SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Commercially supplied radioiodinated triolein has been shown by thin-layer chromatography and silicic acid column chromatography to contain impurities, consisting mainly of diglycerides and monoglycerides, but also a small amount of free fatty acid. The effect of these impurities on the radioiodinated triolein absorption test requires further investigation.
The value of the oral triolein-I(131) "tolerance" test in the study of patients with coronary heart disease was assessed. Thirtynine patients were divided into three groups: those with clinical evidence of coronary heart disease, those with increased risk, and those with no increased risk of coronary heart disease. The variability of the results precluded differentiation between the groups on the basis of this test. A minority of the patients with coronary heart disease showed strikingly elevated blood levels of lipid-bound radioactivity following the oral ingestion of triolein-I(131). It was concluded that this test is of no use in the diagnosis of coronary heart disease but may identify those patients with coronary heart disease who dispose of orally ingested fat in a grossly abnormal fashion.
The intestinal absorption rate of dissolved griseofulvin was determined from: (a) an aqueous phase, (b) an aqueous phase containing a micellar phase composed of taurodeoxycholate, monoolein, and oleic acid, and (c) an aqueous phase containing the micellar phase and emulsified triolein. The triolein digestion mixtures were recirculated through 20-cm segments of in situ rat jejunum. Lipid concentrations were maintained constant by infusing the lipids into the digestion mixture at the same rate as they disappeared. Griseofulvin distribution among the aqueous, micellar, and oil phases was determined by solubility and equilibrium dialysis experiments. Analysis with a linear kinetic model indicated that griseofulvin absorption from the micellar and oil phases was negligible compared to its absorption from the aqueous phase.
Male Wistar rats were pretreated with 3 ml triolein orally for 4 days in addition to their normal diet. A similar control group were allowed free access to normal laboratory food. When given an oral fat load (1 ml triolein) plasma gastric inhibitory polypeptide (GIP) and triglyceride levels were significantly higher in the fat pretreated group. Inhibition of fat-stimulated GIP release by exogenous insulin was demonstrated in the untreated control group (plasma GIP: 663 +/- 49 versus 853 +/- 92 ng/l, mean +/- SEM p less than 0.025), but pretreatment with an oral fat load abolished this effect (plasma GIP: 1008 +/- 95 versus 1116 +/- 100 ng/l, p NS). Plasma glucose levels were significantly higher in fat pretreated rats given oral fat and intraperitoneal insulin compared with untreated controls (plasma glucose nadir 2.6 +/- 0.48 versus 1.6 +/- 0.15 mmol/l, p less than 0.05). Fat-pretreated rats showed significantly higher insulin and glucose levels compared with the untreated rats when given oral glucose (plasma insulin: 6.2 +/- 1.2 versus 2.5 +/- 0.59 micrograms/l, p less than 0.01; plasma glucose: 10.2 +/- 0.39 versus 8.9 +/- 0.41 mmol/l, p less than 0.025). Pretreatment of rats on a high fat diet causes (1) increased GIP secretion in response to an oral fat load, (2) abolition of the feed-back inhibition of exogenous insulin on fat-stimulated GIP release, and (3) some degree of insulin resistance.
Lipolysis of emulsified glycerol tri[9,10-3H]oleate by lipoprotein lipase purified from bovine milk (E.C.3.1.1.34) and by hepatic lipase purified from rat liver perfusate was studied as a function of the phosphatidylcholine molecular species and the cholesterol content of the emulsions. Overall, the activities of the two enzymes were similar on a molar basis. Lipoprotein lipase initial lipolysis rates also were comparable for emulsions made with egg phosphatidylcholine or with saturated (dimyristoyl, dipalmitoyl and distearoyl) phosphatidylcholines when cholesterol was low. Increasing the cholesterol content of the emulsion from 2-3 mole percent to 7-14 mole percent reduced triolein lipolysis by lipoprotein lipase in emulsions made with saturated phosphatidylcholines. Rat hepatic lipase was more sensitive to increased cholesterol in emulsions made with saturated phosphatidylcholines than was lipoprotein lipase. The ability to maintain triolein lipolysis during longer incubations differed strikingly among the emulsions and for the two enzymes. Lymph chylomicrons were better substrates for both enzymes than any of the emulsions.
Refeeding a chow meal containing [1-14C]triolein to food-restricted rats results in increased accumulation of [14C]lipid in carcass and epididymal adipose tissue and lower oxidation to [14C]CO2 compared to ad libitum-fed rats (Biochem. J. 285, 773-778, 1992). In the present experiments the effects of treatment with triiodothyronine (T3) for three days on lipid accumulation in refed food-restricted rats has been examined. T3 decreased accumulation of [14C]lipid in carcass and epididymal adipose tissue (32 and 77%, respectively) of food-restricted rats on refeeding the chow-[1-14C]triolein meal. This decreased accumulation of [14C]lipid was accompanied by increased [14C]CO2 production (77%) and decreased heparin-elutable lipoprotein lipase activity in the epididymal fat pad (90%) and subcutaneous adipose tissue (80%). Accumulation of [14C]lipid in the latter did not decrease significantly. In contrast, T3 treatment of ad libitum-fed rats increased [14C]lipid deposition in carcass (44%) and in subcutaneous adipose tissue (240%) on refeeding, when compared to untreated ad libitum rats. Lipoprotein lipase activity in the two adipose tissue depots of the refed ad libitum+T3 rats, however, decreased. Thus, the effects of T3 on [14C]lipid deposition are adipose-tissue-depot-specific and depend on the previous dietary intake (over 14 days) of the rat. T3-treatment increased the lipoprotein lipase activity released from perfused hearts to a similar extent in both food-restricted and ad libitum-fed rats compared to the corresponding untreated groups. The rates of lipogenesis in-vivo in liver, epididymal and subcutaneous adipose tissue of food-restricted rats refed chow were not altered by T3. It is concluded that the increased deposition of dietary lipid in the food-restricted rat can be partially reversed by treatment with T3, suggesting that the low-T3 state associated with this condition may be in part responsible.
The electrical potential across a fine pore membrane doped with trioleoyl glyceride (triolein) and separating aqueous solutions of 0.5M NaCl and 0.5M KCl, respectively, was studied. It was found that this system showed rhythmic and sustained oscillations of electrical potential between the two aqueous solutions. These oscillations were attributed to the change of permeability of Na+ and K+ ions across the membrane, which originated from the phase-transition of triolein molecules within the fine pores.
Periodic oscillations of electric potential were induced by DC electric current between identical salt solutions separated by a membrane filter impregnated with triolein. The oscillation period was controlled by the base electric potential, and temperature dependence of base conductance and conductance amplitude were both close to that of the electric conductivity of the aqueous salt solution. Effects of salt concentration on membrane conductance and on oscillation characteristics were experimentally investigated, and the lifetime of the membrane and of each oscillation were much improved by regulating the concentration of the salt solution. Moreover, characteristics of oscillation curves could be controlled. All the experimental results could be explained by a model where the oscillation was generated by a periodic change of the diameter of a hole through the membrane, which opened in one of the pores filled with triolein.
Interleukin 15 (IL-15) has previously been shown to have important effects on lipid metabolism in adipose tissue, particularly influencing the rate of the de novo fatty acid synthesis. The results presented here show that chronic administration to rats (100 microg/kg body weight) has important effects on the metabolic fate of an exogenous [(14)C]-triolein load, decreasing the incorporation of lipid into adipose tissue and significantly increasing the total (14)CO(2) formation from [(14)C]-triolein. Skeletal muscle and possibly liver seem to be the main organs involved in the action of IL-15 on lipid oxidation, since the presence of the cytokine in incubated EDL muscle with [(14)C]-palmitic acid increased (14)CO(2) formation by 39%. Concerning the mechanism, the results suggest that the transport of fatty acids into mitochondria could be involved in the action of IL-15 since the cytokine clearly increases the presence of L-CPT-I and CPT-II in liver tissue. In addition, IL-15 treatment resulted in a significant increment in the gene expression of PPARdelta, a transcription factor clearly related with lipid catabolism in many tissues. Altogether, the results presented here suggest that IL-15 alters exogenous lipid partitioning, limiting adipose tissue uptake and favouring oxidation.
The thermotropic properties of triolein-rich, low-cholesterol dipalmitoyl phosphatidylcholine (DPPC) emulsion particles with well-defined chemical compositions (approximately 88% triolein, 1% cholesterol, 11% diacyl phosphatidylcholine) and particle size distributions (mean diameter, approximately 1000-1100 A) were studied in the absence and presence of apolipoprotein-A1 by a combination of differential scanning and titration calorimetry. The results are compared to egg yolk PC emulsions of similar composition and size. Isothermal titration calorimetry at 30 degrees C was used to saturate the emulsion surface with apo-A1 and rapidly quantitate the binding constants (affinity Ka = 11.1 +/- 3.5 x 10(6) M-1 and capacity N = 1.0 +/- 0.09 apo-A1 per 1000 DPPC) and heats of binding (enthalpy H = -940 +/- 35 kcal mol-1 apo-A1 or -0.92 +/- 0.12 kcal mol-1 DPPC). The entropy of association is -3070 cal deg-1 mol-1 protein or -3 cal deg-1 mol-1 DPPC. Without protein on the surface, the differential scanning calorimetry heating curve of the emulsion showed three endothermic transitions at 24.3 degrees C, 33.0 degrees C, and 40.0 degrees C with a combined enthalpy of 1.53 +/- 0.2 kcal mol-1 DPPC. With apo-A1 on the surface, the heating curve showed the three transitions more clearly, in particular, the second transition became more prominent by significant increases in both the calorimetric and Van't Hoff enthalpies. The combined enthalpy was 2.70 +/- 0.12 kcal mol-1 DPPC and remained constant upon repeated heating and cooling. Indicating that the newly formed DPPC emulsion-Apo-A1 complex is thermally reversible during calorimetry. Thus there is an increase in delta H of 1.17 kcal mol-1 DPPC after apo-A1 is bound, which is roughly balanced by the heat released during binding (-0.92 kcal) of apo-A1. The melting entropy increase, +3.8 cal deg-1 mol-1 DPPC of the three transitions after apo-A1 binds, also roughly balances the entropy (-3 cal deg-1 mol-1 DPPC) of association of apo-A1. These changes indicate that apo-A1 increases the amount of ordered gel-like phase on the surface of DPPC emulsions when added at 30 degrees C. From the stoichiometry of the emulsions we calculate that the mean area of DPPC at the triolein/DPPC interface is 54.5 A2 at 41 degrees C and 54.2 A2 at 30 degrees C. The binding of apo-A1 at 30 degrees C to the emulsion reduces the surface area per DPPC molecule from 54.2 A2 to 50.8 A2. At 30 degrees apo-A1 binds with high affinity and low capacity to the surface of DPPC emulsions and increases the packing density of the lipid domain to which it binds. Apo-A1 was also titrated onto DPPC emulsions at 45 degrees C. This temperature is above the gel liquid crystal transition. No heat was released or adsorbed. Furthermore, egg yolk phosphatidylcholine emulsions of nearly identical composition were also titrated at 30 degrees C with apo-A1 and were euthermic. Association constants were previously measured using a classical centrifugation assay and were used to calculate the entropy of apo-A1 binding (+28 cal deg-1 mol-1 apo-A1). This value indicates that apo-A1 binding to a fluid surface like egg yolk phosphatidylcholine or probably DPPC at 45 degrees C is hydrophobic and is consistent with hydrocarbon lipid or protein moities coming together and excluding water. Thus the binding of apo-A1 to partly crystalline surfaces is entropically negative and increases the order of the already partly ordered phases, whereas binding to liquid surfaces is mainly an entropically driven hydrophobic process.
Interfacial tensions of egg yolk phosphatidylcholine (PC) and cholesterol monolayers adsorbed at the triolein-saline interface were measured in the presence and absence of pig apolipoprotein A-1 (apoA-1) in the saline phase. In the absence of apoA-1, the adsorptions of PC and cholesterol at the interface from the triolein phase are cooperative, showing large lateral attractive interactions between the PC molecules and the cholesterol molecules in the monolayer. In the presence of apoA-1, the PC adsorption is anti-cooperative, indicating strong lateral attractive interactions between the PC and the apoA-1 molecules, i.e., apparently, repulsive lateral interactions between the PC molecules. On the other hand, lateral interactions of very low magnitude are observed between the cholesterol and apoA-1 molecules in the monolayer. Values of the lateral interaction energy are evaluated from the adsorption data by the Defay-Prigogine-Flory theory of monolayers. The large difference in lateral interaction energy with apoA-1 between PC and cholesterol in a mixed monolayer is discussed in connection with current problems in lipoprotein catabolism: reverse cholesterol transport, alterations in affinity of lipid particles to apoA-1, and formation of high-density lipoproteins and abnormal lipoproteins.
In this paper we report an extension of our previous work on the triolein-embedded cellulose acetate membrane (TECAM) as a passive sampling device (PSD) and describe the results from simultaneous exposure of TECAMs and triolein-containing semipermeable membrane devices (SPMDs) to PAHs in lake water for 16 days. The data obtained provided a comparison of the uptake rates of specific PAHs by the two PSDs. Using 16-day accumulation tests, similar PAH distribution patterns in TECAMs and in SPMDs (R2 = 0.89, p < 0.0001) were observed. However, it was noted that TECAMs could take up greater amounts of PAHs than SPMDs (735 ng/g of TECAM vs 630 ng/g of SPMD). Uptake rate constants of TECAMs and SPMDs for 16 priority pollutant (PP) PAHs, corrected for dissolved organic carbon, ranged from 0.28 to 2.94 L d(-1) and from 0.16 to 0.91 L d(-1), respectively. The elimination rate constants of TECAMs were 1.4-6.7 times greater than those observed for SPMDs, thereby indicating that PAHs required shorter times to achieve equilibrium in TECAMs than in SPMDs. Thus, the results of the present study suggest that TECAMs have significant potential as a good monitor to assess the pollution of hydrophobic pollutants in aquatic environments.
The effect of high-temperature treatment on the stability of alpha-tocopherol (1) in triolein was assessed under a reduced-pressure atmosphere (4-40 mbar) simulating the deodorization step of the refining of vegetable oils. A marked degradation of 1 was observed, which increased with increasing temperature (180-260 degrees C) and heating time (20-80 min). The degradation of 1 in triolein at 240 degrees C was inhibited by the addition of the synthetic antioxidant TBHQ or when heating was performed under nitrogen atmosphere, indicating oxidative degradation. The oxidation products were isolated and identified as alpha-tocopherolquinone (2), 4a,5-epoxy-alpha-tocopherolquinone (3), and 7,8-epoxy-alpha-tocopherolquinone (4).
1. The effects of starvation and refeeding on the disposal of oral [14C]triolein between 14CO2 production and 14C-lipid accumulation in tissues of virgin rats, lactating rats and lactating rats with pups removed were studied. 2. Starvation (24 h) increased 14CO2 production in lactating rats and lactating rats with pups removed to values found in virgin rats. This increase was accompanied by decreases in 14C-lipid accumulation in mammary gland and pups of lactating rats and in white and brown adipose tissue of lactating rats with pups removed. 3. Short-term (2 h) refeeding ad libitum decreased 14CO2 production in lactating rats and lactating rats with pups removed, and restored the 14C-lipid accumulation in mammary glands plus pups and in white and brown adipose tissue respectively 4. Insulin deficiency induced with mannoheptulose inhibited the restoration of 14C-lipid accumulation in white adipose tissue on refeeding of lactating rats with pups removed, but did not prevent the restoration of 14C-lipid accumulation in mammary gland. 5. Changes in the activity of lipoprotein lipase in mammary gland and white adipose tissue paralleled the changes in 14C-lipid accumulation in these tissues. 6. It is concluded that 14C-lipid accumulation in mammary gland may not be affected by changes in plasma insulin concentration and that it is less sensitive to starvation than is lipogenesis or lactose synthesis. This has the advantage that the milk lipid content can still be maintained from hepatic very-low-density lipoprotein for a period after withdrawal of food. The major determinant of the disposal of oral 14C-triolein appears to be the total tissue activity of lipoprotein lipase. When this is high in mammary gland (fed lactating rats) or white adipose tissue (fed lactating rats with pups removed), less triacylglycerol is available for the muscle mass and consequently less is oxidized.
The effects of insulin deficiency (streptozotocin-induced) or insulin plus prolactin deficiency on the disposal of orally administered [1-14C]triolein between oxidation to 14CO2, uptake by mammary gland and transfer to suckling pups were studied. Insulin deficiency decreased mammary-gland total weight (by 40%), but caused no change in total tissue DNA. A greater proportion of the [1-14C]triolein was oxidized to 14CO2 (120% increase) in the insulin-deficient rats, and there was a tendency for total transfer of [14C]lipid to mammary gland and suckling pups to be decreased. A parallel decrease in total mammary-tissue lipoprotein lipase activity occurred. Combined hormone deficiency caused more dramatic changes in all parameters measured. Replacement of insulin (24 h) in insulin-deficient rats decreased 14CO2 production, increased the uptake of [14C]lipid into the mammary gland and tended to increase total lipoprotein lipase activity. In contrast, administration of prolactin to insulin-deficient rats had no effect on any of the parameters measured. Replacement of insulin (24 h) in the combined hormone-deficient rats increased uptake of [14C]lipid and lipoprotein lipase approx. 3-fold, whereas prolactin again had no significant effects. Replacement of both hormones increased (6-fold) transfer of [14C]lipid to the pups, but did not increase overall uptake of [14C]lipid (mammary gland, milk clot and pups) above the value for insulin alone. It is concluded that insulin is the primary regulator of triacylglycerol uptake and of lipoprotein lipase activity in the lactating mammary gland of the rat and that the action of prolactin on these processes is indirect. Prolactin, but not insulin, appears to have a direct effect on milk lipid transfer to pups.
Orlistat, a selective inhibitor of gastrointestinal lipases, was used to investigate triacylglycerol absorption. Using mice and a variety of emulsified dietary lipids we found that the absorption of radiolabelled tripalmitin (containing the fatty acid 16:0), but not of triolein (18:1n-9) or tri-gamma-linolenin (18:3n-6), was incomplete from meals rich in esterified palmitate. Further, the absorption of radiolabelled tri-gamma-linolenin, from both saturated and unsaturated dietary triacylglycerols, was 1.3- to 2-fold more potently inhibited by orlistat than that of triolein and tripalmitin. These radiolabelled triacylglycerols, which have the same fatty acid in all three positions, may not always be accurate markers of the absorption of dietary triacylglycerols. Orlistat was more effective at inhibiting the absorption of radiolabelled triacylglycerols with which it was codissolved than those added separately, which indicates that equilibration between lipid phases in the stomach may not always be complete. The saturation of the dietary lipid had little or no effect on the potency of orlistat. Orlistat provides a novel approach for studying the role of triacylglycerol hydrolysis in the overall process of triacylglycerol absorption.
The absorption of 14C triolein in a standard fat meal was measured in 60 controls and 66 patients with gastrointestinal disorders by 14CO2 breath sampling. A reference range based upon cumulative eight hour values of the controls was independent of height, weight, and sex. The range was of log normal distribution and declined with age (p less than 0.05). Acceptable 'within-day' and 'between-day' reproducibility was found. All patients tested with untreated coeliac disease, pancreatic insufficiency and most with symptomatic small intestinal Crohn's disease had subnormal values. Twenty per cent of those with irritable bowel syndrome had subnormal values. Patients with ulcerative colitis were all normal. The reagents used and the breath samples after collection were stable. In our experience the 14C triolein test is simple, inexpensive, and helpful in the detection of diseases associated with fat malabsorption. It is of value in monitoring the response to treatment of individual patients with coeliac disease.
The 14C-triolein breath test, a recognised index of fat absorption, and the p-aminobenzoic acid (PABA) test, a 'tubeless' test of exocrine pancreatic function, have both been widely used in the diagnosis of malabsorption and exocrine pancreatic insufficiency. This study evaluates the potential of a combination of both tests in the investigation of fat absorption and exocrine pancreatic function. Combination of the tests has become technically feasible because of the introduction of high pressure liquid chromatography as the preferred method of analysis for PABA, and use of p-aminosalicylic acid (PAS) as the marker for PABA absorption and metabolism. We studied 25 healthy subjects, 11 patients with exocrine pancreatic disease and 12 patients with gastrointestinal disease. The combined test identified subjects with reduced fat absorption and distinguished subjects with exocrine pancreatic insufficiency from those with an intestinal cause of fat malabsorption. The test could be completed in 7 h and had high patient acceptability. These findings suggest that the combined 14C-triolein breath test and PABA test can be used as a non-invasive, 1-day investigation of fat absorption and exocrine pancreatic function.