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PubMed1979

Effect of dietary egg on human serum cholesterol and triglycerides.

One hundred sixteen male volunteers between the ages of 32 and 62 years (mean age 46) consumed two whole fresh eggs daily in their customary diets for 3 months and also eliminated eggs for 3 months before or after eating eggs. The men had had normal-range serum cholesterol and triglycerides for the past 7 years. Four-day food records kept by them in each experimental period were assessed for nutrient intake. A Latin square design allowed analyses for season and sequential effects on serum lipids. The serum cholesterol and triglyceride levels at the end of 6 months were compared with their initial levels on customary free choice diets as well as their levels after the first 3 months of study. No significant increase in mean serum cholesterol was found nor was there a significant association of dietary cholesterol intake with either serum cholesterol or triglyceride.

Adult↗
PubMed1980

Dietary fat-induced postprandial lipemia: effect on arterial oxygen saturation and plasma lactate, triglyceride, and cholesterol levels in subjects with angina pectoris.

The effects of dietary fat-induced lipemia on arterial oxygen tension and plasma lactate, cholesterol, and triglyceride levels were examined in 11 male subjects (average age 60) with a diagnosis of arteriosclerotic coronary vascular disease and angina pectoris. All subjects were alternately fed three isocaloric formula meals consisting of 100 g of cream fat, 100 g of saffola oil, and an isocaloric nonfat cornstarch control meal. Resting values of arterial blood gases and plasma lactate, triglyceride, and cholesterol were measured before (fasting) and at 3 and 5 hr postprandially. Both types of dietary fat produced significant postprandial decreases in plasma lactate, significant increases in plasma triglyceride and cholesterol levels, and no significant changes in arterial oxygen tension. The control meal had no effect upon any value except to transiently increase the plasma lactate. The role of postprandial lipemia in the atherosclerotic process is discussed and a hypothesis for the plasma cholesterol elevation due to dietary fats is presented.

Aged↗
PubMed1982

Carnitine metabolism in Macaca arctoides: the effects of dietary change and fasting on serum triglycerides, unesterified carnitine, esterified (acyl) carnitine, and beta-hydroxybutyrate.

Serum triglycerides and serum total, esterified, and free (unesterified) carnitine were measured in 21 male Macaca arctoides that were switched from a low fat (5.2% w/w), high carbohydrate diet to a high fat (15.9% w/w), low carbohydrate diet for 90 days and then returned to the original low fat diet for a subsequent 76-day period. Serum triglycerides and total carnitine levels fell significantly (p less than 0.05) during the initial 2 wk of feeding the high fat diet and the ratio of esterified/unesterified carnitine rose significantly (P less than 0.05) on the high fat diet. A return to the low fat diet reversed these changes; triglycerides rose significantly (p less than 0.05) within 3 days and the ratio of esterified/unesterified carnitine fell significantly (p less than 0.05) within 3 days and the ratio of esterified/unesterified carnitine fell significantly (p less than 0.05) during the same period. A return of total carnitine levels to those initially observed on the low fat diet was slower to develop. Fasting for 24 to 48 h resulted in increases of 65 to 75% in total serum carnitine. This increase reflected elevations of both the esterified and unesterified carnitine fractions but was largely attributable to increases in esterified carnitine which rose from 10 to 41 nmol/ml by 48 h while unesterified carnitine rose from 55 to 72 nmol/ml during the same period. In addition, the ratio of esterified/unesterified carnitine ratio rose from 0.183 +/- 0.023 to 0.583 +/- 0.069 (n = 8) with a 48-h fast and was significantly correlated with serum beta-hydroxybutyrate levels at both 24 and 48 h.

3-Hydroxybutyric Acid↗
PubMed1986

Effects of dietary polyenylphosphatidylcholine on metabolism of cholesterol and triglycerides in hypertriglyceridemic patients.

This study was carried out primarily to determine whether the feeding of lecithin (polyenylphosphatidylcholine) has systemic effects on metabolism of cholesterol and triglycerides in patients with endogenous hypertriglyceridemia (type 4 hyperlipoproteinemia). Ten patients were studied during control periods and lecithin feeding. In the former period, 7 g of safflower oil were added to the diet to balance the addition of 10 g of lecithin in the latter period. Lecithin feeding had no influence on levels of plasma cholesterol and triglycerides, or lipoprotein-cholesterol, transport of VLDL-triglycerides, or total steroid balance. However, lecithin feeding did significantly increase the molar percent of bile acids and decrease the molar percent lecithin in gallbladder bile suggesting that it has a systemic effect. In addition, it had a small but significant inhibitory effect on intestinal absorption of cholesterol.

Absorption↗
PubMed1986

Thermic effect of medium-chain and long-chain triglycerides in man.

The thermic effects of 400 kcal meals of medium-chain triglycerides (MCT) and long-chain triglycerides (LCT) were compared in seven healthy men. Metabolic rate was measured before the meals and for 6 h after the meals by indirect calorimetry. Mean postprandial oxygen consumption was 12% higher than basal oxygen consumption after the MCT meal but was only 4% higher than the basal oxygen consumption after the LCT meal. There was a 25-fold increase in plasma beta-hydroxybutyrate concentration and a slight increase in serum insulin concentration after MCT ingestion but not after LCT ingestion. Plasma triglyceride concentrations increased 68% after the LCT meal and did not change after the MCT meal. These data raise the possibility that long-term substitution of MCT for LCT would produce weight loss if energy intake remained constant.

3-Hydroxybutyric Acid↗
PubMed1987

Effects of soy polysaccharide on postprandial plasma glucose, insulin, glucagon, pancreatic polypeptide, somatostatin, and triglyceride in obese diabetic patients.

The effect of soy polysaccharide on postprandial plasma glucose levels was examined in a crossover experiment involving seven obese noninsulin dependent maturity-onset diabetic patients fed a standard meal without or with 10 g of this fiber source. Postprandial concentrations of plasma insulin, glucagon, pancreatic polypeptide, and somatostatin were measured to explore the mechanism of action. The effect on plasma triglyceride levels was also studied. Supplementation of soy polysaccharide significantly enhanced return of serum glucose levels towards fasting level during the latter half of the meal test. Addition of soy polysaccharide had no effect on plasma insulin levels but appeared (p greater than 0.05) to lessen postprandial increases in glucagon and pancreatic polypeptide levels while it raised somatostatin levels. Soy polysaccharide significantly reduced the rise of postprandial plasma triglyceride levels. The changes in plasma glucagon, pancreatic polypeptide, and somatostatin levels may have been instrumental in the observed postprandial glucose and triglyceride effects.

Adult↗
PubMed1989

Fructose-induced in vivo insulin resistance and elevated plasma triglyceride levels in rats.

Insulin action was assessed by using the hyperinsulinemic (approximately 800 pmol/L) euglycemic clamp in rats fed equal amounts of glucose or fructose (35% of calories) for 4 wk. The glucose infusion rate required to maintain euglycemia was decreased in fructose-fed animals (14.6 +/- 1.4 vs 21.8 +/- 1.1 for glucose-fed rats, p less than 0.001) with this whole-body effect contributed to equally by an impairment in hepatic insulin action and a reduction in peripheral glucose disposal in a range of tissues. There was no difference in basal glucose turnover, energy expenditure, or postprandial blood glucose and insulin responses to the diets. In the fructose-fed rats there was an increase in fasting triglyceride levels by 2 wk. Euglycemic clamp glucose disposal correlated positively and clamp hepatic glucose output correlated negatively with fasting triglyceride levels. In summary, fructose but not glucose feeding led to impaired insulin action in both the liver and peripheral tissues, effects that may depend on antecedent circulating triglyceride levels.

Animals↗
PubMed1991

Lack of effect of chronic administration of oral beta-carotene on serum cholesterol and triglyceride concentrations.

Previous studies suggest that chronic oral administration of retinol and other retinoids causes elevation of plasma triglyceride concentrations. The effects of chronic oral administration of beta-carotene, a carotenoid partially metabolized to retinol, on plasma lipid concentrations have not been well studied; therefore, we studied 61 subjects over 12 mo while they were enrolled in a skin-cancer-prevention study in which patients were randomly assigned to receive either placebo (n = 30) or 50 mg beta-carotene/d orally (n = 31). At study entry and 1 y later, fasting blood samples were obtained for measurement of triglycerides, total cholesterol, HDL cholesterol, retinol, and beta-carotene. Retinol concentrations changed minimally in both groups; beta-carotene concentration increased an average of 12.1 +/- 47 nmol/L in the placebo group and 4279 +/- 657 nmol/L in the active-treatment group. Both groups experienced similar small increases in triglyceride and total cholesterol concentrations and small decreases in HDL cholesterol. Daily oral administration of 50 mg beta-carotene/d did not affect plasma lipid concentrations.

Administration, Oral↗
PubMed1991

Experimental short-bowel syndrome: effect of an elemental diet supplemented with short-chain triglycerides.

To determine whether short-chain triglycerides (SCTs, 1:1 triacetin:tributyrin, wt:wt) enhance intestinal adaptation in short-bowel syndrome (SBS), male Sprague-Dawley rats underwent 60% distal small-bowel resection with cecectomy and received either a chemically defined diet (CD) or a CD containing 40% of nonprotein energy as either medium-chain triglycerides (MCTs) or SCTs. After 12 d the SCT group had significantly increased jejunal mucosal weight compared with the MCT and CD groups and had significantly increased segment weight and mucosal protein compared with the CD group. In the colon the SCT group had significantly increased segment and mucosal weights and mucosal protein and DNA compared with both the MCT and CD groups. Body-weight change and measurements of serum ketones, albumin, glucose, and triglycerides revealed no significant differences among groups. SCTs improved jejunal and colonic adaptive growth and maintained comparable nutritional status in SBS when compared with CD alone or CD with MCTs.

3-Hydroxybutyric Acid↗
PubMed1992

Fat elimination in acute renal failure: long-chain vs medium-chain triglycerides.

Elimination and hydrolysis of fat emulsions containing long-chain (LCT; Intralipid) or long- and medium-chain triglycerides (MCT; Lipofundin MCT) were compared in seven patients with acute renal failure (ARF) and six healthy control subjects. In control subjects, clearance of MCT was slightly higher than that of LCT (1.93 +/- 0.34 vs 1.55 +/- 0.3 mL.kg body wt-1.min-1, P less than 0.05). The rise in plasma triglycerides was similar and the release of free fatty acids was higher during MCT (P less than 0.02). In ARF, clearance of both LCT and MCT was equally reduced (0.53 +/- 0.12 vs 0.59 +/- 0.14 mL.kg body wt-1.min-1, P less than 0.01 vs control subjects). Again, the rise in triglycerides was comparable. Free fatty acid release was higher during MCT but lower than in control subjects. Plasma concentrations of glucose and lactate were not affected in control subjects but increased during both LCT and MCT in ARF. Thus elimination of both LCT and MCT is profoundly decreased in ARF. The impaired lipolysis in ARF cannot be circumvented by the use of MCT.

Acute Kidney Injury↗
PubMed1992

Plasma lipids and lipoproteins during 6 d of maintenance feeding with long-chain, medium-chain, and mixed-chain triglycerides.

This study assessed fasting plasma lipids and lipoproteins and postprandial plasma lipids in healthy male subjects fed liquid-formula diets containing 40% of total energy as long-chain (LCT, primarily C18:1 and C18:2), medium-chain (MCT, C8:0-C10:0), or mixed-chain (structured lipid, STL, mostly C8:0, C10:0, and C22:0) triglycerides for 6 d. None of the diets altered plasma cholesterol concentrations. HDL cholesterol was decreased 14% by the STL diet (P < 0.044) and 15% by the MCT diet (P < 0.004) but was unchanged by the LCT diet. Plasma triglycerides were elevated 42% by the MCT diet (P < 0.006), but were unaltered by either the STL or LCT diets. Neither the STL nor the MCT diets produced changes in fasting lipoprotein lipid composition; however, during the LCT diet, VLDLs became enriched in triglyceride and LDLs became enriched in cholesterol. Postprandial triglyceridemia was significantly greater after subjects consumed the LCT diet than it was after they consumed either the STL or MCT diets, which were similar. Short-term feeding of MCT and STL diets produces significant changes in lipid metabolism. An understanding of the long-term effects of these diets awaits further study.

Adult↗
PubMed1995

Fat elimination in chronic hepatic failure: long-chain vs medium-chain triglycerides.

Elimination and hydrolysis of fat emulsions containing long-chain (LCT) or long- and medium-chain triglycerides (MCT, 50:50) were compared in eight patients with advanced chronic hepatic failure (CHF) and six healthy control subjects by using a two-stage constant infusion protocol. In control subjects clearance of MCT was slightly higher than that of LCT (1.93 +/- 0.34 vs 1.55 +/- 0.3 mL.kg-1.min-1, P < 0.05). The rise in plasma triglycerides was similar and the release of free fatty acids was higher during MCT (P < 0.02). In CHF patients, clearance of both LCT and MCT was comparable with that in healthy subjects and the rise in plasma triglycerides and release of free fatty acids was identical. We conclude that a clinically relevant infusion rates the elimination of lipid emulsions containing LCT or LCT and MCT and the release of free fatty acids thereof is not altered in patients with CHF and that intravenous lipids are a suitable source of energy and essential fatty acids (and phospholipids) for parenteral nutrition.

Blood Glucose↗
PubMed1984

Fasting plasma glucose, uric acid, and triglycerides as predictors of the ratio of total cholesterol to HDL-C.

It was reported previously that a score composed of glucose, uric acid, and triglyceride was correlated closely with the total cholesterol:high density lipoprotein cholesterol (TC:HDL) ratio and could be used to predict those subjects for whom the more expensive HDL measurement would be useful. The authors tested this score using multiple regression and discriminant function analysis in a population sample of 209 men aged 40-79 years, Triglyceride was the only component of the score that contributed to the prediction or classification of the TC:HDL ratio. Although the correlations of the score with the TC:HDL ratio were relatively good (r = 0.72 or greater), the discriminant function analysis showed that subjects with high or low scores could have high or low TC:HDL ratios. The authors conclude that the score (essentially the triglyceride level) is inadequate to permit the classification of any individual as having a definite high or low TC:HDL ratio.

Adult↗
PubMed1991

Changes in blood pressure, plasma triglyceride and aldosterone concentration, and red cell cation concentration in patients with hyperinsulinemia.

Blood pressure, plasma concentration of triglyceride, aldosterone, renin activity (PRA), and atrial naturietic peptide (ANP), and red blood cell, urine, and plasma sodium and potassium concentration were determined in 24 healthy individuals divided into two groups defined as being either hyperinsulinemic or normoinsulinemic. The results demonstrated that the hyperinsulinemic group had significantly higher values for both systolic (P less than .01) and diastolic (P less than .05) blood pressure. In addition, plasma concentrations of triglyceride (P less than .02), aldosterone (P less than .05) and potassium (P less than .05) were higher in hyperinsulinemic individuals as compared to those who were normoinsulinemic. Furthermore, red cell potassium was lower (P less than .01) and red cell sodium higher (P less than .01) in the hyperinsulinemic group. Finally, the magnitude of hyperinsulinemia correlated directly with systolic (r = 0.50, P less than .01) and diastolic (r = 0.44, P less than .05) blood pressure, concentration of plasma triglyceride (r = 0.55, P less than .01) and aldosterone (r = 0.46, p less than .05), and erythrocyte sodium concentration (r = 0.57, p less than .01). In contrast, plasma insulin response was negatively correlated with erythrocyte potassium concentration (r = 0.40, P less than 0.05). These observations provide further support for the view that hyperinsulinemia, presumably secondary to resistance to insulin-stimulated glucose uptake, is associated with a cluster of variables that may play important roles in the etiology and clinical course of hypertension.

Aldosterone↗
PubMed1975

Structural analyses of triglycerides containing isotopically-labelled fatty acids.

The stereospecific analysis of triglycerides is a complex, multistep procedure and some losses inevitably occur at every stage. Such losses are particularly important when the triglycerides contain isotopically-labelled fatty acids incorporated by incubation in vitro with the relevant enzyme systems, but they can be compensated for by adding, prior to the analysis, a triglyceride containing only the same labelled odd-chain fatty acid in each position.

Carbon Radioisotopes↗
PubMed1993

Abetalipoproteinemia is caused by defects of the gene encoding the 97 kDa subunit of a microsomal triglyceride transfer protein.

Abetalipoproteinemia is an inherited disorder of lipoprotein metabolism. Affected individuals produce virtually no circulating apolipoprotein B-containing lipoproteins (chylomicrons, very low density lipoprotein, low density lipoprotein and lipoprotein (a)). Malabsorption of the antioxidant vitamin E occurs, leading to spinocerebellar and retinal degeneration. Biochemical and genetic studies show that abetalipoproteinemia is not a defect of lipid biosynthesis or of the apolipoprotein B gene. Instead a microsomal triglyceride transfer protein, which exists as a complex with protein disulphide isomerase in the endoplasmic reticulum, has been implicated. We have cloned and sequenced the human cDNA encoding microsomal triglyceride transfer protein. The predicted amino acid sequence shows extensive homology to vitellogenin, the precursor of the lipovitellin complex, which has been shown by X-ray crystallography to contain a large lipid storage cavity. Microsomal triglyceride transfer protein is expressed in ovary, testis and kidney, in addition to liver and small intestine. A homozygous mutation that disrupts splicing has been identified in affected siblings with classical abetalipoproteinemia. These results elucidate a key process in the packaging of apolipoprotein B with lipid, and should increase our understanding of the processes regulating the production of atherogenic lipoproteins.

Abetalipoproteinemia↗
PubMed1998

Characterization of lpd (lipid defect): a novel mutation on mouse chromosome 16 associated with a defect in triglyceride metabolism.

Recent epidemiological studies have identified plasma triglyceride as a risk factor for atherogenesis. We have generated a mouse transgenic line that carries a recessive mutation designated lpd (lipid defect). Homozygous lpd mice develop as runts and die by age 10-15 days with striking liver pathology characterized by the presence of numerous lipid-containing vacuoles and extensive accumulation of triglycerides. Cloning of the mutant insertion locus and the wild-type lpd locus have revealed a duplication of host genomic sequences at the site of integration. Mapping of the lpd locus with the Jackson Laboratory BSS interspecific backcross panel of (C57BL/6JEi x SPRET/Ei) F1 x SPRET/Ei placed the lpd locus to the distal part of chromosome 16. These observations suggest that the transgene disrupts a putative gene at the lpd locus and that lpd is a novel locus related to triglyceride metabolism. The lpd mutant mice may serve as models for human disorders of fatty livers or hypertriglyceridemia.

Animals↗
PubMed1998

Targeted disruption of the mouse lysosomal acid lipase gene: long-term survival with massive cholesteryl ester and triglyceride storage.

Lysosomal acid lipase (LAL) is essential for the hydrolysis of the triglycerides and cholesteryl esters in lysosomes. Its deficiency produces two phenotypes, a severe infantile-onset variant, Wolman disease (WD), and a later onset variant, cholesteryl ester storage disease (CESD). A mouse model with a LAL null mutation was produced by targeting disruption of the mouse gene. Homozygote knockout mice (lal -/lal-) produce no LAL mRNA, protein or enzyme activity. The lal-/lal- mice are born in Mendelian ratios, are normal appearing at birth, and follow normal development into adulthood. However, massive accumulation of triglycerides and cholesteryl esters occurs in several organs. By 21 days, the liver develops a yellow-orange color and is approximately 1.5-2.0x larger than normal. The accumulated cholesteryl esters and triglycerides are approximately 30-fold greater than normal. The lal+/lal- mice have approximately 50% of normal LAL activity and do not show lipid accumulation. Male and female lal-/lal- mice are fertile and can be bred to produce progeny. This mouse model is a phenotypic model of human CESD, and a biochemical and histopathologic mimic of human WD. The lal-/lal- mice provide a model to determine the role of LAL in lipid metabolism and the pathogenesis of its deficiency states.

Animals↗