Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “triglycerides”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,171 records · Page 65Linked to original sources

Metabolism of triglyceride-rich emulsions in rats with protein malnutrition.

Knowledge of chylomicron metabolism is very important in understanding and treating protein malnutrition, since these particles are the primary carriers of dietary fat in lymph and plasma. In the bloodstream, fat transported in chylomicrons is hydrolyzed by the action of lipoprotein lipase and the resulting fatty acids and glycerol are taken up by the body tissues. Chylomicron remnants are then rapidly removed by the liver. To clarify chylomicron metabolism in protein malnutrition, triglyceride-rich emulsions known to behave metabolically like lymph chylomicrons and labeled with 14C-cholesteryl ester and 3H-triglycerides were injected intraarterially into control rats and rats fed a protein-deficient diet for 40 days. Plasma kinetics and organ uptakes of the labeled lipids were determined. Hydrolysis of the emulsion triglycerides by lipoprotein lipase was not different in the malnourished rats (TG-FCR = 0.250 +/- 0.027 m-1 vs 0.250 +/- 0.070 m-1 in controls), but plasma clearance of the resulting triglyceride-depleted emulsion remnant particles was markedly lower compared to controls (cholesteryl-ester FCR = 0.088 +/- 0.009 and 0.146 +/- 0.019 m-1, respectively, p < 0.001). These results were obtained regardless of the amount of emulsion lipid that was injected. Liver atrophy seem to account for the delayed remnant uptake in protein-depleted rats. These data provide insight into the consequences of parenteral nutrition with lipid emulsions when administered in states of protein malnutrition.

Animals↗

Is apolipoprotein A5 a novel regulator of triglyceride-rich lipoproteins?

Hypertriglyceridemia is an independent risk factor for the development of cardiovascular disease and is often associated with diabetes, inflammation and the metabolic syndrome. Recently, apolipoprotein A5 (APOA5) was identified as a novel member of the APOA1/C3/A4 gene cluster. Data from mice over-expressing or lacking APOA5 provide direct evidence that this apolipoprotein plays a role in triglyceride metabolism. Moreover, plasma triglyceride levels were found to be strongly associated with APOA5 polymorphisms. The human APOA5 gene is regulated by transcription factors known to affect triglyceride metabolism such as PPARa, RORa, LXR and SREBP-1c and this supports its function. Insulin and interleukins regulate APOA5 gene expression and provide novel clues for the role of this apolipoprotein. To date, the triglyceride lowering action of apoA-V is attributed to the activation of lipoprotein lipase and an acceleration of very low density lipoprotein catabolism. Recent findings indicate that APOA5 could also influence cholesterol homeostasis and probably play a role in hypertriglyceridemia associated with diabetes and inflammation. This review aims to give a comprehensive summary of the current literature and supports the view that APOA5 plays a relevant role in lipid metabolism.

Animals↗

Metabolic effects in neonates receiving intravenous medium-chain triglycerides.

UNLABELLED: The effects of two lipid emulsions, one with 50% each of medium-chain and long-chain triglycerides, and a long-chain triglycerides lipid emulsion as a control, were evaluated for lipid and carnitine metabolism and respiratory quotient when given to neonates after major surgery during a short period of total parenteral nutrition. Each group included 10 neonates, and all tolerated the total parenteral nutrition well. The relative contents of linoleic acid and alpha-linolenic acid increased in all lipid esters in plasma and adipose tissue in both groups, indicating that the content of these fatty acids is sufficient even in the medium-chain triglycerides emulsion. The serum concentration of ketones was within normal limits. Free fatty acids in plasma did not increase in either group. The total plasma carnitine concentration decreased in both groups but the distribution of free carnitine and acylcarnitine did not change. The total muscle carnitine did not change significantly but the ratio of acylcarnitine to free carnitine tended to increase in muscle in the treatment group, probably an effect of the medium-chain triglyceride supplementation. CONCLUSIONS: The two groups displayed the same fatty acid pattern in plasma and adipose tissue and the same respiratory quotient during the treatment period. Regarding carnitine status, essentially the same changes were seen in the two groups. However, discrete changes were seen in muscle tissue in the treatment group.

Carnitine↗

Fasting levels of serum glucose, cholesterol and triglyceride at age eleven to twelve years in stunted and non-stunted Jamaican children.

AIM: To determine whether fasting serum concentrations of glucose, cholesterol and triglyceride at age 11-12 y (a) differed between children stunted in early childhood and those who were never stunted, (b) were related to birthweight or current anthropometry and (c) were related to stunting after controlling for current size. METHODS: Anthropometry, serum glucose and lipid concentrations were measured in 112 children stunted in early childhood and 181 non-stunted children. RESULTS: Children who were stunted in infancy remained shorter, weighed less and were significantly less fat than non-stunted children but had a more central distribution of fat. They were also less likely to have entered puberty. Non-stunted children had higher fasting serum triglyceride concentrations than stunted children (p < 0.05). There were no significant correlations between birthweight and fasting glucose or any measure of serum lipids. The percentage of variance in biochemical measures explained by anthropometry was low: between 2.1 for HDL cholesterol and 14.6 for triglyceride. Nutritional status in early childhood (stunted or non-stunted) made no additional contribution to the variance. CONCLUSIONS: Linear growth retardation in early childhood was not independently related to fasting serum concentrations of glucose, cholesterol and triglyceride at age 11-12 y. However, despite being thinner, stunted children had a more central distribution of fat.

Analysis of Variance↗

Triglyceride-rich lipoproteins prevent septic death in rats.

Triglyceride-rich lipoproteins bind and inactive bacterial endotoxin in vitro and prevent death when given before a lethal dose of endotoxin in animals. However, lipoproteins have not yet been demonstrated to improve survival in polymicrobial gram-negative sepsis. We therefore tested the ability of triglyceride-rich lipoproteins to prevent death after cecal ligation and puncture (CLP) in rats. Animals were given bolus infusions of either chylomicrons (1 g triglyceride/kg per 4 h) or an equal volume of saline for 28 h after CLP. Chylomicron infusions significantly improved survival (measured at 96 h) compared with saline controls (80 vs 27%, P < or = 0.03). Chylomicron infusions also reduced serum levels of endotoxin, measured 90 min (26 +/- 3 vs 136 +/- 51 pg/ml, mean +/- SEM, P < or = 0.03) and 6 h (121 +/- 54 vs 1,026 +/- 459 pg/ml, P < or = 0.05) after CLP. The reduction in serum endotoxin correlated with a reduction in serum tumor necrosis factor, measured 6 h after CLP (0 +/- 0 vs 58 +/- 24 pg/ml, P < or = 0.03), suggesting that chylomicrons improve survival in this model by limiting macrophage exposure to endotoxin and thereby reducing secretion of inflammatory cytokines. Infusions of a synthetic triglyceride-rich lipid emulsion (Intralipid; KabiVitrum, Inc., Alameda, CA) (1 g triglyceride/kg) also significantly improved survival compared with saline controls (71 vs 27%, P < or = 0.03). These data demonstrate that triglyceride-rich lipoproteins can protect animals from lethal polymicrobial gram-negative sepsis.

Animals↗

Effects of a progestogen and a sequential type oral contraceptive on plasma vitamin A, vitamin E, cholesterol and triglycerides.

Fasting blood samples were taken from 13 college students who had never been on oral contraceptives in two menstrual cycles. During the first cycle, the control cycle, each girl donated three blood samples; the first sample was given between days 1 and 5, the second sample between days 13 and 17, and the third sample between days 22 and 26 of the menstrual cycle. In the second menstrual cycle, the experimental cycle, nine girls were given Micronor, a progestogen type oral contraceptive and four girls were given Ortho-Novum SQ, a sequential type oral contraceptive. Four blood samples were obtained from each of the subjects: the first three samples were obtained in the three periods corresponding to those in the control cycle, and the fourth was taken 2 days after the subjects had stopped taking the oral contraceptive. Results showed that estrogen significantly raised plasma vitamin A and triglycerides. The progestogen, at low concentration, had little or no effect on these two lipid materials. At a higher concentration the progestogen enhanced the effect of the estrogen on plasma vitamin A and triglycerides. These effects were extended to at least 2 days after subjects had ceased taking the oral contraceptive. Plasma vitamin E levels in the subjects given Ortho-Novum SQ, were consistently but not statistically higher in the experimental cycle than in the control cycle. The correlation coefficient between vitamin E and triglycerides was statistically significant while those between the vitamin A and vitamin E and between vitamin A and triglycerides were not. Cholesterol was not affected by either Micronor or Ortho-Novum SQ.

Adult↗

Efficacy of diet and exercise in the reduction of serum cholesterol and triglyceride in free-living adult males.

Young males with levels of serum cholesterol or triglyceride in the upper quartile of the distribution for volunteers tested, participated in a program designed to determine the effect of diet and exercise on serum lipids. Dietary modifications involved caloric restriction superimposed on either the National Institutes of Health (NIH) recommendations for type II or IV hyperlipoproteinemia, as appropriate, or superimposed on a fat-controlled regimen in which fat of an unspecified nature was restricted to 30% of total calories. Participants with elevated levels of cholesterol responded significantly better when instructed in the diet meeting NIH criteria, 21% change in cholesterol, than when instructed in a diet controlled in fat, 11% change in cholesterol. For those with elevated levels of triglyceride, the NIH type IV diet was no more effective at the end of 6 months than the diet controlled in fat where caloric restriction was a part of both dietary regimens. The mean change in triglyceride for this group was 32%. Those with elevated levels of both cholesterol and triglyceride were less amenable to change than those with a single hyperlipidemia. For some diagnostic types, the results were suggestive of a beneficial effect of exercise in addition to diet in accelerating or maintaining reductions in serum lipids.

Adult↗

Effect of oral alanine loads on the serum triglycerides of oral contraceptive users and normal subjects.

The effect of orally administered L-alanine loads on serum triglycerides, and plasma insulin and glucose, was studied in 23 women using an estrogen-containing oral contraceptive and 13 healthy female controls. Oral contraceptive users had significantly higher fasting serum triglycerides than the controls. Serum triglycerides concentrations udnerwent little changes in the controls after alanine ingestion, whereas the oral contraceptive users showed increases which were maintained throughout the 3-hr sampling period. The two groups had similar elevations in plasma insulin after alanine loading; the glucose concentrations were unchanged. The changes in serum triglycerides may have resulted from increased metabolism of alanine to pyruvate, and its incorporation into lipids under the stimulus of elevated insulin levels.

Adult↗

Effect of high carbohydrate feeding with dextrose or sucrose on adipose tissue lipoprotein lipase activity and plasma triglyceride levels in hemodialysis patients.

The acute effect of feeding high concentration carbohydrate meals containing equicaloric amounts of dextrose or sucrose on the activity of adipose tissue lipoprotein lipase and the concentration of plasma triglyceride was assessed in 11 hemodialysis patients. Dextrose feeding resulted in higher postprandial glucose levels and a greater insulin response than sucrose. The relationship between the postprandial change in the activity of adipose tissue lipoprotein lipase and the insulin response to feeding almost reached statistical significant (rs = 0.40, P = 0.08, n = 20), and the increase in the activity of the enzyme after dextrose feeding was greater than after sucrose (P less than 0.01). There was a significant decrease in plasma triglyceride levels after dextrose feeding (P less than 0.01), but no change was observed after the ingestion of sucrose. These results indicate that the inability of the administered sucrose to raise the plasma insulin concentration to the same level as isocaloric amounts of dextrose probably accounts for the smaller increase in the activity of adipose tissue lipoprotein lipase after sucrose. The failure of plasma triglyceride levels to fall after sucrose feeding suggests that the extent to which the activity of adipose tissue lipoprotein lipase increases postprandially may be important in the regulation of triglyceride metabolism in hemodialysis patients.

Adipose Tissue↗

Triglyceride integrated concentrations: effect of variation of source and amount of dietary carbohydrate.

The effect of changes in the amount of dietary carbohydrate (45 or 65% of total energy) and in the source of carbohydrate (sucrose or corn syrup) on plasma triglyceride and cholesterol concentrations was studied in eight healthy males. Subjects ingested each of the four formula diets for 10 days in a latin square sequence. Diet-induced response was assessed by measurement of plasma lipid concentrations in blood obtained after overnight fast and by measurement of the mean plasma lipid concentrations--designated the integrated concentration--of blood obtained by 24 hr continuous blood withdrawal. The fasting plasma triglyceride concentration increased significantly during ingestion of the high carbohydrate diet (P less than 0.005) but was not significantly influenced by the source of carbohydrate calories. The 45% carbohydrate diets induced larger meal associated plasma triglyceride variation than 65% diets. Sucrose-containing diets induced significantly higher plasma triglyceride integrated concentrations than corn syrup diets, whether provided as 45% (P less than 0.05) or 65% (P less than 0.005) of total energy. Diet-induced changes in fasting or integrated plasma cholesterol concentration were minimal.

Adult↗

Serum triglyceride responses to fatty meals: effects of meal fat content.

To determine the dose response of serum triglyceride concentrations to fat feeding, serum triglyceride responses to meals containing 40, 80, and 120 g fat (in the form of dairy cream) were measured in 12 normotriglyceridemic men. Mean postprandial lipemia (measured as the integrated area under the curve of serum triglyceride concentration plotted against time) was 251 +/- 129 mg.dL-1.8 h-1 (2.83 +/- 1.46 mmol.L-1.8 h-1) after the 40-g-fat meal, 503 +/- 233 mg.dL-18 h-1 (5.68 +/- 2.63 mmol.L-1.8 h-1) after the 80-g-fat meal, and 712 +/- 281 mg.dL-1.8 h-1 (8.04 +/- 3.17 mmol.L-1.8 h-1) after the 120-g-fat meal. These data indicate that in normotriglyceridemic men the magnitude of lipemia that follows the ingestion of a fat meal is directly proportional to the fat content of the meal. The results also suggest that the mechanism whereby triglyceride is removed from the intravascular compartment is not saturated by meals containing the amounts of fat typically consumed by men following a Western diet.

Adult↗

Intestinal beta-carotene absorption and cleavage in men: response of beta-carotene and retinyl esters in the triglyceride-rich lipoprotein fraction after a single oral dose of beta-carotene.

Postprandial response curves of beta-carotene and retinyl esters in a triglyceride-rich lipoprotein (TRL) fraction were evaluated as a potential measure of beta-carotene uptake and cleavage. beta-Carotene, retinyl ester, and triglyceride concentrations in the TRL fraction (density < 1.006 kg/L) and plasma were measured in 10 men for 8 or 16 h after an oral dose of 15 mg beta-carotene. The beta-carotene response, unlike the triglyceride and retinyl ester response, can be evaluated in the TRL fraction but not in plasma. Intraindividual variations in the triglyceride-adjusted response of beta-carotene and retinyl palmitate in TRL fractions were 23% and 20% and interindividual variations were 42% and 36%, respectively. A low beta-carotene response was associated with a high ratio between retinyl palmitate and beta-carotene responses (r = -0.56, P = 0.013). In conclusion, the measurement of beta-carotene and retinyl esters in the TRL fraction after a dose of beta-carotene with a vitamin A-free meal may be an appropriate method to study beta-carotene uptake and cleavage.

Administration, Oral↗

Serum triglyceride: a possible risk factor for ruptured abdominal aortic aneurysm.

BACKGROUND: We aimed to determine the relationship between ruptured abdominal aortic aneurysm (AAA) and serum concentrations of lipids and apolipoproteins. METHODS: A cohort of 21 520 men, aged 35-64 years, was recruited from men attending the British United Provident Association (BUPA) clinic in London for a routine medical examination in 1975-1982. Smoking habits, weight, height and blood pressure were recorded at entry. Lipids and apolipoproteins were measured in stored serum samples from the 30 men who subsequently died of ruptured AAA and 150 matched controls. RESULTS: Triglyceride was strongly related to risk of ruptured AAA. In univariate analyses the risk in men on the 90th centile of the distribution relative to the risk in men on the 10th (RO10-90) was 12 (95% confidence interval [CI] : 3.8-37) for triglyceride, 5.5 (95% CI: 1.8-17) for apolipoprotein B (apoB) (the protein component of low density lipoprotein [LDL]), 0.15 (95% CI : 0.04-0.56) for apo A1 (the protein component of high density lipoprotein [HDL]), 3.7 (95% CI: 1.4-9.4) for body mass index and 3.0 (95% CI: 1.1-8.5) for systolic blood pressure. Lipoprotein (a) (Lp(a)) was not a significant risk factor (RO10-90 = 1.6, 95% CI: 0.6-3.0). In multivariate analysis triglyceride retained its strong association. CONCLUSION: Triglyceride appears to be a strong risk factor for ruptured AAA, although further studies are required to clarify this. If this and other associations are cause and effect, then changing the distribution of risk factors in the population (by many people stopping smoking and adopting a lower saturated fat diet and by lowering blood pressure) could achieve an important reduction in mortality from ruptured AAA.

Adult↗

Effects of diets of homogeneous saturated triglycerides on cholesterol balance in rats.

The effects of a diet of 10% homogeneous triglycerides of 12 to 18-carbon chain saturated fatty acids on cholesterol absorption and turnover were studied in rats. Cholesterol absorption was successively significantly less in rats fed tristearin than in groups fed tripalmitin, trimyristin and trilaurin. Lesser fatty acid absorption may explain the differences in part, since cholesterol absorption was significantly correlated with fat absorption. Cholesterol removal from plasma was fastest in rats fed tristearin. Plasma cholesterol levels were increased with the trilaurin diet although the rate of cholesterol accumulation in lymph after gavage was slower with trilaurin. Lymph triglycerides were highest with trilaurin and trimyristin diets perhaps indicating endogenous mobilization of triglyceride for lipoprotein formation. Lymph triglycerides were, however, decreased with tristearin. Sterol turnover (production, absorption plus synthesis) was increased with tristearin or trilaurin by kinetic or balance methods.

Animals↗

Response of normal and diabetic rats to increasing dietary medium-chain triglyceride content.

Replacing dietary long-chain triglycerides (LCT) with medium-chain triglycerides (MCT) has not previously been shown to produce reliable changes in caloric intake. However, diabetic rats are particularly sensitive to changes in the fat content of their diet, and thus were used for comparison to normal rats in the studies reported below. Rats were fed synthetic diets that contained either corn oil or MCT. Food intake and plasma metabolic fuels were measured as the fat content of the diet was increased from 5 to 15 to 25%. Both normal and diabetic MCT-fed rats adjusted their caloric intake more quickly than LCT-fed rats as the fat content of the diet was increased. The relative preference of MCT- and LCT-fed rats for high and low concentrations of dietary fat was assessed. It was found that both normal and diabetic LCT-fed rats preferred high dietary fat, whereas MCT-fed rats did not. In normal rats, plasma triglycerides and glycerol were decreased and plasma ketones increased by MCT feeding. In diabetic rats, the only effect of MCT feeding was to decrease plasma glycerol and triglycerides. The relative importance of hedonic and metabolic feedback to the rapid caloric regulation of MCT-fed rats is discussed.

Animals↗

Hepatic fatty acid synthesis and triglyceride secretion in rats fed fructose- or glucose-based diets containing corn oil, tallow or marine oil.

The effects of three dietary fats, corn oil (CO), tallow (T) and marine oil (MO), on serum triglycerides, hepatic lipogenic enzyme activity and lipogenesis in vivo using 3H2O were measured in fed and fasted rats that had been consuming diets in which the carbohydrate was either glucose or fructose. Hepatic triglyceride secretion was also measured in fasted rats fed the same diets. In both the fed and fasted state, hepatic enzyme activity and lipogenesis in vivo were greater in fructose-fed rats than in glucose-fed rats and less in both CO- and MO-fed rats than in T-fed rats. In rats fed glucose, serum triglycerides were lower in fasted rats fed MO than in fasted rats fed CO. In rats fed glucose or fructose, hepatic triglyceride secretion was lower in rats fed MO than in those fed CO or T.

Adipose Tissue↗

Long-chain fatty acid composition of maternal liver lipids during pregnancy and lactation in the rat: comparison of triglyceride to phospholipid.

The change in long-chain fatty acid composition in maternal liver was studied during pregnancy and lactation in the rat. Maternal liver triglycerides and phospholipids transiently accumulated and were depleted of long-chain fatty acids during pregnancy and lactation. During pregnancy, maternal liver accumulated triglyceride, but triglyceride fatty acid composition changed little. However, maternal liver total phospholipid fatty acid composition changed significantly without a change in the total pool size throughout pregnancy or lactation. The change in composition of (n-3) and (n-6) essential fatty acids in maternal liver triglyceride and total phospholipid occurred in an apparently dyssynchronous manner throughout pregnancy and lactation.

Animals↗

Effect of various triglycerides on plasma cholecystokinin levels in rats.

In the rat model, polyunsaturated vegetable oil has been shown to stimulate pancreatic secretion and promote pancreatic carcinogenesis, whereas dietary fish oil has been found to protect against carcinogenesis. Because cholecystokinin (CCK), a hormonal polypeptide secreted from the upper small intestine after food stimulation, is the most important known humoral stimulus of pancreatic secretion and also because this gut hormone has been shown to promote pancreatic carcinogenesis in the rat, we decided to study the effects of various triglycerides on CCK secretion in this species. Small amounts (2.5 mL) of corn oil, beef tallow, fish oil, medium-chain triglyceride (MCT) oil or saline (control) were administered to groups of five fasted rats. Plasma CCK levels were measured using a specific and sensitive radioimmunoassay. The maximal CCK increments for corn oil, beef tallow, fish oil and MCT oil were 3.0 +/- 0.5, 2.1 +/- 0.6 and 7.2 +/- 0.4 pmol/L, respectively. All the increments were significantly greater (p less than 0.05) than the change found after saline administration (-0.8 +/- 0.3 pmol/L). In another experiment, plasma CCK levels after intragastric administration of MCT oil reached a peak increment of 6.4 +/- 0.4 pmol/L after 240 min and continued to be significantly increased for the entire 480-min study period. It was concluded that all four triglycerides caused a significant CCK release in the rat and that the MCT oil was the most powerful stimulator of CCK secretion among the triglycerides studied.

Analysis of Variance↗