating low density lipoprotein (LDL) acts to feed back on VLDL secretion is discussed. The decreased TGSR associated with the diet-induced cholesterolemia also implies clearance of VLDL is impaired under these conditions.

Animals↗
PubMed1978

Triglyceride synthesis from dihydroxyacetone phosphate and palmitate by microsomes from mammary glands of lactating mice.

Both di- and triglycerides were synthesized when microsomes isolated from mammary glands of lactating mice were incubated with dihydroxyacetone phosphate (DHAP), 1(-14)C)palmitate, ATP, CoASH, GSH, KF, MgC12, and NADPH. When NADH replaced NADPH, glyceride synthesis was very low. In the absence of either NADPH or NADH, DHAP was acylated to palmityl-DHAP. Since microsomes do not have glycerol 3-phosphate NAD:oxidoreductase activity , we inferred that glycerol 3-phosphate (GP) is not an intermediate in triglyceride biosynthesis from DHAP. This reductase, present in the cytosol, was active only with NADH. With the same concentration of either GP or DHAP, microsomes yielded essentially similar amounts of di- and triglycerides. Mitochondria, while capable of synthesizing palmityl-DHAP, did not produce di- and triglycerides.

Animals↗
PubMed1980

Intercorrelations among plasma high density lipoprotein, obesity and triglycerides in a normal population.

The interrelationships among fatness measures, plasma triglycerides and high density lipoproteins (HDL) were examined in 131 normal adult subjects: 38 men aged 27-46, 40 men aged 47-66, 29 women aged 27-46 and 24 women aged 47-66. None of the women were taking estrogens or oral contraceptive medication. The HDL concentration was subdivided into HDL2b, HDL2a and HDL3 by a computerized fitting of the total schlieren pattern to reference schlieren patterns. Anthropometric measures employed included skinfolds at 3 sites. 2 weight/height indices and 2 girth measurements. A high correlation was found among the various fatness measures. These measures were negatively correlated with total HDL, reflecting the negative correlation between fatness measures and HDL2 (as the sum of HDL2a and 2b). Fatness measures showed no relationship to HDL3. There was also an inverse correlation between triglyceride concentration and HDL2. No particular fatness measure was better than any other for demonstrating the inverse correlation with HDL but multiple correlations using all of the measures of obesity improved the correlations. Partial correlations controlling for fatness did not reduce any of the significant correlations between triglycerides and HDL2 to insignificance. The weak correlation between fatness and triglycerides was reduced to insignificance when controlled for HDL2.

Adult↗
PubMed1989

Changes in lipid composition of liver microsomes and fatty acyl-CoA desaturase activities induced by medium chain triglyceride feeding.

Changes in fatty acid composition, microsomal delta 9- and delta 6-desaturase activities and liver contents of cholesterol and phospholipids were studied in rats fed medium chain triglyceride-supplemented diets. Weanling rats were divided into four groups and fed for three weeks a basal diet with different 10%-fat supplements: corn oil, medium chain triglyceride-corn oil, olive oil and medium chain triglyceride-olive oil. The highest relative content of saturated fatty acids corresponded to corn oil-fed animals. Both monounsaturated fatty acid content and delta 9-desaturase activity were higher in the animals fed olive oil diets than in corn oil-fed rats. The long chain polyunsaturated fatty acids of the n-3 series were increased in the olive oil and medium chain triglyceride-olive oil-fed groups probably due to the lower linoleic/alpha-linolenic ratios found in these two diets. The cholesterol/phospholipid molar ratio was unaffected by diet and the unsaturation index was only slightly changed in the four groups. Thus, some mechanism may be operative under these conditions to maintain the homeostasis of the membrane.

Acyl-CoA Dehydrogenase, Long-Chain↗
PubMed1982

Positional distribution of fatty acids in triglycerides from milk of several species of mammals.

Milk triglycerides from the echidna, koala, Tammar wallaby, guinea pig, dog, cat, Weddell seal, horse, pig and cow were subjected to fatty acid and stereospecific analysis to determine the positional distribution of the fatty acids in the triglycerides. The samples presented a wide range of fatty acids, most of which varied in content among species. The compositions of the acids at the 3 positions also varied among species, reflecting the content of these acids in the triglycerides. However, there was a general similarity in fatty acid positional distribution patterns for all the species with the exception of the echidna. The echidna exhibited a completely different fatty acid positional distribution pattern. The saturated acids were preferentialy esterified at the sn-1-position whereas the unsaturated acids were selectively esterified at the sn-2-position. The triglyceride carbon number distribution of milk from the above species (with the exception of the Weddell seal) was determined by gas liquid chromatography and compared to that predicted by the 1-random-2-random-3-random fatty acid distribution hypothesis. Agreement was excellent between observed and predicted composition for echidna, koala, Tammar wallaby, guinea pig and pig milk, and agreement was reasonable for dog, cat, horse and cow milk. Results are discussed in relation to biochemical mechanisms.

Animals↗
PubMed1991

Effect of n-3 fatty acids on the key enzymes involved in cholesterol and triglyceride turnover in rat liver.

The effect of long-chain n-3 fatty acids on hepatic key enzymes of cholesterol metabolism and triglyceride biosynthesis was investigated in two rat models. In the first model, rats were intravenously infused for two weeks with a fat emulsion containing 20% of triglycerides in which either n-6 or n-3 fatty acids predominated. The treatment with n-3 fatty acids led to a reduction primarily of serum cholesterol (45%), but also of serum triglycerides (18%). HMG-CoA reductase activity and cholesterol 7 alpha-hydroxylase activity were reduced by 45% and 36%, respectively. There were no significant effects on diacylglycerol acyltransferase (DGAT) or phosphatidate phosphohydrolase (PAP) activities. In the second model, rats were fed a diet enriched with sucrose, coconut oil and either sunflower oil (n-6 fatty acids) or fish oil (long-chain n-3 fatty acid ethyl esters). The treatment with n-3 fatty acids decreased serum triglycerides (41%) and, to a lesser extent, serum cholesterol (17%). Neither glycerol 3-phosphate acyltransferase (GPAT) or DGAT were affected by n-3 fatty acids. In contrast, PAP activity was reduced by 26%. HMG-CoA reductase was not significantly affected, whereas cholesterol 7 alpha-hydroxylase activity was reduced by 36%. The results indicate that part of the TG-lowering effect of long-chain n-3 fatty acids may be mediated by inhibition of the soluble phosphatidate phosphohydrolase. The effect on serum cholesterol may be partly due to inhibition of HMG-CoA reductase.

Acyltransferases↗
PubMed1987

Medium chain triglycerides and structured lipids.

Lipids are an essential component of our body composition and necessary in our daily food intake. Conventional fats and oils are composed of glycerides of long chain fatty acids and are designated as long chain triglycerides (LCT). Body fat as well as the fats and oils in our daily intake fall into this category. In enteral and parenteral hyperalimentation, we can identify such LCT fats and oils. Soy, corn, safflower and sunflowerseed oils are typical of the LCT oils. In the search for alternative noncarbohydrate fuels, medium chain triglycerides (MCT) are unique and have established themselves in the areas of malabsorption syndrome cases and infant care and as a high energy, rapidly available fuel. Structure lipids with a MCT backbone and linoleic acid built into the triglyceride molecule have been developed to optimize the triglyceride structure that is best for patients, particularly the critically ill. Structured lipids with built-in essential fatty acid components or other polyunsaturated fatty acids promise greater flexibility in patient care and nitrogen support.

Animals↗
PubMed2003

The single nucleotide polymorphism -1131T>C in the apolipoprotein A5 (APOA5) gene is associated with elevated triglycerides in patients with hyperlipidemia.

The -1131T>C polymorphism in the newly identified apolipoprotein A5 (APOA5) gene has been associated with elevated plasma triglycerides. We determined its incidence in 915 patients attending a lipid outpatient clinic. The frequency of the C allele was significantly higher in patients with triglycerides above the 90th percentile and patients with type III hyperlipidemia compared to those with hypercholesterolemia. The C allele was associated with increased plasma triglycerides and decreased plasma HDL cholesterol, conditions associated with an increased risk of coronary heart disease. The effects on plasma lipids were only observed in overweight (BMI>25) patients and were greater in patients who were also carriers of a least one epsilon4 allele in the APOE gene. Thus additional genetic and/or metabolic factors are required in order for the triglyceride raising and HDL lowering effect of the -1131T>C polymorphism in APOA5 to be expressed.

Alleles↗
PubMed2006

Glucagon-like peptide 1 abolishes the postprandial rise in triglyceride concentrations and lowers levels of non-esterified fatty acids in humans.

AIMS/HYPOTHESIS: Diabetic dyslipidaemia contributes to the excess morbidity and mortality in patients with type 2 diabetes. Exogenous glucagon-like peptide 1 (GLP-1) lowers postprandial glycaemia predominantly by slowing gastric emptying. Therefore, the effects of GLP-1 on postprandial lipid levels and gastric emptying were assessed. METHODS: 14 healthy male volunteers were studied with an i.v. infusion of GLP-1 (1.2 pmol kg(-1) min(-1)) or placebo over 390 min in the fasting state. A solid test meal was served and gastric emptying was determined using a (13)C-labelled sodium octanoate breath test. Venous blood was drawn frequently for measurement of glucose, insulin, C-peptide, glucagon, GLP-1, triglycerides and NEFA. RESULTS: GLP-1 administration lowered fasting and postprandial glycaemia (p<0.0001). Gastric emptying was delayed by GLP-1 compared with placebo (p<0.0001). During GLP-1 administration, insulin secretory responses were higher in the fasting state but lower after meal ingestion. After meal ingestion, triglyceride plasma levels increased by 0.33+/-0.14 mmol/l in the placebo experiments (p<0.0001). In contrast, the postprandial increase in triglyceride levels was completely abolished by GLP-1 (change in triglycerides, -0.023+/-0.045 mmol/l; p<0.05). During GLP-1 infusion, plasma concentrations of NEFA were suppressed by 39% in the fasting state (p<0.01) and by 31+/-5% after meal ingestion (p<0.01). CONCLUSIONS/INTERPRETATION: GLP-1 improves postprandial lipidaemia, presumably as a result of delayed gastric emptying and insulin-mediated inhibition of lipolysis. Thus, by lowering both glucose and lipid concentrations, GLP-1 administration may reduce the cardiovascular risk in patients with type 2 diabetes.

Adult↗
PubMed1999

The role of microsomal triglyceride transfer protein and dietary cholesterol in chylomicron production in diabetes.

AIMS/HYPOTHESIS: The aim of this study was to examine factors involved in chylomicron production in the streptozotocin diabetic rat, our hypothesis being that the synthesis of the chylomicron is abnormal in diabetes. METHODS: Diabetic rats (n = 20) were paired with control rats (n = 20). Cholesterol emulsion was given by gavage and the lymph duct was cannulated. Lymph was collected for 4 h. Chylomicrons were prepared from the lymph by ultracentrifugation. Lymph apolipoprotein B48 was isolated by gradient gel electrophoresis and quantified by densitometric scanning. Intestinal microsomal triglycerol transfer protein mRNA was measured by solution hybridisation nuclease protection, using a rat specific [32P]-labelled cRNA probe. RESULTS: Serum triglyceride and cholesterol were greatly increased in diabetic compared with control animals (258 +/- 77 and 8.9 +/- 6.4 mg/ml vs 1.04 +/- 0.37 and 0.54 +/- 0.03 mg/ml, p < 0.0001). Lymph chylomicron triglyceride and cholesterol were also higher in diabetic rats (29.4 +/- 27.3 and 0.28 +/- 0.3 mg/h vs 16.8 +/- 10.6 and 0.18 +/- 0.09 mg/h, p < 0.05). Lymph chylomicron apo B48 was similar in the two groups. Intestinal microsomal triglycerol transfer protein mRNA was higher in the diabetic rats (12.6 +/- 3.2 vs 3.8 +/- 3.0 amol/microgram RNA, p < 0.0001) and there was a positive correlation between lymph triglyceride and microsomal triglycerol transfer protein mRNA in the whole group (r = 0.65, p < 0.01). CONCLUSION/INTERPRETATION: The study shows that microsomal triglycerol transfer protein mRNA is raised in diabetes without an increase in apolipoprotein B48 in the lymph suggesting that microsomal triglycerol transfer protein regulates chylomicron triglyceride content but not particle number.

Animals↗