Absorption, Distribution and Excretion
In the small intestine, most triglycerides are split into monoglycerides, free fatty acids, and glycerol, which are absorbed by the intestinal mucosa. Within the epithelial cells, resynthesized triglycerides collect into globules along with cholesterol and phospholipids and are encased in a protein coat as chylomicrons. Chylomicrons are transported in the lymph to the thoracic duct and eventually to the venous system. The chylomicrons are removed from the blood as they pass through the capillaries of adipose tissue. Fat is stored in adipose cells until it is transported to other tissues as free fatty acids which are used for cellular energy or incorporated into cell membranes.
When (14)C-labeled long-chain triglycerides are administered intravenously, 25% to 30% of the radiolabel is found in the liver within 30 to 60 minutes, with less than 5% remaining after 24 hours. Lesser amounts of radiolabel are found in the spleen and lungs. After 24 hours, nearly 50% of the radiolabel has been expired in carbon dioxide, with 1% of the carbon label remaining in the brown fat. The concentration of radioactivity in the epididymal fat is less than half that of the brown fat.
Rats were fed an emulsion diet (via stomach tube) consisting of 95 parts triolein (Glycerol Trioleate) and 5 parts glycerol 1- (14)C-trioleate. The percentage of administered glycerol 1- (14)C-trioleate that was identified in the lymph in 24 hours was 88%. In an earlier study four male rats (weights 250 g) were dosed orally with [1-(14)C]triolein. The percentage of radioactivity that was absorbed in 24 hours ranged from 57% to 92% (mean =78.2%). The percentage of absorbed activity that was recovered in the lymph fat from the thoracic duct ranged from 51% to 83% (mean =65.5%).
After a single dose of [1- (14)C]triolein was administered intravenously into fasted rats, a high rate of uptake was noted within the first hour in the following organs: liver, myocardium, gastric mucosa, and diaphragm. However, after 24 hours, radioactivity in these tissues had decreased markedly. A similar pattern of distribution was noted in mice; however, large amounts of radioactivity were also noted in the brown fat, white adipose tissue, and spleen, even after 24 hours.
For more Absorption, Distribution and Excretion (Complete) data for TRIOLEIN (7 total), please visit the HSDB record page.

---

Metabolism / Metabolites
Hydrolysis of /Triolein/ by hepatic triacylglycerol lipase in plasma from ICR mice has been demonstrated in vitro.
The metabolism of triolein in vitro was evaluated using isolated perfusion of a rat liver in tandem with an isolated rat hind-end. This permitted the study of lipid transfer between the two. In the absence of added triolein, a net removal of free fatty acids was demonstrated in both tissue beds when fatty acid gradients across tissue beds were measured. Following the addition of 100 mg of triolein (as [(3)H]-glycerol-[(14)C]triolein) to either reservoir in the system, an appreciable net production of free fatty acid was noted for the hind-end gradient at 30 minutes. This hind-end free fatty acid efflux amounted to more than one third of the catabolism of triolein.
In experimental studies, embolization of the cerebral hemisphere with triolein emulsion has revealed reversible magnetic resonance imaging (MRI) findings in the subacute stage. /The aim of this study was/ to investigate the changes in the major metabolites, by proton magnetic resonance spectroscopy (MRS), in a cerebral fat embolism induced by a triolein emulsion.The internal carotid arteries of 19 cats were injected with a triolein emulsion, and multivoxel MRS was performed 30 min, 1 day, and 7 days later. In the control group, six cats were injected with normal saline. The MR spectra were evaluated for N-acetyl aspartate (NAA), creatine (Cr), and choline (Cho), along with the presence of lipid and lactate. Semiquantitative analyses of NAA/Cr, Cho/Cr, NAA/Cho, and lipid/Cr ratios compared the median values of the ipsilateral metabolite ratios with those of the contralateral side and in the control group for each point in time.The NAA/Cr, Cho/Cr, and NAA/Cho ratios in the ipsilateral cerebral hemisphere of the embolized group after 30 min, 1 day, and 7days were not significantly different from the contralateral hemisphere of the embolized and control groups (P>0.05). The lipid/Cr ratio in the ipsilateral cerebral hemisphere of the embolized group was significantly higher when compared with the control group (P=0.012 at 30 min, P=0.001 on day 1, and P=0.018 on day 7). Cerebral fat embolism induced by a triolein emulsion resulted in no significant change in the major metabolites of the brain in the acute stage, except for an elevated lipid/Cr ratio, which suggests the absence of any significant hypoxic-ischemic changes in the lesions embolized using a fat emulsion.
Effects of protopanaxdiol (PDG) and protopanaxatriol (PTG) types of ginsenosides isolated from the leaves of American ginseng on porcine pancreatic lipase activity were determined in vitro. PDG inhibited the pancreatic lipase activity in a dose-dependent manner at the concentrations of 0.25-1 mg/mL. It inhibited hydrolysis of about 83.2% of triolein at about 1 mg/mL of PDG. However, PTG showed no inhibitory activity. Therefore, anti-obesity activity of PDG was evaluated in mice fed a high-fat diet. The results demonstrated that PDG was effective in preventing and healing obesity, fatty liver and hypertriglyceridemia in mice fed with a high-fat diet.

---

Biological Half-Life
/Half-life/ 4.5 minutes.

Interactions
IM administration of tetracycline hydrochloride 250 mg/kg /to rats/ significantly decreased the intestinal absorption of intragastrically administration triolein.
The oral administration of 2 g neomycin/kg, twice daily, reduced in rats the in vivo intestinal absorption of (14)C-labeled triolein.
The purpose of this study is to evaluate the effect of dexamethasone on the damaged blood-ocular barrier caused by triolein emulsion, using contrast-enhanced MR imaging. An emulsion of 0.1-mL triolein in 20 mL of saline was infused into the carotid arteries of 32 cats, 12 cats were placed in the treatment group and 18 cats were placed in the Control group. Thirty minutes after the infusion of triolein emulsion, a set of orbital pre- and post-contrast T1-weighted MR images (T1WIs) were obtained. Infusion of 10 mg/kg dexamethasone into the ipsilateral carotid artery of each of the cats in the treatment group cats and 20 mL saline in each of the cats in the control group was given. A second set of pre- and post-contrast orbital T1WIs were obtained three hours following triolein emulsion infusion. Qualitative analysis was performed for the the anterior chamber (AC), the posterior chamber (PC), and in the vitreous humor of the ipsilateral and contralateral eyes. The signal intensity ratios of the ipsilateral eye over the contralateral eye were quantitatively evaluated in the three ocular chambers on the first and second set of T1WIs, and were then statistically compared. Qualitatively, the AC, the PC or the vitreous did not show immediate contrast enhancement on the first and the second set of post-contrast T1WIs. However, the AC and the PC showed delayed contrast enhancement for both groups of cats on the second pre-contrast T1WIs. No enhancement or minimally delayed enhancement was seen for the vitreous humor. Quantitatively, the signal intensity ratios in the PC of the treatment group of cats were statistically lower than the ratios of the control group of cats for the second set of T1WIs (p = 0.037). The AC and vitreous showed no statistically significant difference between the feline treatment group and control group (p > 0.05). Contrast-enhanced MR images revealed increased vascular permeability in the PC of the eye after infusion of triolein emulsion. Dexamethasone seems to decrease the breakdown of the blood-aqueous barrier in the PC.
Fat embolization (FE) is an often overlooked and poorly understood complication of skeletal trauma and some orthopedic procedures. Fat embolism can lead to major pulmonary damage associated with fat embolism syndrome (FES). A model of FE in unanesthetized rats, using intravenous injection of the neutral fat triolein, was used to study the potential therapeutic effect on lung histopathology of altering the production of, or response to, endogenous angiotensin (Ang) II. Either captopril, an Ang I converting enzyme inhibitor, or losartan, an Ang II type 1 receptor blocker, was injected 1 hour after FE by triolein injection. After euthanasia at 48 hours, histopathologic evaluation was used to compare the drug-treated animals with control animals that received only triolein. Histology of the lungs of rats treated only with triolein revealed severe, diffuse pathology. Alveolar septa showed severe, diffuse inflammation. Bronchial lumina showed severe mucosal epithelial loss. The media of the pulmonary small arteries and arterioles was thicker, and the lumen patency was reduced 60% to 70%. Trichrome staining confirmed the abundant presence of collagen in the media and adventitia, as well as collagen infiltrating the bronchial musculature. Both captopril and losartan treatments reduced the inflammatory, vasoconstrictor, and profibrotic effects present at 48 hr (p<0.001). With treatment, the vascular lumen remained patent, and the fat droplets were reduced in size and number. There was a reduction in the number of infiltrating leukocytes, macrophages, myofibroblasts, and eosinophils, along with a significant decrease in hemorrhage and collagen deposition (p<0.001). Pathologic changes in bronchial epithelium were also diminished. The results suggest that the use of drugs that act on the renin-Ang system might provide an effective and targeted therapy for fat embolism syndrome.
For more Interactions (Complete) data for TRIOLEIN (6 total), please visit the HSDB record page.

[1]. Triolein reduces MMP-1 upregulation in dermal fibroblasts generated by ROS production in UVB-irradiated keratinocytes. J Dermatol Sci. 2017 Feb;85(2):124-130.

[2]. Triolein and trilinolein ameliorate oxidized low-density lipoprotein-induced oxidative stress in endothelial cells. Lipids. 2014 May;49(5):495-504.

Triolein is a triglyceride formed by esterification of the three hydroxy groups of glycerol with oleic acid. Triolein is one of the two components of Lorenzo's oil. It has a role as a plant metabolite and a Caenorhabditis elegans metabolite. It is functionally related to an oleic acid.
Glyceryl Trioleate has been investigated for the treatment of Adrenoleukodystrophy.
Triolein has been reported in Panax pseudoginseng, Grifola frondosa, and other organisms with data available.
TG(18:1(9Z)/18:1(9Z)/18:1(9Z)) is a metabolite found in or produced by Saccharomyces cerevisiae.
(Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.
See also: Coix lacryma-jobi seed (part of).

---

Therapeutic Uses
/The aim of this study was/ To identify asymptomatic boys with X-linked adrenoleukodystrophy who have a normal magnetic resonance image (MRI), and to assess the effect of 4:1 glyceryl trioleate-glyceryl trierucate (Lorenzo's oil) on disease progression. Eighty-nine boys (mean +/- SD baseline age, 4.7 +/- 4.1 years; range, 0.2-15 years) were identified by a plasma very long-chain fatty acids assay used to screen at-risk boys. All were treated with Lorenzo's oil and moderate fat restriction. Plasma fatty acids and clinical status were followed for 6.9 +/- 2.7 years. Changes in plasma hexacosanoic acid levels were assessed by measuring the length-adjusted area under the curve, and a proportional hazards model was used to evaluate association with the development of abnormal MRI results and neurological abnormalities. Of the 89 boys, 24% developed MRI abnormalities and 11% developed both neurological and MRI abnormalities. Abnormalities occurred only in the 64 patients who were aged 7 years or younger at the time therapy was started. There was significant association between the development of MRI abnormalities and a plasma hexacosanoic acid increase. (For a 0.1-ug/mL increase in the length-adjusted area under the curve for the hexacosanoic acid level, the hazard ratio for incident MRI abnormalities in the whole group was 1.36; P = .01; 95% confidence interval, 1.07-1.72.) Results for patients aged 7 years or younger were similar (P = .04). In this single-arm study, hexacosanoic acid reduction by Lorenzo's oil was associated with reduced risk of developing MRI abnormalities. We recommend Lorenzo's oil therapy in asymptomatic boys with X-linked adrenoleukodystophy who have normal brain MRI results.
X-linked adrenoleukodystrophy (X-ALD) is an inherited disorder of peroxisomal metabolism, biochemically characterized by deficient beta-oxidation of saturated very long chain fatty acids (VLCFA). The consequent accumulation of these fatty acids in different tissues and in biological fluids is associated with a progressive central and peripheral demyelination, as well as with adrenocortical insufficiency and hypogonadism. Seven variants of this disease have been described, cerebral childhood being the most frequent. The recommended therapy consists of the use of the glyceroltrioleate/glyceroltrierucate mixture known as Lorenzo's Oil (LO), combined with a VLCFA-poor diet, but only in asymptomatic patients will this treatment prevent the progression of the symptomatology. In the present study we evaluated the biochemical course of patients with cerebral childhood (CCER) and asymptomatic clinical forms of X-ALD treated with LO associated with a VLCFA-restricted diet. We observed that hexacosanoic acid plasma concentrations and hexacosanoic/docosanoic ratio were significantly reduced in CCER patients during treatment when compared with diagnosis. Hexacosanoic acid plasma level was significantly reduced when compared with that at diagnosis and achieved the normal levels only in asymptomatic patients under LO treatment. In asymptomatic patients the magnitude of hexacosanoic acid decrease was higher than that of the CCER patients. These results show the good biochemical response of LO treatment in asymptomatic X-ALD patients. It is possible to suppose that this could be correlated with the prevention of the appearance of neurological signals in this group of patients treated with LO.
/The study/ investigated the possible therapeutic effect of decreasing plasma levels of very-long-chain fatty acids (C26:0) with a synthetic oil containing trioleate and trielucate (Lorenzo's oil) as well as increasing docosahexaenoic acid (DHA) in red blood cells (RBC) with DHA ethyl ester in four patients with Zellweger syndrome. /The study/ investigated serial changes of plasma C26:0 levels and DHA levels in RBC membranes by gas-liquid chromatography/mass spectrometry (GC/MS). After death, the fatty acid composition of each patient's cerebrum and liver was studied. Dietary administration of Lorenzo's oil diminished plasma C26:0 levels. Earlier administration of Lorenzo's oil was more effective and the response did not depend on the duration of administration. DHA was incorporated into RBC membrane lipids when administrated orally, and its level increased for several months. The final DHA level was correlated with the duration of administration and was not related to the timing of initiation of treatment. DHA levels in the brains and livers of treated patients were higher than in untreated patients. Early initiation of Lorenzo's oil and the long-term administration of DHA may be useful for patients with Zellweger syndrome.

C57H104O6

885.4321

884.783

122-32-7

5497163

Colorless to light yellow liquid

0.9±0.1 g/cm3

818.7±55.0 °C at 760 mmHg

-5,5°C

302.7±31.5 °C

0.0±3.0 mmHg at 25°C

1.477

23.71

0

6

53

63

1010

0

O(C(C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])/C(/[H])=C(/[H])\C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])[H])=O)C([H])(C([H])([H])OC(C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])/C(/[H])=C(/[H])\C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])[H])=O)C([H])([H])OC(C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])/C(/[H])=C(/[H])\C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])[H])=O

PHYFQTYBJUILEZ-IUPFWZBJSA-N

InChI=1S/C57H104O6/c1-4-7-10-13-16-19-22-25-28-31-34-37-40-43-46-49-55(58)61-52-54(63-57(60)51-48-45-42-39-36-33-30-27-24-21-18-15-12-9-6-3)53-62-56(59)50-47-44-41-38-35-32-29-26-23-20-17-14-11-8-5-2/h25-30,54H,4-24,31-53H2,1-3H3/b28-25-,29-26-,30-27-

propane-1,2,3-triyl trioleate

Glyceryl trioleate Lorenzo oil Lorenzo's oil Oleic triglyceride Raoline Triolein

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage.  (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~112.94 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (2.35 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

---

Solubility in Formulation 2: ≥ 2.08 mg/mL (2.35 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

---

View More

Solubility in Formulation 3: ≥ 2.08 mg/mL (2.35 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

---

 (Please use freshly prepared in vivo formulations for optimal results.)