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PubMed1994

Serum triglycerides in the prediction of coronary artery disease (an Italian experience).

An occupational group living in Rome and composed of 3,007 men aged 46 to 65 years who were free from previous major coronary events was screened for a number of coronary risk factors and then followed up for 10 years. In all, 107 coronary deaths occurred in 10 years. There was a positive relation between coronary death rate and increasing levels of triglycerides, but the difference between the extreme quintile classes was not any more significant after adjustment for cholesterol levels. A cross-classification involving low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol and triglyceride levels showed a higher coronary artery disease (CAD) mortality in subjects with a higher LDL cholesterol/HDL cholesterol ratio and higher triglycerides. However, the excess risk in this subgroup was largely explained by the mean levels of total cholesterol. The multivariate proportional-hazards Cox model with coronary deaths as the end point, and age and triglycerides as predictors, produced a significant coefficient for triglycerides that became nonsignificant when other lipids alone or in combination (total, HDL and LDL cholesterol and some of their ratio) were fed into the model as further covariates. It is concluded that there is no evidence of an independent role of triglycerides in the prediction of coronary deaths.

Age Factors↗
PubMed1988

Preparation of human cord sera for enzymatic triglyceride assays: removal of free glycerol by ultrafiltration.

Enzymatic triglyceride assays that generate glycerol from triglycerides as a part of the enzymatic process in quantitating serum triglyceride levels give elevated values when external free glycerol is present. Our objective was to develop an ultrafiltration technique that would remove exogenous and/or endogenous free glycerol from small aliquots of human cord sera so that accurate serum triglyceride values could be obtained with the commercially available triglyceride assay kits. Exogenous glycerol was completely removed from cord sera when the samples were washed twice with saline in Amicon Centricon-30 microconcentrators. This ultrafiltration technique lowered cord serum triglyceride levels significantly (P less than 0.001), but had no effect on cord total serum cholesterol levels. A comparison of washed and unwashed cord sera by either polyacrylamide or agarose gel electrophoresis indicated that the serum protein and lipoprotein profiles were not altered by the ultrafiltration process.

Cholesterol↗
PubMed1979

Validation of a procedure for exogenous isotopic labeling of lipoprotein triglyceride with radioactive triolein.

A procedure has been developed for the exogenous isotopic labeling of triglyceride-rich lipoproteins (chylomicrons and very low density lipoproteins) using high specific activity radioactive triglyceride in the presence of aqueous dimethyl sulfoxide. The labeled product lipoproteins showed unchanged chemical and physical properties. When the particles had also been labeled biologically by incorporation of unesterified fatty acids into the triglycerides of lipoproteins secreted by liver or intestine, both endogenous and exogenous labels were removed at the same rates in the isolated perfused heart and liver or in intact or functionally hepatectomized rats. These experiments additonally indicated that the triglyceride fatty acid composition of chylomicrons and very low density lipoproteins was unchanged during triglyceride depletion in the peripheral tissues. Using such labeled lipoproteins it has been shown that uptake of remnant lipoprotein cholesteryl ester and triglyceride by the liver is simultaneous. The labeling procedure described should prove suitable for kinetic studies of the disposition of the various lipoprotein non-polar ('core') lipids.

Animals↗
PubMed1986

The role of the hepatocellular redox state in the hepatic triglyceride accumulation following acute ethanol administration.

The role of the increased hepatocellular redox-state [( NADH]/[NAD+] ratio) as a mechanism underlying hepatic triglyceride deposition after acute ethanol dosing has been investigated in the rat. Following a single dose of ethanol (2 g/kg i.p.) in fasted rats, increases were observed at 1.5 hr in the hepatic [lactate]/[pyruvate] (133%), [3-hydroxybutyrate]/[acetoacetate] (69%) ratios, and the liver triglyceride concentration (129%). At the same time point, ethanol increased radioactivity incorporated into hepatic total lipid and triglyceride, after an injection of [U-14C] palmitic acid, by 76% and 158% respectively. Treatment of animals with Naloxone hydrochloride (2 mg/kg i.p.) at 1.0 hr and 2.5 hr after ethanol abolished these ethanol-mediated redox-state changes, without inhibiting ethanol oxidation or affecting hepatic acetaldehyde levels. This, however, did not prevent completely the triglyceride accumulation in the liver or reverse the enhanced uptake of radio-labelled palmitate caused by ethanol. Administration of sorbitol (3.5 g/kg i.p.) caused 109%, 57% and 200% increases in the hepatic [lactate]/[pyruvate], [3-hydroxybutyrate]/[acetoacetate] ratios and glycerol-3-phosphate concentrations respectively. However, the hepatic triglyceride concentration and the incorporation of [U-14C] palmitic acid into hepatic lipids were not influenced by this treatment. In vitro studies in which rat liver slices were incubated with [1-14C] palmitic acid also indicated that the altered [NADH]/[NAD+] ratio was not responsible for the decreased rate of fatty acid oxidation seen after ethanol administration or after the addition of ethanol to the incubation medium. In conclusion, these experiments indicate that increases in the hepatic [NADH]/[NAD+] ratio resulting from ethanol oxidation may not be directly implicated in the altered hepatic fatty acid utilisation and triglyceride deposition observed after acute ethanol administration in rats.

Acetaldehyde↗
PubMed1991

Fatty acid composition of hepatic triglycerides in Reye's syndrome: implications for hepatic desaturase abnormalities.

Serum NEFA profiles in Reye's syndrome are reportedly unique with a disproportionate percent made up of polyunsaturated fatty acids some of which are not ordinarily found in the serum. This pattern is also reflected in the serum triglyceride composition as well. As the liver is probably the sole source of the serum triglyceride in Rye's syndrome because patients are vomiting or in coma, the fatty acid acid composition of the liver triglyceride was examined for insight regarding the lipid abnormalities in this disease. Palmitic acid (16:0) and the sum of all the saturated fatty acids in the liver triglycerides were significantly decreased whereas the sum of the monoenoic fatty acids and the products of delta 9 desaturase activity were increased in Reye's samples. When these data were compared to the fatty acid composition of the serum triglyceride from a separate cohort of Reye's and control subjects, certain inferences regarding hepatic delta 9, delta 6, delta 5, and delta 4 desaturase activities and the elongases can be drawn from the liver and serum triglyceride fatty acid profiles which are unique. Collectively, these data reflect considerable intrahepatic fatty acid desaturation and elongation activity and/or acyl transfer from lipid to lipid of various polyunsaturated fatty acids in Reye's syndrome.

Adolescent↗
PubMedDate not supplied

Transport kinetics of plasma free fatty acid, very low density lipoprotein triglycerides and apoprotein in patients with endogenous hypertriglyceridaemia: effects of 2,2-dimethyl, 5(2, 5-xylyoxy) valeric acid therapy.

The effects of C1-719 on plasma lipid and lipoprotein concentrations have been examined in four patients with endogenous hypertriglyceridaemia maintained on an isocaloric diet for a period of 6 months. During therapy (400 mg/day) the mean plasma triglyceride and cholesterol concentrations were reduced by 35% and 15% respectively, while the administration of 800 mg/day reduced these by 49% and 31%. This hypolipidaemic effect was due to a reduction in the circulating level of very low density lipoproteins (VLDL) without a change in their composition. Before treatment the plasma VLDL triglyceride turnover, and FFA flux, were higher than that of normal subjects maintained on a similar diet. The plasma VLDL B-apoprotein turnover was similarly higher than in the controls. Administration of C1-719 decreased the plasma VLDL triglyceride turnover, FFA flux and VLDL B-approtein turnover. The drug reduced the insulin response following a glucose load with some decrease in glucose levels. The results suggest that the increase in plasma triglyceride concentration in patients with endogenous hypertriglyceridaemia is due to increased production of plasma VLDL triglyceride and its apoptein associated with an enhanced supply of FFA for hepatic triglyceride synthesis. C1-719 exerts a hypolipidaemic effect through a reduction of VLDL production, consequent upon inhibition of lipolysis as well as decreased synthesis of the apoprotein carrier. These effects could in part be explained by an improvement in peripheral tissue responsiveness to insulin and decreased exposure of the liver to high levels of insulin. However, a direct effect of the drug on adipose tissue and liver metabolism has to be considered.

Adult↗
PubMed1979

Species differences in the activity of a serum triglyceride transferring factor.

Low density lipoproteins (LDL), endogenously labelled with 3H in the triglyceride moiety, were isolated from rabbit serum and subsequently incubated in vitro at 37 degrees C with unlabelled preparations of rabbit high density lipoproteins (HDL) or very low density lipoproteins (VLDL). In incubations performed in the presence of phosphate buffer, there was no significant transfer of [3H]triglyceride from LDL to either HDL or VLDL; but when rabbit lipoprotein-free serum (the dialysed 1.21 g/ml infranatant) was added, transfer was apparent to both HDL and VLDL. The triglyceride transferring activity of the lipoprotein-free serum was abolished by heating at 85 degrees C for 10 min; all the transferring activity was found in the fraction which precipitated with ammonium sulphate at a concentration of less than 50% saturation. In direct contrast to the rabbit studies, rat serum failed to show a comparable process of triglyceride transfer. In subsequent experiments, mixtures of labelled LDL and unlabelled VLDL isolated either from rabbits or from rats were incubated with lipoprotein-free rabbit, rat or human serum. The lipoprotein-free serum of both the rabbit and man was effective in promoting transfer of 30--50% of LDL [3H]triglyceride into VLDL, regardless of the species origin of the lipoproteins. By contrast the lipoprotein-free serum of rats was only slightly more effective than buffer alone in promoting such transfers. It has been concluded that rabbit and human serum contains a triglyceride transferring factor of far greater activity than that in rat serum.

Adolescent↗
PubMed1983

Effects of dietary fat saturation and triglyceride and cholesterol load on lipid absorption in the rat.

Lipid absorption was studied in non-fasting thoracic lymph duct-cannulated rats receiving continuous intraduodenal infusions of oils varying in triglyceride fatty acid saturation (P/S = 4.6 or 0.2), triglyceride load (66 or 165 mumoles/h) and cholesterol load (0 and 3.5 mumoles/h at the low oil infusion rate, and 0 and 11 mumoles/h at the high infusion rate). Triglyceride absorption averaged 95% for rats receiving the low and high infusion rates of the polyunsaturated oil (groups defined as 10P and 25P, respectively), and 77% for those receiving the saturated oil (10S and 25S). Estimated average relative lymph lipoprotein size was significantly larger during infusion of the high vs. low triglyceride load, and of the P vs. S oil (25P greater than 25S greater than 10P greater than 10S). Lymph cholesterol flux during infusion of oil only averaged 3.2 mumoles/h for all groups and was not significantly influenced by dietary fat saturation or triglyceride load. The initial rapid rise in lymph cholesterol after addition of cholesterol (mass + tracer) to the oils was due primarily to endogenous cholesterol. Thus, absorption of dietary cholesterol resulted in an initial displacement of endogenous cholesterol into the lymph. However, in samples collected 18--24 h after addition of cholesterol to the oil, 87--107% of the increased lymph cholesterol flux was exogenous (labeled). This increased flux was not significantly influenced by fat saturation of the infused oil and averaged 5.6 mumoles/h for rats in the low oil/lower cholesterol infusion groups, and 9.5 mumoles/h for those in the higher infusion groups. The percent esterified cholesterol in lymph of rats in the low oil infusion groups was significantly higher in the S vs. P animals during both infusion of oil only and of oil + cholesterol. The observed effects of fat saturation on lymph triglyceride flux, cholesterol esterification and lipoprotein size may have important consequences for subsequent metabolism of absorptive lipoproteins, and for their ultimate effects on plasma lipid levels.

Absorption↗
PubMed1983

Cholesterol content as a possible determinant in the removal of chylomicron triglyceride by the liver.

The nature of chylomicron removal from the circulation and the role of the liver in this process have been investigated by measuring the removal of chylomicron triglyceride and cholesterol from the plasma of normal and functionally hepatectomized rats. The rate of removal of chylomicron triglyceride exceeded that of both free and esterified cholesterol in all animals. Whereas chylomicrons were completely removed from the circulation of normal rats soon after intravenous injection, chylomicron remnant particles accumulated in the plasma very low density lipoprotein and chylomicron fractions of hepatectomized rats. The rate of removal of chylomicron triglyceride from the blood of the hepatectomized rats decreased when the cholesterol content of the chylomicrons was elevated. In addition, more chylomicron triglyceride remained in the circulation of the hepatectomized rats when the chylomicrons were enriched with cholesterol and the remnant particles derived from these chylomicrons were of lower average density. These observations indicate that the cholesteryl ester content of the chylomicrons influences the degree of triglyceride removal in extrahepatic tissue capillaries and thereby the amount of residual triglyceride in the remnant particles subsequently removed by the liver.

Animals↗
PubMed1984

Accelerated turnover of very low density lipoprotein triglycerides in chronic alcohol users. A possible mechanism for the up-regulation of high density lipoprotein by ethanol.

The concentration of high density lipoproteins (HDL) is related to the catabolism of triglyceride-rich lipoproteins. In order to elucidate the mechanisms by which alcohol increases plasma HDL levels we measured the turnover kinetics of very low density lipoprotein (VLDL) triglycerides in 10 alcoholic men without liver disease and in nonalcoholic control men matched for age, weight and plasma VLDL triglyceride level. The study was repeated in the alcoholics after a 2-week abstinence period. The alcoholic men had elevated HDL cholesterol but reduced low density lipoprotein (LDL) cholesterol as compared to the controls. The fractional catabolic rate and the total turnover (production) rate of VLDL triglycerides were both significantly increased (P less than 0.05) in the alcoholic men before abstinence. After withdrawal of alcohol both the synthetic rate and the catabolic rate of VLDL triglycerides returned to normal and the HDL (HDL2 and HDL3) cholesterol fell. The per cent decrease in HDL2 cholesterol during abstinence was positively correlated to the respective fall of VLDL triglyceride fractional catabolic rate (r = +0.51). The results suggest that the absence of hypertriglyceridemia and the elevated levels of HDL in regular alcohol users may be partly based on increased metabolic clearance of VLDL particles and on subsequent accelerated transfer of the VLDL surface components to HDL.

Adult↗
PubMed1985

Lipoprotein fractions, lipoprotein lipase and hepatic triglyceride lipase during short-term and long-term uptake of ethanol in healthy subjects.

In short-term experiments, healthy fasting persons were given a basic dose of 0.5 g of ethanol/kg body weight, followed by hourly maintenance doses of 0.15 g of ethanol/kg body weight. After 10 h there was a significant increase of triglycerides in the VLDL, LDL, and HDL, the main rise (from 42 to 92 mg/dl) being found in the VLDL triglycerides. Other subjects, who received nourishment isocaloric with ethanol, likewise showed a significant rise of triglycerides in all lipoprotein fractions. Chylomicron triglycerides increased from 9.3 to 35.5 mg/dl. There was no significant change in postheparin HTGL, but postheparin LPL activity decreased after 10 h from 17.9 to 12.2 mmol FFA/ml/h in the fasting subjects, and from 28.5 to 10.2 mmol/FFA/ml/h in the persons receiving food. In long-term experiments after 4 weeks of 70 - 80 g of ethanol and isocaloric food daily, triglycerides increased, especially in the VLDL (from 50 to 82 mg/dl). The increase in the HDL, however, was also significant. After 4 weeks of ethanol, the chylomicron triglycerides in the plasma of the fasting subjects reached a value of 29.3 mg/100 ml, LDL cholesterol decreased, and HDL cholesterol increased. After 4 weeks of ethanol there was an increase in the lipoprotein lipase of the adipose tissue.

Adult↗
PubMed1988

Evidence for an inverse relation between plasma triglyceride and aortic cholesterol in the coconut oil/cholesterol-fed rabbit.

Rabbits fed a commercial chow diet containing 0.5% cholesterol and 14% coconut oil developed more severe hyperlipidemia and atherosclerosis than rabbits fed the same diet containing olive oil in place of coconut oil. Average plasma cholesterol was twice as high in the coconut oil/cholesterol-fed rabbits than in olive oil/cholesterol-fed rabbits. Final plasma triglycerides, although highly variable, were approx. 20-fold higher than basal plasma triglyceride in coconut oil/cholesterol-fed rabbits; plasma triglyceride in olive oil/cholesterol-fed rabbits remained unchanged throughout the study period. In coconut oil/cholesterol-fed rabbits, a direct relationship between plasma triglyceride and aortic cholesterol was not found. Plasma cholesterol and aortic cholesterol were also not correlated at a statistically significant level (r = 0.26, P greater than 0.25). However, when both plasma cholesterol and triglyceride were simultaneously introduced as predictors of aortic cholesterol, the correlation between these plasma lipids and aortic cholesterol became highly significant (r = 0.64, P less than 0.02). Aortic cholesterol increased in proportion to plasma cholesterol concentrations but appeared to be inversely related to plasma triglyceride levels.

Animals↗
PubMed1991

An investigation of the role of lecithin:cholesterol acyltransferase and triglyceride-rich lipoproteins in the metabolism of pre-beta high density lipoproteins.

Small high density lipoproteins (HDL) with pre-beta electrophoretic mobility (pre-beta HDL) have recently been shown to be the primary acceptor of cholesterol from cultured cells. We studied the metabolism of these particles by incubating serum at 37 degrees C in the presence and absence of active lecithin: cholesterol acyltransferase (LCAT). We found that the serum pre-beta HDL concentration decreased in the presence of LCAT, but when LCAT was inhibited the concentration remained constant, or increased, depending on the method of inhibition. This suggests that pre-beta HDL are a substrate for LCAT. We also found a significant negative correlation between levels of LCAT activity and pre-beta HDL in 28 fasting healthy subjects, this provides evidence that the activity of LCAT regulates, at least in part the concentration of these particles in vivo. During the early phase of incubation there was a more rapid decrease in pre-beta HDL concentration which was greater in the post-prandial than fasting state. When we infused a triglyceride emulsion into 6 subjects or added this to serum in vitro we observed an immediate fall in pre-beta HDL concentration. These findings suggest that pre-beta HDL interact with triglyceride rich particles. We investigated the origin of pre-beta HDL from blood lipoproteins during their lipolysis, in vivo and in vitro and found that they were produced from both triglyceride-rich and high-density lipoproteins. Formation from triglyceride-rich lipoproteins was evident by the rise in pre-beta HDL concentration during heparin-induced lipolysis when fasting and post-prandially. The rise was greater post-prandially and particularly marked in 4 hypertriglyceridaemic patients following a fat load. Generation from alpha-HDL was evident when we prolonged the action of the heparin-released lipases by incubation of post-heparin sera at 37 degrees C. Continued formation of pre-beta HDL occurred at an equal rate in the fasting and post-prandial samples suggesting release by lipolysis of alpha-HDL. This was supported by the action of lipases on serum and isolated HDL in vitro, where triglyceride lipase rather than phospholipase activity appeared more effective at releasing pre-beta HDL. These findings suggest binding and release of pre-beta HDL by triglyceride-rich lipoproteins depending on the prandial state and production from alpha-HDL through the action of lipases.

Adolescent↗
PubMed1993

Metabolism of apolipoprotein B-100 and of triglyceride-rich lipoprotein particles in the absence of functional lipoprotein lipase.

Cholesterol and triglyceride in the various lipoprotein fractions were determined in five patients without functional lipoprotein lipase (LPL) while on their habitual therapeutic diet of 'low fat' content (20-25 g/day). They were also studied following 3 days on either a 'minimal fat' diet (< 15 g/day) or a 'moderate fat' diet (45-50 g/day). Values obtained were compared with the respective levels measured in five control subjects on a 'normal fat' (70-90 g/day) diet. The patients had hypertriglyceridaemia (type V hyperlipoproteinaemia) under all dietary conditions. Cholesterol and triglyceride levels in plasma and in the chylomicron fraction increased in the patients with increasing dietary fat. In the very low density lipoprotein (VLDL) fraction from the patients, triglyceride levels also increased with the dietary fat intake, but cholesterol levels were similar under all dietary conditions. In the patients, cholesterol concentrations in the low (LDL) and high density (HDL) lipoprotein fractions were significantly lower than the respective levels in controls, but the ratio of cholesterol to triglyceride levels in both of these lipoprotein fractions decreased with the dietary fat intake. VLDL apolipoprotein B-100 (apo B-100) pool size was similar in the patients on the two test diets (P = 0.95) and 3.5-fold higher than in five healthy volunteers on a normal fat diet. Using a stable isotope enrichment method, the kinetics of apo B-100 were investigated in the patients under the last two dietary conditions. The fractional and absolute secretion rates of the apolipoprotein in the patients did not vary with fat intake, but fractional secretion rates were significantly lower and the absolute secretion rates were significantly higher in the patients than the respective values in the controls. These results are consistent with the hypothesis that in the absence of LPL activity the metabolism of chylomicron and VLDL particles in the circulation results in triglyceride-rich LDL and HDL particles that are taken up by the liver at increased rates, thus reducing the plasma LDL and HDL cholesterol concentrations, whereas the products of hydrolysis of these particles induce an increased rate of synthesis of triglyceride and an increased rate of secretion of VLDL apo B-100.

Adult↗
PubMed1994

Role of plasma triglyceride in the regulation of plasma low density lipoprotein (LDL) subfractions: relative contribution of small, dense LDL to coronary heart disease risk.

The concentration of plasma LDL subfractions is described in four groups of normocholesterolaemic (total plasma cholesterol < 6.5 mmol/l) male subjects consisting of men with and without coronary artery disease (CAD+/-), as determined by angiography, post-myocardial infarct survivors (PMI) and normal, healthy controls. The CAD(+) and PMI groups were distinguished from the CAD(-) and controls by raised concentrations of plasma triglyceride, very low density lipoprotein (VLDL) cholesterol, small, dense LDL (LDL-III density (d) 1.044-1.060 g/ml) and lower concentrations of high density lipoprotein (HDL) cholesterol and large, buoyant LDL (LDL-I d 1.025-1.034 g/ml). In all groups, a subfraction of intermediate density, LDL-II (d 1.034-1.044 g/ml), was the predominant LDL species but was not related to coronary heart disease risk. Plasma triglyceride showed a positive association with LDL-II (r = 0.51, P < 0.001) below a triglyceride level of 1.5 mmol/l. Above this threshold of 1.5 mmol/l, LDL-II and LDL-I showed significant negative associations with triglyceride (LDL-II r = -0.5, P < 0.001; LDL-I r = -0.45, P < 0.001). Small, dense LDL-III showed a weak positive association with triglyceride that became highly significant above the 1.5 mmol/l threshold (r = 0.54, P < 0.001). While age was positively related to LDL-II within the control subjects (r = 0.3, P < 0.05), there was no difference in the percentage abundance or concentration of LDL-III within control and CAD(-) subjects above and below the age of 40 years. Smoking was associated with a relative deficiency of the LDL-I subfraction (LDL-I to LDL-III ratio in smokers = 0.77, in ex-smokers = 0.95, in non-smokers = 1.89; P < 0.01), as was beta-blocker medication (% LDL-I, users vs. non-users, P < 0.05). Both of these effects could be explained by their primary influence on plasma triglyceride. Analysis of the frequency distributions for the three LDL subfractions revealed the concentration of small, dense LDL-III to be bimodal around a concentration of 100 mg (lipoprotein mass)/100 ml plasma. The calculation of odds ratios based on this figure indicated relative risk estimates of 4.5 (chi 2: P < 0.01) for the presence of coronary artery disease and 6.9 (chi 2: P < 0.001) for myocardial infarction.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

The effects of immobilization stress on serum triglycerides, nonesterified fatty acids, and total cholesterol in male rats after dietary modifications.

The effects of acute immobilization stress on triglycerides, nonesterified fatty acids (NEFA) and total cholesterol were determined in serum samples obtained by indwelling jugular catheters from male Sprague-Dawley rats. Stress was evaluated in three groups of rats: (1) those maintained on a regular Purina Chow diet and then fasted for 24 hours; (2) those maintained on this same diet but not fasted (nonfasted) before experimentation; and (3) those maintained on a Purina Chow diet supplemented with cholesterol (1%) and fat (10%) for 6 weeks and nonfasted prior to experimentation. Samples were taken by catheter in the home cage prior to, four times during a one hour stress/nonstress period and thirty minutes after being returned to the home cage for recovery. Nonstressed rats remained in the home cage during the entire 90 minute period. In each dietary state studied, stress affected serum triglycerides and NEFA but not total cholesterol levels. Triglyceride levels in fasted rats increased during the stress period. On the other hand, triglycerides decreased in response to stress in nonfasted rats. In stressed, nonfasted high cholesterol-fed animals, triglycerides were elevated in comparison to their nonstressed counterparts. In both fasted, regular diet-fed and nonfasted, cholesterol-fed rats, NEFA sharply declined from baseline after 5 minutes of stress; NEFA did however increase after fifteen minutes. NEFA levels in both stressed and nonstressed, nonfasted rats also rapidly decreased from baseline and never recovered throughout the session. Total cholesterol did not change in response to stress or dietary modifications. The rats maintained on a high cholesterol diet showed only a diet-induced increase in total cholesterol. Thus, acute immobilization stress affected serum triglyceride and NEFA values and these effects were diet- and time-dependent. Total cholesterol levels were unaffected by stress.

Animals↗
PubMed1993

Lymphatic transport of eicosapentaenoic and docosahexaenoic acids as triglyceride, ethyl ester and free acid, and their effect on cholesterol transport in rats.

Lymphatic transport of docosahexaenoic (DHA) and eicosapentaenoic (EPA) acids given in the forms of triglyceride, ethyl ester of free acid and their effect on cholesterol transport was compared in lymph-cannulated rats. Lymphatic recovery of DHA and EPA given by stomach tube in the form of triglyceride in which they were mainly located at the 2-position was significantly higher than that of the ethyl ester or free acid during the first 6 hr after the administration and the tendency continued until 9 hr. In contrast, the 9 to 24 hr recovery of DHA and EPA in the forms of ethyl ester and free acid was considerably higher than that of triglyceride. Consequently, cumulative 24 hr recovery of EPA was comparable among the three forms. However, the 24 hr recovery of DHA was highest in free acid, lowest in ethyl ester and intermediate in triglyceride. Recovery of the free acid between 9 and 24 hr after administration was significantly higher than that given in the forms of triglyceride or ethyl ester. Cholesterol recovery in lymph of rats given with ethyl ester or free acid was lower than that given with triglyceride at an early stage after the administration in both EPA and DHA. Cumulative 24 hr recovery of cholesterol in rats given these fatty acids as ethyl ester was significantly lower than in those given as the other two forms.

Animals↗
PubMed1978

Increased production of triglyceride-rich lipoproteins after partial biliary diversion in the rhesus monkey.

An interrelationship between bile acid and triglyceride metabolism is suggested by observations in patients with endogenous hypertriglyceridemia and in subjects treated with bile acid-binding resins or chenodeoxycholic acid. We investigated this possible interrelationship in the rhesus monkey. The effect of 14 days of partial bile diversion on plasma concentration and secretion rates of triglyceride-rich lipoproteins was studied by means of a stream-splitting device that permitted controlled interruption of the enterohepatic circulation. Diversion of 25% of the enterohepatic circulation resulted in increased bile acid synthesis and decreased bile acid secretion and pool size, and was associated with a 75% increase in fasting serum triglyceride concentration and a twofold increase in the rate of secretion of triglyceride-rich lipoproteins into plasma. Intraduodenal replacemtn of cholic acid during the period of bile diversion completely prevented the increase in lipoprotein secretion and partially prevented the increase in fasting plasma triglycerides, suggesting that these changes resulted from loss of bile acid rather than other components of bile. These studies show that partial removal of bile acids from the enterohepatic circulation augments the secretion of triglyceride-rich lipoprotein into plasma in the rhesus monkey. Elucidation of the mechanism of this effect may provide important new information concerning the control of hepatic lipoprotein secretion.

Animals↗