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PubMed1994

Rapid, sensitive fluorometric determination of serum triglyceride by measuring lipase-liberated fatty acids.

A continuous fluorescence displacement assay was developed for the measurement of long-chain fatty acids and utilized in the study of triglyceride lipase-catalyzed reactions (Wilton, DC. Biochem J 1991;276:129-33). We now describe a method for the rapid measurement of triglyceride in serum with the fluorescence displacement assay. The method involves the hydrolysis of a diluted sample equivalent to 0.1 microL of original serum with excess lipase (EC 3.1.1.3) from Rhizopus arrhizus and measuring the fatty acid released after a set time interval, normally 1 min. Under the conditions of the timed assay, about 2 mol of fatty acid are released per mole of triglyceride. The released fatty acid is monitored by fluorescence change and is proportional to the concentration of triglyceride in the original serum sample. The effective range of serum triglyceride concentration that could be measured was 0.5-10 mmol/L (0.44-8.8 g/L), based on triolein standard. The assay is unique in that it measures lipase-liberated fatty acids rather than liberated glycerol and as such is not subject to many of the criticisms of the glycerol-based methods. Comparison of fasted serum samples established a high correlation between the fatty acid and glycerol methods.

Animals↗
PubMed1993

Dietary cholesterol stimulates hepatic biosynthesis of triglyceride and reduces oxidation of fatty acids in the rat.

Experiments were conducted in the intact rat and in the isolated, perfused rat liver to investigate the possibility that the increase in the concentration of hepatic triglyceride and increase in the secretion of the very low density lipoprotein (VLDL)-triglyceride (TG) resulting from addition of cholesterol to the diet are due to stimulation of synthesis of triglyceride, reduced fatty acid oxidation, or both. Male rats were fed for 7 days with either a cholesterol-free diet to which 5% (w/w) corn oil was added, or with the same diet supplemented with 0.5% cholesterol. Fed animals received [1-14C]oleic acid via the tail vein, as a complex with rat serum, and were killed 2 h later. Feeding cholesterol for 7 days increased hepatic triglyceride and cholesteryl ester (CE) concentrations, moderately elevated free cholesterol, but did not affect phospholipid (PL) levels, as we had previously observed after a feeding period of 3 weeks. Incorporation of [1-14C]oleic acid into hepatic and plasma triglyceride increased significantly (60 and 48%, respectively) with cholesterol feeding. Incorporation of [1-14C]oleic acid into hepatic and plasma cholesteryl esters increased by 63 and 79%, respectively, while incorporation into phospholipid was unaffected. Increasing the fat (corn oil) content of the diet to 20% (w/w) did not change these effects of dietary cholesterol. Studies using isolated, perfused rat livers were carried out in vitro after rats were fed the 5% corn oil diet for 3 weeks. [Perfusions lasted 4 h. The perfusion medium contained 3% bovine serum albumin and 30% washed bovine erythrocytes in Krebs-Henseleit-HCO3 buffer.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Effects of free fatty acids on activity of hepatic microsomal 3-hydroxy-3-methylglutaryl coenzyme A reductase and on secretion of triglyceride and cholesterol by liver.

The output of triglyceride and cholesterol, and the activity of microsomal 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase) were measured following perfusion of the isolated rat liver with a medium containing free fatty acids. The activity of the enzyme and the output of cholesterol and triglyceride are regulated by the quantity and structure of the free fatty acid. The activity of HMG-CoA reductase was linearly proportional to uptake of oleic acid (18:1) by the liver. Output of triglyceride and cholesterol in the presence of oleate was also stimulated although, under these experimental conditions, the maximal secretory rate for cholesterol was observed while reductase activity was still increasing. When equimolar quantities of palmitic (16:0), oleic (18:1), or linoleic acid (18:2) were infused, the observed activity of the enzyme was in the order 18:1 greater than 18:2 = 16:0. Output of triglyceride was in the order 18:1 = 18:2 greater than 16:0. Output of free and esterified cholesterol was in the order 18:1 greater than 18:2 greater than 16:0. The stimulation by free fatty acids of hepatic cholesterogenesis, as estimated by the activity of HMG-CoA reductase, probably is the result of stimulation by free fatty acids of secretion of triglyceride in the very low density lipoprotein, and the obligatory requirement for cholesterol as a component of the lipoprotein.

Alcohol Oxidoreductases↗
PubMed1977

Relation between concentrations of free glycerol and triglycerides in human sera.

The concentrations of total glycerol, unesterified glycerol, and glycerol deriving from triglycerides (triacylglycerols) were measured in 468 fresh human sera from unselected outpatients of a municipal hospital. The distribution mode of free glycerol was log-normal; that of triglycerides was neither normal nor log-normal. A weak but statistically approved correlation between these variables was demonstrated. A comparison of triglyceride concentrations corrected for unesterified glycerol with those based on total glycerol shows that, for the triglycerides determination, analysis for total glycerol and substraction of 0.11 mmol/liter from the resulting value appears to be justified in clinical routine. Subtraction of individual sample-blank values is unnecessary. In a triglyceride concentration range from 1.71 to 2.85 mmol/liter the 95 percentile for the possible error of this procedure ranges from + 0.04 to - 0.08 mmol/liter.

Glycerol↗
PubMed1995

Plasma triglycerides cosegregate with erythrocyte sodium content in F2 rats of HTG x Lewis cross.

The possible association of plasma lipids (triglycerides and cholesterol) with erythrocyte Na+ content (Na+i) and/or with alterations in red cell Na+ and K+ (Rb+) transport was studied in a population of F2 hybrids obtained by crossing hypertensive Prague hereditary hypertriglyceridaemic (HTG) rats with normotensive Lewis rats. The obtained data indicated a strong cosegregation (p < 0.001) of plasma triglycerides with erythrocyte Na+ content. This was the cause for the close correlation of plasma triglycerides with the Na(+)-K+ pump activity (measured as ouabain-sensitive Na+ extrusion). On the contrary, there was only marginal association (p < 0.05) of erythrocyte Na+ content with plasma cholesterol which was significantly (p < 0.01) related to burnetanide-sensitive Rb+ uptake mediated by the Na(+)-K+ cotransport system. Na+ leak (bumetanide-resistant net Na+ uptake) correlated positively with blood pressure in female but not in male F2 rats. The close association between plasma triglycerides and erythrocyte Na+ content suggests that ion transport alterations might contribute to mechanisms responsible for the cosegregation of blood pressure with plasma triglycerides in HTG x Lewis F2 hybrids.

Animals↗
PubMed1995

MDL 29311, a phenolic antioxidant, interferes with the interaction of apoC with VLDL: a possible explanation for its triglyceride-lowering effect.

MDL 29311 is an antioxidant that lowers plasma triglycerides and raises high density lipoprotein (HDL) cholesterol in rats. It lowers triglycerides in rats by enhancing the clearance of very low density lipoprotein (VLDL) by the liver (Sheetz, M. J., et al. 1994. Metabolism. 43: 232-240). In this paper, the possibility that MDL 29311 enhances VLDL clearance by altering the apolipoprotein (apo) content of lipoproteins is examined. Treatment of rats with 1% MDL 29311 in the diet for 7 days lowered plasma triglycerides and markedly increased total lipoprotein-associated apoE. The increase in apoE was confined to the HDL fraction; no increase in VLDL-associated apoE was detected. No apparent alterations in the amount of total lipoprotein-associated apoC were observed, although there was a decrease in VLDL-associated apoC-II and C-III-0. Consistent with this finding, the amount of 125I-labeled apoC transferred from HDL to VLDL in plasma from MDL 29311-treated rats was only 40% of the amount transferred in control plasma. Sepharose 6B gel filtration of mixtures of 125I-labeled apoC with increasing concentrations of MDL 29311 in the absence of plasma or lipid revealed that proportionally increasing amounts of the 125I-labeled apoC eluted in a high molecular weight (HMW) complex with MDL 29311. An HMW complex was not formed when MDL 29311 was mixed with 125I-labeled soybean trypsin inhibitor. The 125I-labeled apoC in the HMW complex bound to VLDL only 20% as well as uncomplexed 125I-labeled apoC. MDL 29311 also caused the dissociation of 125I-labeled apoC from VLDL at concentrations of MDL 29311 similar to those obtained in vivo. Other phenolic antioxidants related to MDL 29311 caused the formation of HMW 125I-labeled apoC-containing complexes to an extent proportional to their abilities to lower triglycerides in rats. These studies support the hypothesis that MDL 29311 lowers triglycerides in rats by interfering with apoC association with VLDL, thereby relieving the apoC-mediated inhibition of hepatic VLDL uptake.

Animals↗
PubMed1996

[High triglyceride, low HDL-cholesterol and risk of coronary heart disease].

Hypercholesterolaemia is a strong risk factor of coronary artery disease (CAD). The importance of high triglyceride and low HDL cholesterol in predicting risk of CAD is less well-established. This review presents data showing that high triglyceride and low HDL cholesterol are important risk factors of CAD and suggests that combined lipid profiles of triglyceride, HDL cholesterol, and total cholesterol provide more information about risk of CAD than total cholesterol alone. High triglyceride and low HDL cholesterol is the characteristic dyslipidaemia seen in subjects with insulin resistance, a basic abnormality in glucose- and insulin metabolism. Since insulin resistance and raised triglyceride and decreased HDL cholesterol can be identified in children of patients with NIDDM, essential hypertension, and CAD, we suggest that efforts to prevent CAD should include interventions against all these associated abnormalities in glucose-, insulin-, and lipid metabolism and not only high cholesterol.

Cholesterol, HDL↗
PubMed1996

HDL content and composition in acute phase response in three species: triglyceride enrichment of HDL a factor in its decrease.

High density lipoprotein (HDL) levels decrease during the acute phase response (APR). We have used the APR model of rabbit, baboon, and mouse to study the factors that influence HDL level. In the baboons and rabbits there was massive hypertriglyceridemia, triglyceride enrichment of HDL (60-80% of core lipids), decreases of HDL-cholesterol and apolipoprotein (apo)A-I (to 10% of baseline), and increases of apoA-I in the non-lipoprotein bottom fraction suggesting dissociation of apoA-I from the particles. Detailed analyses of serum amyloid A (SAA)-rich HDL done in the rabbit revealed large, triglyceride-enriched (> 60% of core lipids) particles containing > 95% SAA. These particles had a high surface to core ratio (13.4 +/- 1.94, control = 3.0 +/- 0.12) and a very high protein (79.71 +/- 5.25 weight %, control = 37.2 +/- 0.43) proportion, large (r = 5.95 nm) when examined by non-denaturing gradient electrophoresis but small when examined by electron microscopy (r = 4.2 nm). In the mouse there was no hypertriglyceridemia, no triglyceride enrichment of HDL, no decrease of HDL cholesterol. ApoA-I decreased to about 61.4% of baseline but did not increase in the bottom fraction although large but dense SAA-enriched HDL particles were also produced. These results suggest that hypertriglyceridemia, triglyceride-enrichment of HDL, and dissociation of apoA-I from the particles, possibly by displacement of apoA-I by SAA, are important factors in the decline of HDL during the APR. Whether differences in triglyceride metabolism account for the differences in the HDL response in the species studied requires further experimentation.

Acute-Phase Reaction↗
PubMed1998

Participation of the microsomal triglyceride transfer protein in lipoprotein assembly in Caco-2 cells: interaction with saturated and unsaturated dietary fatty acids.

This study was designed to gain insight into the role of microsomal triglyceride transfer protein (MTP) in the association of apolipoprotein (apo) B with lipid during intestinal lipoprotein assembly. The MTP-inhibiting compound BMS-200150 (Jamil et al. 1996. Proc. Natl. Acad. Sci. USA 93: 11991-11995) was used to inhibit the lipid transfer activity of MTP in Caco-2 cells. MTP inhibition reduced the number of apoB-containing lipoproteins that were secreted from the cells. Secretion of apoB-100 appeared to be more sensitive to BMS-200150 than apoB-48 secretion, which appeared to be relatively insensitive. BMS-200150 caused a decrease in the triglyceride content of the secreted lipoproteins, compared with control incubations without MTP inhibition. This indicated that, in Caco-2 cells, MTP is not only involved in the first step of lipoprotein synthesis, i.e., the rescue of apoB from intracellular degradation through early lipidation of the protein, but also in further steps involving the association of lipoproteins with triglycerides. When 0.5 mM oleic acid (18:1) was used to stimulate cellular lipid synthesis, secreted lipoproteins were predominantly of chylomicron/VLDL density and their secretion could be efficiently inhibited with BMS-200150. With 0.5 mm palmitic acid (16:0), lipoproteins of distinct densities (i.e., chylomicron/VLDL and IDL/LDL) were secreted by Caco-2 cells, as reported before (van Greevenbroek et al. 1995. J. Lipid Res. 36: 13-24). Secretion of the lipoproteins at chylomicron/VLDL density was strongly reduced by inhibition of MTP activity by BMS-200150, whereas the IDL/LDL density lipoproteins were relatively insensitive. In conclusion, specific inhibition of MTP activity in Caco-2 cells with BMS-200150 resulted in reduced secretion of apoB-containing lipoproteins (predominantly apoB-100) by Caco-2 cells and furthermore reduced the triglyceride content of these lipoproteins. MTP inhibition preferentially reduced the secretion of triglyceride-rich lipoproteins (d < 1.006 g/ml).

Apolipoproteins B↗
PubMed1998

Plasma triglyceride as a risk factor for cardiovascular disease.

OBJECTIVES: To determine whether cardiovascular disease can be predicted from plasma triglyceride levels independent of high density lipoprotein (HDL) cholesterol levels. DATA SOURCES AND STUDY SELECTION: Seventeen prospective population-based studies, ranging in publication date from 1965 to 1994, were selected based on uniform criteria. Among the studies, 16 were conducted in men, comprising data for more than 46,000 men, with an average follow-up period of more than eight years. The data from women came from five studies, including nearly 11,000 women with an 11-year average follow-up. DATA EXTRACTION: The meta-analysis protocol comprised the following steps: estimating the relative risk of triglyceride for each individual study; standardizing the relative risks to a 1 mmol/l increase; estimating the variance and weighting relative risks by the inverse of the variance, and estimating the summary relative risk by averaging the weighted relative risks. DATA SYNTHESIS: Among studies of men, relative risks ranged from 1.1 to 2.0, and the summary relative risk was 1.32 (P < 0.05). All five studies of women were statistically significant, with relative risks ranging from 1.7 to 2.0. The summary relative risk was 1.76, higher than that for men, indicating a 76% increase in risk for women. For the studies among men in which HDL cholesterol data were available, multivariate adjusted relative risk was attenuated to 1.14 but was still statistically significant. Although only two studies of women included HDL cholesterol adjustments, the summary relative risk for triglyceride remained statistically significant, with a value of 1.37. CONCLUSIONS: When all available data are taken into account, increased triglyceride level is a risk factor for cardiovascular disease, independent of HDL cholesterol level. Clinical trials are urgently needed to determine whether lowering plasma triglyceride levels reduces subsequent risk of cardiovascular disease.

Cardiovascular Diseases↗
PubMed1976

Results for serum cholesterol and triglycerides by gas-liquid chromatography, as compared with a continuous-flow technique.

We assessed the usefulness of gas-liquid chromatography forthe routine and reference measurement of cholesterol and triglycerides (triacylglycerols). Compared with results obtained by an AutoAnalyzer II method, correlation was good with both serum specimens (triglycerides, r = 0.88; cholesterol, r = 0.90) and lipoprotein fractions isolated by ultracentrifugation (triglycerides, r = 0.98; cholesterol, r = 0.98). However, none of the comparisons was completely free of analytical bias, and in general the AutoAnalyzer method underestimated the cholesterol value and overestimated triglycerides. The obvious advantage of the AutoAnalyzer is its greater analytical speed, but the chromatographic method appeared to be more accurate and precise and to suffer less from interfering substances, and in addition gave information about the cholesterol ester and triglyceride composition. We expect gas-liquid chromatography to be of major importance in the calibration of other analytical methods.

Autoanalysis↗
PubMed1998

Effect of pulsed magnetic fields on triglyceride and cholesterol levels in plasma of rats.

BACKGROUND: Liver is a crucial organ in metabolism. For instance liver is the main source of circulating lipoproteins. METHODS: In this paper cholesterol and triglyceride plasma levels were measured in male rats previously exposed to pulsed magnetic fields (PMF) used in therapy. Rats underwent a one-hour exposure to a 6 mT 12 Hz PMF. RESULTS: Twenty-four hours after the end of the exposure to the PMF the rats' livers were heavier, cholesterol and triglyceride plasma levels decreased. All these variations were significantly different according to a variance ratio test as was a rebound in triglyceride level 48 hours after the end of the exposure. Normal values were observed 48 and 96 hours after the end of exposure respectively for cholesterol and triglycerides. CONCLUSIONS: These alterations may be due to a reversible accumulation of either triglycerides or of their precursors in liver following acute exposure to a 12 Hz PMF.

Animals↗
PubMed1998

Human pancreatic triglyceride lipase expressed in yeast cells: purification and characterization.

A cDNA clone encoding human pancreatic triglyceride lipase was cloned into a yeast expression vector so that the yeast PHO1 signal peptide replaced the native signal peptide. Pichia pastoris cells were transfected with the vector, and clones expressing human pancreatic triglyceride lipase were isolated. Recombinant human pancreatic lipase was expressed in broth cultures and was purified from the medium by DEAE blue Sepharose and hydroxyapatite chromatography. The highly purified lipase had specific activities for various triglyceride substrates identical to those of tissue-purified human pancreatic triglyceride lipase; it was inhibited by bile salts, required colipase for activity, and demonstrated interfacial activation. This expression system is suitable for the rapid, efficient production of human pancreatic triglyceride lipase in amounts adequate for biophysical studies.

Amino Acid Sequence↗
PubMed2001

Diaminoindanes as microsomal triglyceride transfer protein inhibitors.

The synthesis and biological activities of biarylamide-substituted diaminoindanes as microsomal triglyceride transfer protein (MTP) inhibitors are described. One of the more potent compounds, 8aR, inhibited both the secretion of apoB from Hep G2 cells and the MTP-mediated transfer of triglycerides between synthetic acceptor and donor liposomes with IC(50) values of 0.7 and 70 nM, respectively. In normolipidemic rats and dogs, oral administration of 8aR dose-dependently reduced both plasma triglycerides and total cholesterol. Moreover, in rats and dogs, 8aR also prevented the postprandial rise in plasma triglycerides following a bolus administration of a fat load. Because MTP inhibitors decrease very low density lipoprotein assembly in the liver, the potential for hepatic lipid accumulation was evaluated. In normolipidemic rats, hepatic cholesterol and triglyceride contents were dose-dependently increased by 8aR. However, hepatic lipid accumulation resulted in negligible change in total liver weight and was reversible after withdrawal of the compound.

Animals↗
PubMed2007

Spontaneous formation of fractal structures on triglyceride surfaces with reference to their super water-repellent properties.

Alkylketene dimer (AKD), a kind of wax, has been known to form fractal surfaces spontaneously and show super water-repellency. Such formation of water-repellent and fractal surfaces was also found in this work for triglycerides. Since the crystal phase transitions of these waxes were well studied, we studied the formation of their fractal surfaces through contact angle measurements, differential scanning calorimetry (DSC), and X-ray diffraction (XRD). From time-dependent contact angle measurements, it was found that the formation of super water-repellent surfaces with fractal structures occurred spontaneously also on the triglyceride surfaces at different temperatures. The freshly solidified triglyceride surfaces were almost transparent, and their initial contact angles of water were close to 110 degrees. The surfaces then became rough and clouded after being incubated for a certain time at a specified temperature. The super water-repellent surfaces were quite rough and showed fractal structures with the dimension of ca. 2.2 calculated from the scanning electron microscopic (SEM) images by the box-counting method. The phase transformation from a metastable state to a stable cystalline one after the solidification from the melt of triglycerides was clearly observed by DSC and XRD measurements. The fractal crystalline structures and the super water-repellency resulted from this phase transformation and the crystal growth. Ensuring the initial sample solidified into the metastable state and curing the surface at an appropriate temperature are key factors for the successful preparation of fractal triglyceride surfaces by the solidification method.

Journal Article↗
PubMed2001

Decreased activities of lipoprotein lipase and hepatic triglyceride lipase in patients with gout.

Postheparin plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) activities were measured in 30 male primary gout patients as well as in control subjects. The activities of these lipolytic enzymes were significantly decreased in the patients as compared with the controls (gout v control; LPL, 5.4 +/- 0.4 v 7.9 +/- 0.9 U; HTGL, 14.6 +/- 2.0 v 17.9 +/- 3.4 U) when matched with serum triglyceride concentration. Further, LPL activity was negatively correlated with serum- and very-low-density lipoprotein (VLDL)-triglyceride in gout patients, while that of HTGL was negatively correlated with low-density lipoprotein (LDL)-triglyceride in both gout patients and control subjects. These results suggest that decreased activities of LPL and HTGL may contribute, in part, to the increased concentrations of serum-, VLDL-, and LDL-triglyceride seen in gout patients, leading to a higher risk for coronary atherosclerotic diseases in gout.

Adult↗
PubMed1999

The effect of 24 months recombinant human growth hormone (rh-GH) on LDL cholesterol, triglyceride-rich lipoproteins and apo [a] in hypopituitary adults previously treated with conventional replacement therapy.

Hypopituitary adults receiving conventional hormone replacement therapy are reported to have increased cardiovascular mortality. Previous studies indicate that these patients have several abnormalities in lipoprotein metabolism, including reduced low density lipoprotein (LDL) uptake and impaired metabolism of triglyceride-rich lipoproteins. The effects of 24 months of 0.21 IU/kg per week recombinant growth hormone (rh-GH) on the lipoprotein profiles of 22 GH-deficient adults were studied. Samples were collected after a 12-h fast at baseline and 24 months. Total cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, LDL cholesterol, apolipoprotein (apo) A, apo B and apo [a] were determined by routine laboratory methods. LDL particle size was determined by non-denaturing gradient gel electrophoresis. Visceral adiposity was determined by dual energy X-ray absorptiometry (DEXA). Insulin sensitivity was measured in a subset of 17 subjects using a two-stage hyperinsulinaemic-euglycaemic clamp. Significant reductions were observed in total cholesterol (5.3 +/- 0. 17 vs 4.9 +/- 0.23 mmol/l;P<0.05) and LDL cholesterol (3.4 +/- 0.17 vs 2.9 +/- 0.17 mmol/l; P<0.001) at 24 months when compared to baseline. No significant changes were observed in triglyceride level, HDL cholesterol level, apo B, apo A and LDL size. A significant increase in apo [a] [160 (96-416) vs 204 (127-534) U/l;P<0.05] was observed which appeared to be dose-dependent. Visceral adiposity was reduced significantly. Insulin sensitivity did not alter significantly. Replacement for 24 months with rh-GH has a differential effect on the lipid profile with a decrease in LDL, but little effect upon the metabolism of triglyceride-rich lipoproteins, manifested by unchanged triglyceride, HDL cholesterol levels and LDL size, despite the reduction in visceral adiposity. Conversely, apo [a], an independent risk factor for cardiovascular disease was increased. The ultimate effect of GH therapy upon cardiovascular mortality remains to be determined and may be dose-related.

Adult↗
PubMed1992

Total parenteral nutrition with short- and long-chain triglycerides: triacetin improves nitrogen balance in rats.

Little is known about the long-term metabolic effects of parenteral administration of short-chain triglycerides. These studies were undertaken to investigate triacetin, the water-soluble triglyceride of acetate when it is incorporated into nutritionally balanced total parenteral nutrition formulas. Male Sprague-Dawley rats (n = 22) were fed an isovolemic, isocaloric and isonitrogenous diet for 7 d. The lipid energy represented 30% of the nonprotein energy with short-chain triglycerides representing 0, 50 or 90% of the lipid energy. Plasma acetate concentration was determined as well as indicators of protein metabolism: daily and cumulative nitrogen balance, whole body leucine kinetics and rectus muscle and liver fractional protein synthetic rates. No overt toxic effects were observed at any point during the study. As the proportion of short-chain triglycerides in the diet increased from 0 to 50 or 90% of the lipid energy, cumulative nitrogen balance increased 50 or 120%, respectively (P less than 0.05). Whole-body and tissue leucine kinetics (determined during the last 2.5 h of the 7-d study) were unaffected by the lipid composition of the diet. Plasma acetate concentration was not significantly different among groups. These results indicate that incorporation of the short-chain triglyceride, triacetin, in nutritionally balanced total parenteral nutrition formulas improves nitrogen balance with no overt toxic effects. These data indicate that triacetin may have a future role as a parenteral nutrient, and that further studies of its use are warranted.

Acetates↗