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PubMed2000

Limited feeding of potassium nitrate for intracellular lipid and triglyceride accumulation of Nannochloris sp. UTEX LB1999.

Limited feeding of nitrate during culture of Nannochloris sp. UTEX LB1999 for intracellular lipid and triglyceride accumulation was investigated with the aim of obtaining cells superior for liquefaction into a fuel oil. The intracellular lipid contents and the percentage of triglycerides in the lipids of cells grown in a nitrogen-limited medium (0.9 mM KNO3) were 1.3 times as high as those grown in a modified NORO medium containing 2.0-9.9 mM KNO3. However, the cell concentration was too low for the practical production of fuel oil by high-pressure liquefaction of the cell mass. A single feeding of 0.9 mM nitrate after nitrate depletion during cultivation in a nitrate-limited medium increased the cell concentration to twice that obtained without such feeding, and the lipid content was maintained at a high level. The timing of nitrate feeding, i.e., whether it was given during the log phase (before nitrate depletion), the constant growth phase (just after the depletion), or the stationary phase (after the depletion), had negligible effect on the intracellular lipid content and percentage of triglycerides in the lipids. When 0.9 mM nitrate was intermittently fed ten times during the log phase in addition to the initial nitrate feed (0.9 mM), the cell concentration reached almost the same (2.16 g/l) and the intracellular lipid content and the percentage of triglycerides in the lipids increased from 31.0 to 50.9% and 26.0 to 47.6%, respectively, compared with those of cells cultured in a modified NORO medium containing 9.9 mM KNO3 without additional nitrate feeding.

Chlorophyta↗
PubMed2007

Improvements of hypertriglyceridemia and hyperlacticemia in Japanese children with glycogen storage disease type Ia by medium-chain triglyceride milk.

BACKGROUND: Besides profound hypoglycemia with hyperlacticemia, glycogen storage disease type Ia (GSD Ia) presents hypertriglyceridemia that is often resistant to dietary treatment with cornstarch. The present study aimed to evaluate the effects of medium-chain triglycerides (MCT)--which are absorbed via the portal vein without being incorporated into chylomicrons--on hypertriglyceridemia and to explore otherwise metabolic changes in children with GSD Ia. PATIENTS AND METHODS: A 13-year-old boy with GSD Ia who received a dietary treatment with MCT milk after cornstarch administration and two infants also with GSD Ia, ages 6 and 7 months, who received MCT milk after carbohydrate-rich, lipid-poor milk were enrolled. In addition to serum glucose and lactate levels, serum levels of total cholesterol, triglycerides, and high-density lipoprotein (HDL) cholesterol were serially determined. Simultaneously, serum levels of total carnitine, free carnitine, acylcarnitine, and ketone bodies were determined to evaluate fatty acid beta-oxidation. RESULTS: Mean glucose level (mmol/l) of patient 1 remained stable, the value being around 4.5, while those of patients 2 and 3 increased to this level from 4.00 and 3.72, respectively. Lactate levels were significantly decreased in all patients. Mean triglyceride levels (mM) of patient 1 decreased from 3.00 to 2.05. Also, triglyceride levels of patients 2 and 3 decreased from 2.74 and 3.15 to 2.13 and 2.70, respectively. HDL cholesterol, acylcarnitine, and ketone body levels increased in all patients after MCT administration, while total and free carnitine levels decreased. CONCLUSION: We describe here the beneficial effects on lipid and carbohydrate metabolisms in three Japanese children with GSD Ia. In light of the unfavorable influence of lipid restriction on growth and development in infancy, dietary treatment with MCT milk may be a better treatment for infants with GSD Ia. Further investigation should be required to confirm the efficacy of MCT milk in GSD Ia.

Adolescent↗
PubMed2006

Genome-wide linkage scans for loci affecting total cholesterol, HDL-C, and triglycerides: the Family Blood Pressure Program.

Atherosclerosis accounts for 75% of all deaths from cardiovascular disease and includes coronary heart disease (CHD), stroke, and other diseases of the arteries. More than half of all CHD is attributable to abnormalities in levels and metabolism of lipids. To locate genes that affect total cholesterol, high density lipoprotein cholesterol (HDL-C), and triglycerides, genome-wide linkage scans for quantitative trait loci were performed using variance components methods as implemented in SOLAR on a large diverse sample recruited as part of the Family Blood Pressure Program. Phenotype and genetic marker data were available for 9,299 subjects in 2,953 families for total cholesterol, 8,668 subjects in 2,736 families for HDL, and 7,760 subjects in 2,499 families for triglycerides. Mean lipid levels were adjusted for the effects of sex, age, age2, age-by-sex interaction, body mass index, smoking status, and field center. HDL-C and triglycerides were further adjusted for average total alcoholic drinks per week and estrogen use. Significant linkage was found for total cholesterol on chromosome 2 (LOD=3.1 at 43 cM) in Hispanics and for HDL-C on chromosome 3 (LOD=3.0 at 182 cM) and 12 (LOD=3.5 at 124 cM) in Asians. In addition, there were 13 regions that showed suggestive linkage (LOD >or= 2.0); 7 for total cholesterol, 4 for HDL, and 2 for triglycerides. The identification of these loci affecting lipid phenotypes and the apparent congruence with previous linkage results provides increased support that these regions contain genes influencing lipid levels.

Adult↗
PubMed2001

Physical activity modulates the combined effect of a common variant of the lipoprotein lipase gene and smoking on serum triglyceride levels and high-density lipoprotein cholesterol in men.

Physical activity has been identified as a protective factor against the occurrence and progression of coronary heart disease. The lipoprotein lipase (LPL) HindIII polymorphism has been associated with changes in triglyceride and high density lipoprotein (HDL)-cholesterol levels. We have investigated whether the association between the LPL HindIII genetic polymorphism and lipid levels is modified by physical activity. We have also tested the hypothesis that physical activity may interact with smoking and the LPL HindIII polymorphism to determine an individual's plasma lipid concentrations. A total of 520 men were selected from a representative sample used in a population study conducted in Gerona, Spain. The median value (291 kcal/day) of energy expenditure in leisure-time physical activity of the studied sample was selected as a cut-off to define sedentary or active subjects. Serum HDL-cholesterol was positively and significantly associated with the amount of daily energy expenditure in physical activity, whereas inverse associations were seen between physical activity and triglyceride concentration and with the triglyceride to HDL-cholesterol ratio. These effects were consistent across LPL HindIII genotypes. There was a statistically significant interaction between LPL genotype and smoking on lipid concentrations. No statistically significant differences were observed in lipid levels of active or sedentary non-smokers between H- carriers and H+H+ homozygotes for the LPL HindIII polymorphism. In smokers, sedentary H+H+ homozygotes showed significantly higher triglyceride and lower HDL-cholesterol concentrations than sedentary H- carriers. These differences were smaller and not statistically significant when lipid values of active H+H+ homozygotes were compared with active H- carriers. Among all subgroups, sedentary smokers with the H+H+ genotype had the most adverse lipid profile, which was considerably less adverse in H+H+ smokers who were physically active. These findings suggest that the presence of the H+H+ genotype has a deleterious effect on lipid profile in an adverse environment such as smoking, and that the expenditure of more than 291 kcal/day in physical activity attenuates this effect.

Cholesterol, HDL↗
PubMed2002

Triglyceride, cholesterol and weight changes among risperidone-treated youths. A retrospective study.

The purpose of this retrospective chart review was to assess triglyceride, cholesterol and weight changes among risperidone-treated youths. The charts of 22 child and adolescent inpatients were abstracted. The sample's mean (+/- SD) age was 12.8 (+/- 2.6) years, daily risperidone dose 2.7 (+/- 2.2) mg, and average length of exposure 4.9 (+/- 1.0) months. Repeated measures analysis of variance revealed statistically and clinically significant weight gain averaging 7.0 (+/- 4.7) kg (95% confidence interval [CI] for the mean = 4.9,9.1; F = 49.421, df = 1,21, p < 0.001). No significant changes in serum triglyceride or cholesterol levels were seen in the group as a whole. Triglyceride levels and weight were strongly correlated with each other: almost 25% of the variance in triglyceride level changes could be explained by weight gain alone (R2 = 0.22, F = 5.526, p = 0.029), although such association weakened when excluding subjects (N=5) concurrently treated with lithium or divalproex (R2 = 0.06, p > 0.05). On the basis of this preliminary report it seems prudent to be clinically vigilant and conservative, recommending regular laboratory monitoring until a clearer picture emerges regarding lipid dysregulation associated with risperidone and other atypical antipsychotic use in children and adolescents.

Adolescent↗
PubMed2005

Prospective study of the association of serum triglyceride and glucose with colorectal cancer.

To determine if serum triglyceride and glucose levels are associated with colorectal cancer, a prospective study among 7619 Japanese-American men was conducted. From 1968 to 1998, 376 colon and 124 rectal cancer incident cases were diagnosed. A strong positive association of alcohol intake and pack-years of cigarette smoking with colorectal cancer was observed. Body mass index and heart rate were also positively related to colon, but not to rectal cancer. In contrast, serum triglyceride did not predict the development of either colon or rectal cancer. There was a modest association of serum glucose in the highest quartile group with rectal cancer (relative risk = 1.33; 95% confidence interval, 0.79-2.26), but it was not statistically significant. This study did not find a strong positive association of serum triglyceride or glucose with colorectal cancer, but additional studies including other metabolic consequences associated with increased serum triglyceride and glucose may clarify the relationship.

Adult↗
PubMed2006

Effect of monensin on serum lipoproteins, triglycerides, cholesterol and total lipids of periparturient dairy cows.

Serum concentrations of very low-density lipoproteins (VLDL), low-density lipoproteins (LDL), high-density lipoproteins (HDL), triglycerides, cholesterol, and total lipids of a group of monensin-treated cows (n = 7) were compared with those of a control group (n = 6) from about 10 days before calving to 45 days postpartum. Monensin was fed in the diet from about 20 days before predicted calving date to 45 days after parturition. Blood samples were obtained on days 20 and 10 before predicted calving, and on days 4, 15, 25 (phase I), and days 35 and 45 (phase II) post calving. Cholesterol (p = 0.046) and total lipids (p = 0.003) were lower in the treatment group 10 days before calving. Concentrations of serum triglycerides and VLDL (p = 0.017), and that of LDL (p = 0.032) were significantly higher in the treatment group in phase I postpartum. No significant difference was detected between groups during phase II. Comparison of the entire length of the trial showed higher concentrations of triglycerides and VLDL in the treatment group (p = 0.009). It is concluded that monensin is effective in increasing secretion of triglyceride-rich lipoproteins from the liver during the postpartum transition period of dairy cows. This may be effective in reducing the intensity of hepatic lipidosis and the incidence of periparturient diseases resulting from disturbances in energy metabolism.

Animals↗
PubMed1997

Structure analysis of an allene-containing estolide tetraester triglyceride in the seed oil of Sebastiana commersoniana (Euphorbiaceae).

The seed oil of Sebastiana commersoniana (Euphorbiaceae) was separated into triglyceride and an estolide fraction by preparative thin-layer chromatography. The triglyceride band was characterized by spectroscopic methods, and its fatty acids have been analyzed by gas chromatography (GC) and GC-mass spectrometry (MS) as their methyl esters. Linolenic acid was the main fatty acid (65%). The estolide band was examined by a combination of spectroscopic and chromatographic methods (ultraviolet, infrared, nuclear magnetic resonance, fast atom bombardment-MS, GC-MS of the fatty acids before and after silylation) and was identified as a tetraglyceride, where one alpha-carbon of the triglyceride backbone was esterfied with 8-hydroxy-5,6-octadienoic acid, which itself was esterfied with trans-2,cis-4-decadienoic acid. The remaining positions of the triglyceride backbone were occupied by common fatty acids.

Alkadienes↗
PubMed2002

Skeletal muscle triglyceride: marker or mediator of obesity-induced insulin resistance in type 2 diabetes mellitus?

The inability of insulin to stimulate glucose metabolism in skeletal muscle is a classic characteristic of type 2 diabetes, but this insulin resistance entails altered patterns of lipid metabolism as well. An association between intracellular triglyceride and insulin resistance has been well established in both human and animal studies of obesity-related insulin resistance and type 2 diabetes. Skeletal muscle's ability to select substrate for fuel metabolism, a metabolic flexibility, is also lost in insulin resistance, and defects in fatty acid metabolism during fasting or postabsorptive conditions likely play an important role in lipid oversupply to insulin-resistant muscle. These impairments appear to be at least indirectly centered on the ability of mitochondria to oxidize fatty acids, possibly through mediation of lipid metabolite levels such as ceramide or diacylglycerol, which are known to directly attenuate insulin signaling. Moreover, periodic use of muscle triglyceride by exercise may mediate the association between muscle triglyceride and insulin resistance. Thus, it appears that skeletal muscle triglyceride is perhaps a surrogate for other lipid species having a more direct effect on insulin action. Defining mechanisms by which dysregulation of fatty acid metabolism and persistent lipid oversupply alter insulin action may help to target more effective strategies to prevent or treat type 2 diabetes.

Biomarkers↗
PubMed1990

Interrelationship of triglycerides with lipoproteins and high-density lipoproteins.

Triglycerides are transported by the largest and most lipid-rich of the lipoprotein particles, namely, chylomicrons and very low density lipoproteins (VLDL). These particles are buoyant because of the high triglyceride content, which makes up approximately 90% by weight of the chylomicron and 70% by weight of the VLDL. The chylomicron transports exogenous or dietary fat and cholesterol, whereas VLDL transports endogenous triglyceride and cholesterol in lipoproteins synthesized and secreted by the liver. Both chylomicrons and VLDL are hydrolyzed at the capillary surface by the enzyme lipoprotein lipase. Lipoprotein lipase catalyzes the hydrolysis of triglyceride in the lipid core of these particles, producing smaller particles known as remnants. We currently believe the remnants are atherogenic and that this is one reason why hypertriglyceridemia may predispose to coronary artery disease. Chylomicron remnants are recognized and removed by hepatic receptors that contain apolipoprotein (apo) E. The rate of clearance of remnant particles depends on which subfraction of apo E is present. Particles containing apo EII are removed more slowly than those with apo EIII and EIV. The dietary cholesterol from the chylomicron remnant particles is thought to down-regulate the hepatic low-density lipoprotein (LDL) receptors. VLDL remnants, also called intermediate-density lipoprotein (IDL), contain apo E and may be removed by the liver through the LDL or B/E receptor. The decrease in activity of these receptors results in apparent oversynthesis of LDL, the end-product of VLDL and IDL metabolism. LDL is the major cholesterol carrier, followed by high-density lipoprotein (HDL).(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1994

Effects of heparin and cardiac catheterization on serum lipoprotein and triglyceride levels.

This study determined whether heparin administration and procedures involving heparin significantly affect lipid measurement. Serum lipid and lipoprotein analyses (total cholesterol, triglycerides, high-density lipoprotein [HDL] cholesterol, low-density lipoprotein [LDL] cholesterol, apolipoprotein B, and apolipoprotein A-I) were performed at baseline and at several time points after (1) intravenous heparin or placebo in 6 healthy volunteers (group 1), (2) cardiac catheterization with heparin in 26 patients (group 2), and (3) peripheral angiography without heparin in 11 patients (group 3). In group 1, after heparinization, triglycerides decreased 50 +/- 12 mg/dl (-57%, p < 0.001 vs baseline and placebo) at 60 minutes. No changes were observed in other lipid or lipoprotein fractions. After cardiac catheterization (group 2), however, decreases were observed not only in triglycerides (58 +/- 26 mg/dl [-40%]), but also in total cholesterol (28 +/- 12 mg/dl [-14%]), LDL cholesterol (19 +/- 22 mg/dl [-15%]), apolipoprotein B (13 +/- 9 mg/dl [-14%]), and apolipoprotein A-I (21 +/- 14 mg/dl [-17%]) (p < 0.001 vs baseline for all), and HDL cholesterol (4 +/- 7 mg/dl [-3%], p = 0.07). With the exception of triglycerides, these values remained significantly decreased for > or = 24 hours. The change in HDL was variable: Whereas most patients had a decrease (n = 24), 2 patients had a dramatic increase (> 100%) after administration of heparin. Similar decreases in total cholesterol, LDL cholesterol, and apolipoproteins B and A-I were observed in group 3 undergoing peripheral angiography without heparin.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins↗
PubMed1992

The Diabetes in Early Pregnancy Study: changes in cholesterol, triglycerides, body weight, and blood pressure. The National Institute of Child Health and Human Development--the Diabetes in Early Pregnancy Study.

This study examined changes in cholesterol, triglycerides, body weight, and blood pressure during pregnancy in 312 diabetic and 356 control women recruited within 21 days after conception. Cholesterol values rose in both groups but were significantly lower in diabetic women at each time point (166 vs 178 mg/dl at week 12, p = 0.0004). Triglyceride values also rose in both groups. Triglyceride levels did not differ between groups up to week 8 of gestation, but by weeks 10 to 12 they were significantly lower in diabetic women than in controls (75 vs 89 mg/dl at week 12, p = 0.0004). Although they were no heavier at entry, diabetic women gained significantly more weight between weeks 6 and 8 (p less than 0.001), resulting in a mean difference between groups of 1 kg. Systolic blood pressure increased steadily and significantly in the diabetic but not the control women (115.8 +/- 16.2 SD vs 109.3 +/- 11.8 mm Hg, p = 0.0006 at term). Diastolic blood pressure was higher in diabetic women on entry (70.7 vs 67.3 mm Hg, p = 0.0006) and throughout gestation. Significant correlations were found in the diabetic group between maternal blood pressure and lipids and infant birth weight. These newly found differences in cholesterol and triglyceride levels, weight gain, and blood pressure between type I diabetic and control women during gestation may have long-term cardiovascular implications.

Adult↗
PubMed1978

Cholesteryl ester and triglyceride hydrolysis by an acid lipase from rabbit aorta.

The properties of the triglyceride- and cholesteryl ester-hydrolyzing activity by an acid lipase from rabbit aortic tissue were compared under different experimental conditions. Radiolabeled cholesteryl oleate or triolein was incorporated into phospholipid vesicles by sonication and the resulting preparations were used for in vitro studies. No distinction was observed between triglyceride lipase and cholesterol esterase activity in the aortic cytosol fraction following either thermal inactivation, inhibition by a mercurial, fractionation by ammonium sulfate or acid precipitation, or DEAE-cellulose chromatography. Addition of rabbit lipoproteins to the assay system resulted in inhibition of both cholesterol esterase and triglyceride lipase activity. Parallel changes in the hydrolysis of both substrates also were observed when exogenously added lipids were added to the incubation system in various physical states. Specificities of the enzyme system towards different cholesteryl esters were examined. No differences in the rate of hydrolysis were observed between cholesteryl oleate, palmitate and linoleate. The data suggest that a single acid lipase, presumably of lysosomal origin, has broad specificity towards triglycerides and cholesteryl esters, and may play a role in the hydrolysis of these lipids during intralysosomal degradation of lipoproteins.

Animals↗
PubMed1985

Requirements of glycerol and fatty acid for triglyceride synthesis and ketogenesis by hepatocytes from normal and triiodothyronine-treated rats.

Hepatocytes from T3-treated rats synthesized less triglyceride and more ketone bodies from [1-14C]oleate at all concentrations from 0-2 mM, than did hepatocytes from euthyroid animals; addition of 1.0 mM glycerol increased triglyceride synthesis and reduced ketogenesis in hepatocytes from T3-treated rats to the rates observed in euthyroid hepatocytes in the absence of added glycerol. Glycerol did not alter triglyceride synthesis, but reduced ketogenesis genesis by euthyroid hepatocytes. It is probable from these and other data (J. Biol. Chem. 259, 8857-8862 (1985)) that, in the hyperthyroid rat, glycero-3-P, and not fatty acid, is rate limiting for synthesis of triglyceride, and, secondarily for reducing rates of ketogenesis in the hepatocyte.

Animals↗
PubMed1991

Effect of the peroxisome proliferator LY171883 on triglyceride accumulation in rats fed a fat-free diet.

LY171883 is a leukotriene D4 antagonist that induces peroxisome proliferation in the rodent liver. Like many peroxisome-proliferating agents, it causes transient lipid accumulation and several other changes in hepatic lipid metabolism. The effect of LY171883 on lipid metabolism was studied further in rats maintained on a fat-free diet. Administration of a fat-free diet for 14 days caused a 5.6-fold increase in liver triglycerides associated with a 3.3-fold increase in fatty acid synthetase. Co-administration of 0.1% LY171883 increased liver triglycerides slightly, whereas 0.3% LY171883 prevented the accumulation of triglycerides. Furthermore, treatment with 0.3% LY171883 reversed the fatty liver in rats pretreated with the fat-free diet for 14 days. Fatty acid synthetase activity increased comparably in all treatment groups, indicating that 0.3% LY171883 did not prevent the lipogenic response to a fat-free diet. In rats treated with 0.3% LY171883, peroxisomal beta-oxidation increased 9.5-fold, mitochondrial beta-oxidation 4.8-fold, carnitine palmitoyltransferase I 1.9-fold, and plasma ketones 3-fold. In the 0.1% dose group the increases in these parameters were smaller. The data indicate that 0.3% LY171883 sufficiently increased mitochondrial and peroxisomal beta-oxidation such that fatty acids generated by lipogenesis were preferentially oxidized rather than esterified to triglycerides. In the 0.1% dose group oxidation was only mildly increased, and the excess fatty acids continued to be esterified.

Acetophenones↗
PubMed1976

Triglyceride lipases in acute hepatitis.

Two triglyceride lipases in postheparin plasma, the lipoprotein lipase (LPL) and the hepatic triglyceride lipase (H-TGL) were separated by heparin-sepharose affinity chromatography and studied in controls and patients during the course of acute hepatitis. All three patients had increased content of triglycerides in the low density lipoproteins, and two of them had hypertriglyceridemia. Low activities of both lipases were found in the acute stage of the disease in all three patients. Concomitantly one of the patients had absolute low lecithin: cholesterol acyltransferase (LCAT) activity, and in the two other patients a relative LCAT deficiency was present. The increased content of triglycerides in LDL that may be found in liver disease, may not only be due to low H-TGL and LPL, but also LCAT deficiency.

Acute Disease↗
PubMed1978

Triglyceride lipase activity in postheparin plasma and plasma lipoproteins in liver disease.

Hepatic lipase activity and lipoprotein lipase activity were studied in postheparin plasma from 14 patients with various liver disorders. Plasma lecithin: cholesterol acyltransferase (LCAT) activity and lipoprotein composition and structure were also estimated. Five patients had lower hepatic lipase activity than the lowest control value, and in three of these no hepatic lipase activity was detected. Lipoprotein lipase was low in 5 patients, but in only one of them was hepatic lipase activity also low. Hepatic lipase was not significantly correlated to the concentration of plasma triglycerides, either in controls or in patients, whereas lipoprotein lipase was negatively correlated with plasma triglycerides both in controls and patients. Lipoprotein lipase and LCAT activity, but not hepatic lipase, was negatively correlated to the triglyceride content of the low density lipoproteins (density 1.019-1.063 g/ml) from the patients. No specific lipid or lipoprotein pattern was found in plasma from the patients with a low or without any hepatic lipase activity. The results suggest an important role of lipoprotein lipase and LCAT, for the increased content of triglycerides in the low density lipoproteins in patients with liver disease. The role of hepatic lipase remains unclear.

Adult↗
PubMed1979

Triglyceride-poor very low density lipoprotein in human serum.

The chemical and physical properties of very low density lipoproteins, isolated from the pool of the sera of 60 persons with high pre-beta and normal triglyceride and cholesterol concentrations, have been studied. These very low density lipoproteins, a designated as triglyceride-poor very low density lipoproteins, consist of 20.5% phospholipids, 30.8% free cholesterol, 15% cholesterol esters and 33.7% triglycerides. Their protein content consists of 54.5% apo B, 26% apo A, 11.5% apo E and only 8% apo C, so they differ from any serum lipoprotein described until now. Triglyceride-poor very low density lipoproteins consist of spherical particles 300-450 A in diameter as revealed by electron microscopy.

Cholesterol↗