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PubMed2002

Microsomal triglyceride transfer protein is essential for hepatic secretion of apoB-100 and apoB-48 but not triglyceride.

Despite a complete lack of microsomal triglyceride transfer protein (MTP), L35 rat hepatoma cells secrete triglyceride-containing lipoproteins, albeit at a rate 25% of that of parental FAO hepatoma cells, which express high levels of MTP. The inability to express MTP was associated with a complete block in the secretion of both apolipoprotein (apo)B-100 and apoB-48. Stable expression of a MTP transgene restored the secretion of both apoB-100 and apoB-48 in L35 cells, indicating that MTP is essential for the secretion of both forms of apoB. Treatment with the MTP inhibitor BMS-200150 reduced the secretion of triglyceride by 70% in FAO cells, whereas the inhibitor did not affect the secretion of triglycerides by L35 cells. Thus, in the presence of the MTP inhibitor, both cell types secreted triglycerides at similar rates. Essentially, all of the triglycerides secreted by L35 cells were associated with HDL containing apoA-IV and apoE but devoid of apoB-100 or apoB-48. These results suggest that these triglyceride-containing lipoproteins are assembled and secreted via a pathway that is independent of both apoB and MTP. Our findings support the concept that apoB and MTP co-evolved and provided a means to augment the secretion of triglyceride through the formation of lipoproteins containing large hydrophobic cores enriched with triglycerides.

Animals↗
PubMed2006

Sustained enrichment of liver phospholipids and triglycerides in eicosapentaenoate after a bolus intravenous injection of a medium-chain triglycerides:fish oil emulsion to streptozotocin (Type 1) and Goto-Kakizaki (Type 2) diabetic rats.

This study deals with the sustained enrichment of liver phospholipids and triglycerides in long-chain polyunsaturated omega3 fatty acids (omega3) found after the bolus intravenous injection of a novel medium-chain triglyceride:fish oil emulsion (MCT:FO) to streptozotocin (Type 1) and Goto-Kakizaki (Type 2) diabetic rats. Twenty hours after injection of the MCT:FO emulsion, the relative concentration of omega3 was indeed higher in liver phospholipids and triglycerides than that found in rats injected with either saline or a control medium-chain triglyceride:long-chain triglyceride emulsion. This coincided with a decrease in the ponderal percentage of C18:3omega3, C20:4omega6 and/or C22:4omega6 in liver triglycerides. The present study further documents differences between streptozotocin-induced and Goto-Kakizaki diabetic rats in terms of body weight, glycemia, liver triglyceride content and the fatty acid pattern of both liver phospholipids and triglycerides, as well as a close correlation in the latter animals between liver and plasma phospholipids or triglycerides as far as the ratio in the relative concentration of selected fatty acids representative of desaturase and elongase activities is concerned. In light of these and previous findings, it is proposed that the beneficial metabolic and functional events of the MCT:FO emulsion may display not solely a rapid but also sustained time course.

Animals↗
PubMed1995

Dietary intake of the short-chain triglyceride triacetin vs. long-chain triglycerides decreases adipocyte diameter and fat deposition in rats.

Diets containing either triacetin (the water-soluble triglyceride of acetate) or long-chain triglycerides (LCT) were fed to rats for 30 d to determine the effect on body weight gain and adipose tissue cellularity. Male Sprague-Dawley rats were allowed free access to one of three diets: a control diet containing 5% of energy as fat or one of two experimental diets that contained 30% triglyceride (by energy). The source of the triglyceride in the two experimental groups was either 100% LCT or 95% triacetin + 5% LCT. Within the experimental groups receiving 30% fat, the source of dietary triglyceride (LCT vs. triacetin) did not affect total energy consumption. There were no significant differences in body weight at the onset of the study; however, animals fed 100% LCT weighed significantly more than the other two groups at the end of the study. In all three fat pads studied, animals fed triacetin had significantly lower pad mass than did animals fed LCT. Mean fat cell size was smaller in fat depots of animals fed short-chain triglyceride. Provision of dietary energy as the short-chain triglyceride triacetin in lieu of LCT resulted in lower weight gain and fat deposition. These data demonstrate the impact of dietary triglyceride composition on body weight regulation.

Adipocytes↗
PubMed1975

Effect of fasting on two postheparin plasma triglyceride lipases and triglyceride removal in obese subjects.

A new method was used for selective measurement of lipoprotein lipase and hepatic lipase in human postheparin plasma. Hepatic lipase was assayed in 1.0 M NaCl withour addition of serum, and the activity of lipoprotein lipase was determined in 0.1 M NaCl after immunoprecipitation of hepatic lipase with specific antiserum. The activity of both these enzymes and the total lipolytic activity were measured in plasma samples taken during a 4-h infusion of heparin. Each of the activities was related to basal serum triglyceride concentration and to the fractional removal constant (K) of Intralipid in 13 obese subjects before and after prolonged fasting. During a normal isocaloric diet the lipolytic activities showed a biphasic response to heparin infusion in all subjects. A peak activity was reached within 30 minutes ("early response") and thereafter the lipase activities decreased to a constant level maintained during the rest of the heparin infusion ("late response"). The early response of lipoprotein lipase showed a significant inverse correlation with the basal serum triglyceride level (r = -0.85) and a significant positive correlation with the fractional removal rate of Intralipid (r = 0.84). The late response of lipoprotein lipase was not related to either of these parameters. The early response of hepatic lipase was not correlated with basal triglyceride concentration or Intralipid removal, whereas the late response of this enzyme showed a significant negative correlation with the removal rate of Intralipid (r = -0.82). After fasting for several days the acute response of all lipolytic activities to heparin was markedly decreased or totally abolished, but the magnitude of the late response was similar to that seen in the fed state. The fractional removal rate of Intralipid was slightly increased by starvation. All correlations between postheparin plasma lipases and serum triglyceride concentration and removal disappeared in fasting subjects. It is concluded that the rapidly releasable lipoprotein lipase probably reflects the activity of the tissue enzyme(s) which is responsible for the primary removal of very low density lipoprotein (VLDL) triglycerides and chylomicrons. It is probable that this component of the postheparin plasma lipolytic activity is derived from the endothelial lipoprotein lipase pool. This enzyme plays a key role in the efflux of plasma triglycerides under normal conditions, and it is thus one determinant of plasma triglyceride level. Prolonged fasting obviously changes the triglyceride removal sites and mechanism but does not impair the removal efficiency.

Adult↗
PubMed2002

Hepatic expression of microsomal triglyceride transfer protein and in vivo secretion of triglyceride-rich lipoproteins are increased in obese diabetic mice.

Secondary hyperlipidemia is a major cardiovascular risk factor in individuals with type 2 diabetes. Increased hepatic production of apolipoprotein B (apoB)-containing lipoproteins contributes to the elevated plasma levels, but the mechanism is poorly understood. Recent results have established that microsomal triglyceride transfer protein (MTP) is rate limiting for the assembly and secretion of apoB-containing lipoproteins. To better understand the mechanism of type 2 diabetes-associated hyperlipidemia, we quantified hepatic MTP mRNA levels, hepatic microsomal triglyceride transfer activity, and in vivo triglyceride secretion from the liver in two diabetic mouse models. Obese diabetic (ob/ob) mice had 45% higher (P = 0.006) hepatic MTP mRNA levels, 54% higher (P < 0.0001) microsomal triglyceride transfer activity, and 70% higher (P < 0.0001) in vivo triglyceride secretion rates compared with ob/+ control mice. In contrast, in lean streptozotocin-treated diabetic mice, hepatic MTP mRNA levels were unchanged, whereas microsomal triglyceride transfer activity and in vivo triglyceride secretion rates were marginally decreased. These studies suggest that obesity-induced type 2 diabetes in mice confers increases in hepatic MTP expression and secretion of triglyceride-rich lipoproteins. High blood glucose and altered hepatic expression of sterol regulatory element binding protein genes play a minor role in this diabetic response.

Animals↗
PubMed1989

Gastric lipolysis and fat absorption in preterm infants: effect of medium-chain triglyceride or long-chain triglyceride-containing formulas.

The extent of gastric lipolysis, fat absorption, and infant weight gain was studied in 12 preterm infants (gestational age 28.75 +/- 0.50 weeks, postnatal age 6.08 +/- 0.81 weeks) fed medium-chain triglyceride or long-chain triglyceride formula for 1 week in a crossover design. The former formula contained 42% of 8:0 and 10:0 and 19% of 12:0, 14:0, and 16:0; the latter formula contained only 7% of 8:0 and 10:0 and 46% of 12:0, 14:0, and 16:0. Gastric aspirates were obtained on the second and third day of formula feeding for quantitation of lipase activity and of the extent of gastric lipolysis. Fat balance studies were conducted during the last three days of each feeding regimen. The study showed that (1) there was marked hydrolysis of formula fat in the stomach during feeding of either medium-chain triglyceride formula or long-chain triglyceride formula (20% and 16%, respectively); (2) lipase activity in the gastric aspirates was less during feeding of medium-chain triglyceride formula than before the meal, which suggested stimulation of lipase secretion by long-chain fatty acid released from long-chain triglyceride formula fat or more rapid binding of lipase to ingested lipid in the medium-chain triglyceride formula; (3) fatty acid distribution in glycerides and free fatty acids showed preferential release of medium-chain (8:0, 10:0) and long-chain unsaturated (18:1, 18:2) fatty acids in the stomach. The low content of 8:0 and 10:0 in gastric triglyceride and free fatty acids suggested that medium-chain fatty acids were absorbed directly in the stomach.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Weight↗
PubMed1989

Role of triglyceride-rich lipoproteins from the liver and intestine in the etiology of postprandial peaks in plasma triglyceride concentration.

Plasma triglyceride concentration in human subjects peaks once, twice or three times in the twelve-hour period following the ingestion of a fat-rich meal. Triglyceride-rich lipoproteins (TRL) containing apolipoprotein (apo)B-48 (of intestinal origin), and TRL containing apoB-100 (predominantly of hepatic origin) both contribute to postprandial changes in plasma triglyceride concentration. To test the hypothesis that earlier peaks in postprandial triglyceridemia are due predominantly to the secretion of TRL from the intestine, while later peaks are due to the secretion of TRL from the liver, TRL apoB-48, TRL apoB-100 and retinyl ester (a marker of intestinal lipoproteins) were measured in plasma samples from subjects fed a fat-rich meal (1 g fat/kg body wt). Data from seven subjects (four fed 40 retinol equivalents vitamin A/kg body wt, three fed 20 retinol equivalents vitamin A/kg body wt, with the fat meal), showed that postprandial peaks in plasma triglyceride were always associated with increases in plasma retinyl ester concentration. In four subjects, who were selected because they had two clearly defined postprandial triglyceride peaks, the plasma concentration of TRL triglyceride, apoB-48, apoE and apoC increased in conjunction with both the earlier (three hour) and later (nine hour) peaks in plasma triglyceride. Increase in TRL apoB-100 was associated with both peaks in two of the four subjects. Our data suggest that 1) TRL from the liver and intestine contribute to both earlier and later peaks in postprandial triglyceridemia; and 2) the rate of appearance of TRL from the intestine is not constant after dietary fat absorption.

Adult↗
PubMed1972

Studies on the mode of uptake of blood triglycerides by the mammary gland of the lactating goat. The uptake and incorporation into milk fat and mammary lymph of labelled glycerol, fatty acids and triglycerides.

1. The mode of uptake of the precursors of milk fat by the mammary gland of the lactating goat has been examined by infusing radioactive fatty acids, glucerol or doubly labelled triglycerides into the mammary artery or jugular vein of animals surgically prepared to permit samples of arterial and venous blood to be withdrawn without disturbance to the animal. 2. Acetate was taken up by the mammary gland and incorporated into milk fat. The decrease in the specific radioactivity of blood acetate across the gland was evidence of acetate production, but there was no significant release of labelled lipid from the mammary gland. 3. When labelled long-chain fatty acids or glycerol were infused into the lactating goat, there was extensive transfer of radioactivity into milk in spite of the absence of net uptake of substrate by the mammary gland. The decrease in the specific radioactivity of each substrate across the mammary gland, however, showed that both fatty acids and glycerol were simultaneously taken up and released by mammary tissue. 4. The infusion of chylomicra and triglyceride emulsions labelled with (3)H and (14)C revealed that both glycerol and fatty acids were released during triglyceride uptake by mammary tissue. Changes in the (3)H/(14)C ratio during the transfer of triglyceride from blood into milk showed that at least 80% of the triglyceride was hydrolysed during uptake, but the potential re-utilization of both products of hydrolysis for triglyceride synthesis in mammary tissue implied that only a minimum value could be obtained from the change in the ratio. 5. The time-course of the transfer of (3)H and (14)C into milk and lymph were closely similar after the infusion of [2-(3)H]glycerol tri[1-(14)C]oleate or of a mixture of [2-(3)H]glycerol and [1-(14)C]oleate. 6. The results were consistent with the hypothesis that plasma triglycerides are extensively or completely hydrolysed during mammary uptake.

Acetates↗
PubMed2001

Domains of apolipoprotein E contributing to triglyceride and cholesterol homeostasis in vivo. Carboxyl-terminal region 203-299 promotes hepatic very low density lipoprotein-triglyceride secretion.

Apolipoprotein (apo) E has been implicated in cholesterol and triglyceride homeostasis in humans. At physiological concentration apoE promotes efficient clearance of apoE-containing lipoprotein remnants. However, high apoE plasma levels correlate with high plasma triglyceride levels. We have used adenovirus-mediated gene transfer in apoE-deficient mice (E(-)/-) to define the domains of apoE required for cholesterol and triglyceride homeostasis in vivo. A dose of 2 x 10(9) plaque-forming units of apoE4-expressing adenovirus reduced slightly the cholesterol levels of E(-)/- mice and resulted in severe hypertriglyceridemia, due to accumulation of cholesterol and triglyceride-rich very low density lipoprotein particles in plasma. In contrast, the truncated form apoE4-202 resulted in a 90% reduction in the plasma cholesterol levels but did not alter plasma triglyceride levels in the E(-)/- mice. ApoE secretion by cell cultures, as well as the steady-state hepatic mRNA levels in individual mice expressing apoE4 or apoE4-202, were similar. In contrast, very low density lipoprotein-triglyceride secretion in mice expressing apoE4, but not apoE4-202, was increased 10-fold, as compared with mice infected with a control adenovirus. The findings suggest that the amino-terminal 1-202 region of apoE4 contains the domains required for the in vivo clearance of lipoprotein remnants. Furthermore, the carboxyl-terminal 203-299 residues of apoE promote hepatic very low density lipoprotein-triglyceride secretion and contribute to apoE-induced hypertriglyceridemia.

Adenoviridae↗
PubMed2006

The triglyceride-lowering effects of a modest dose of docosahexaenoic acid alone versus in combination with low dose eicosapentaenoic acid in patients with coronary artery disease and elevated triglycerides.

BACKGROUND: Hypertriglyceridemia is a risk factor for coronary artery disease (CAD). The American Heart Association recommends 1000 mg of omega-3 fatty acids, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), daily for cardioprotection and higher doses for triglyceride-lowering in patients with CAD. METHODS: This was a prospective, randomized, double-blind study comparing DHA to DHA + EPA in patients with CAD and triglycerides greater than 200 mg/dL. Subjects were randomized to either 1000 mg of DHA or 1252 mg of DHA + EPA for eight weeks. Baseline and eight-week laboratories were drawn to assess changes in the fasting lipid profile. The primary objective was to evaluate the change in triglycerides between the two groups at eight weeks. RESULTS: A total of 116 subjects were enrolled; 57 in the DHA group and 59 in the DHA + EPA group. Baseline characteristics were similar between groups. The mean age was 69.4 +/- 9.1 years and 70.7% were male. Triglycerides decreased by an average of 21.8% in the DHA group (p < 0.001) and 18.3% in the DHA + EPA group (p < 0.001). The difference between groups was not significant. A greater proportion of subjects in the DHA group achieved triglyceride goal (less than 150 mg/dL) compared to the DHA + EPA group (24.6% versus 10.2%, p < 0.05). CONCLUSIONS: Our results indicate that the American Heart Association recommended cardioprotective dose of omega-3 fatty acids can also significantly lower triglycerides in patients with CAD. There do not appear to be significant differences in triglyceride-lowering between DHA only and DHA + EPA combination products when dosing is based on DHA.

Aged↗
PubMed1978

Relation between triglycerides in human skeletal muscle and serum and the fractional elimination rate of exogenous plasma triglycerides.

Muscle triglycerides, serum lipid and lipoprotein concentrations and an intravenous fat tolerance test were determined on thirteen survivors of myocardial infarction and on fourteen subjects referred to a Lipid Clinic but without myocardial infarction. The mean concentration of triglycerides in muscle and the fractional removal rate k2 of intravenous injected Intralipid were similar in patients with and without MI. In seventeen of these subjects type IV hyperlipoproteinaemia was found. In type IV patients the muscle triglyceride concentration was twice that found in patients without hypertriglyceridaemia. A negative correlation between muscle triglyceride concentration and the k2 value was found for all subjects with a correlation coefficient of -0.62 (P less than 0.001). No independent correlations were found between muscle triglyceride and serum triglyceride concentration or the triglyceride concentrations of the major lipoproteins.

Adult↗
PubMed1992

The relation between triglyceride synthesis in peripheral tissues and postprandial plasma triglyceride levels: preliminary evidence of a role for acylation stimulating protein.

The present study examines the hypothesis that the rate at which peripheral tissues synthesize triglycerides is a key determinant of the rate at which they are removed from plasma. The cells of greatest interest in this regard would, of course, be the adipocytes. However, serial sampling of this tissue is not possible in man. We have approached the question indirectly, by studying triglyceride synthesis in human mononuclear cells before and after an oral fat load. In addition, plasma levels of Acylation Stimulating Protein (ASP) were measured after an overnight fast and 4 h after ingestion of the oral fat load. Similar measurements were made in the same subjects after fasting overnight and with the fast extended for 4 additional hours. With the extended fast, no parameter measured changed significantly. However, after the oral fat load, the following changes were found to be significant: plasma triglycerides increased (63.6 +/- 31.1 vs 101.5 +/- 43 mg/dl, p less than 0.005) as did d less than 1.006 g/ml triglycerides (42.3 +/- 22.8 vs 78.0 +/- 39.7 mg/dl, p less than 0.005) and plasma ASP (10.4 +/- 2.2 vs 14.7 +/- 2.3 mg/dl, p less than 0.005). In addition, the rate of triglyceride synthesis in the mononuclear cells increased significantly (1.22 +/- 0.3 vs 1.52 +/- 0.3 nmol oleate/mg cell protein per h, p less than 0.005). There was also a significant inverse relation between the increase in the d less than 1.006 triglycerides between 0 and 4 h and the increase in triglyceride synthesis in the mononuclear cells (r = 0.91, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Acylation↗
PubMed1995

Endogenous triglyceride-rich lipoproteins accumulate in rat plasma when competing with a chylomicron-like triglyceride emulsion for a common lipolytic pathway.

The rat liver secretes very low density lipoproteins (VLDL) containing either apoB-100 or apoB-48. After oral fat intake, chylomicrons containing apoB-48 and endogenously synthesized VLDL are mixed in the blood and the triglyceride clearance from these triglyceride-rich lipoprotein species compete for the same lipolytic pathway, i.e., lipoprotein lipase. A situation mimicking alimentary lipemia was induced by a short-term intravenous primed infusion of a chylomicron-like triglyceride emulsion to fed and fasted rats. The plasma concentration of apoB-100 and apoB-48 was monitored in triglyceride-rich lipoprotein subfractions after separation with density gradient ultracentrifugation by analytical SDS-PAGE. The net liver secretory output of VLDL was quantified by lipolytic blockade induced by Triton WR 1339. The chylomicron-like triglyceride emulsion induced a linear increase of large VLDL (Sf 60-400 subfraction containing both apoB-100 and apoB-48), almost to the same extent as that induced by Triton. The clearance of postprandial triglyceride-rich lipoproteins and both lipolysis and clearance of intravenously injected labeled rat chylomicrons was efficiently inhibited by the emulsion but not so complete as for fasting VLDL. The linearity of the VLDL increase and the very early response in the Intralipid-treated rats suggest that enhanced synthesis of VLDL is not a major cause for the accumulation. Rather, the present data indicate that a high plasma concentration of a chylomicron-like triglyceride emulsion competes efficiently with liver-derived VLDL for the same lipolytic pathway, which leads to accumulation in plasma of endogenous VLDL in the postprandial state.

Animals↗
PubMed1993

Hypertriglyceridemia in nephrotic rats is due to a clearance defect of plasma triglyceride: overproduction of triglyceride-rich lipoprotein is not an obligatory factor.

This study was conducted to determine whether overproduction of triglyceride-rich lipoprotein is an obligatory factor for experimental hypertriglyceridemia in nephrotic rats. Nephrosis was induced in male Wistar rats by administration of 150 mg/kg puromycin aminonucleoside. Nephrotic rats had slightly increased triglyceride secretion rate (TGSR) estimated using Triton WR1339 (0.53 +/- 0.05 vs. 0.45 +/- 0.04 mg/min, P < 0.05 vs. control rats) and marked hypertriglyceridemia (330.4 +/- 78.6 mg/dl). Rats made diabetic by 40 mg/kg streptozotocin were normotriglyceridemic (66.3 +/- 12.1 mg/dl) but had suppressed TGSR (0.33 +/- 0.09 mg/min). Experimental nephrosis was induced in diabetic rats. Their TGSR remained suppressed (0.35 +/- 0.06 mg/min) but they had marked hypertriglyceridemia (296.6 +/- 72.4 mg/dl) suggesting further impairment of triglyceride removal from the circulation in diabetic rats caused by nephrosis. Endogenously radiolabeled very low density lipoprotein (VLDL)-triglyceride from donor rats was reinjected into normal recipient rats. [3H]VLDL from the experimental groups (the rats with nephrosis, diabetes with nephrosis, and diabetes alone) were more slowly cleared by normal rats than VLDL from normal rats. These results suggest that circulating insulin is essential for increased triglyceride secretion in experimental nephrosis and that nephrotic hypertriglyceridemia can be induced only by a triglyceride removal defect. Therefore, hypersecretion of triglyceride-rich lipoprotein is not an obligatory factor for nephrotic hypertriglyceridemia.

Animals↗
PubMed1999

A cross-over study of the effect of a single oral feeding of medium chain triglyceride oil vs. canola oil on post-ingestion plasma triglyceride levels in healthy men.

Due to its unique absorption and metabolism characteristics, medium chain triglyceride (MCT) oil, consisting of fatty acids with 8-12 carbons, has been used therapeutically since the 1950s in the treatment of fat malabsorption, cystic fibrosis, epilepsy, weight control, and to increase exercise performance. Medium chain triglycerides are easily hydrolyzed in the intestines and the fatty acids are transported directly to the liver via the portal venous system, in contrast to long-chain fatty acids (LCFAs), which are incorporated into chylomicrons for transport through the lymphatic system or peripheral circulation. Medium chain fatty acids (MCFAs) do not require carnitine to cross the double mitochondrial membrane of the hepatocyte, thus they quickly enter the mitochondria and undergo rapid beta-oxidation, whereas most LCFAs are packaged into triglycerides in the hepatocyte. In this single-blind, randomized, cross-over study, 20 healthy men ingested a single dose of either 71 g of MCT oil or canola oil. Blood samples were taken at baseline and at hours one through five post-ingestion to compare the effect of a single oral dosing of MCT oil versus canola oil on post-ingestion plasma triglyceride levels. Mean triglyceride values after canola oil increased 47 percent above baseline (p <0.001), while mean triglyceride values after MCT oil decreased 15 percent from baseline (p <0.001), which is consistent with several other studies involving short- and longer-term feeding with MCT oil. The effect of long-term usage of MCT oil on triglycerides is yet to be established.

Administration, Oral↗
PubMed1985

Purification and characterization of human lipoprotein lipase and hepatic triglyceride lipase. Reactivity with monoclonal antibodies to hepatic triglyceride lipase.

Human lipoprotein lipase and hepatic triglyceride lipase were purified to homogeneity from post-heparin plasma. These enzymes were purified 250,000- and 100,000-fold with yields of 27 +/- 15 and 19 +/- 6%, respectively. Molecular weight determination by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate and reducing agents yielded Mr of 60,500 +/- 1,800 and 65,200 +/- 400, respectively, for lipoprotein lipase and hepatic triglyceride lipase. These lipase preparations were shown to be free of detectable antithrombin by measuring its activity and by probing of Western blots of lipases with a monospecific antibody against antithrombin. In additions, probing of Western blots with concanavalin A revealed no glycoproteins corresponding to the molecular weight of antithrombin. Four stable hybridoma-producing distinct monoclonal antibodies (mAb) to hepatic triglyceride lipase were isolated. The specificity of one mAb, HL3-5, was established by its ability to immunoprecipitate hepatic triglyceride lipase catalytic activity. Interaction of HL3-5 with this lipase did not inhibit catalytic activity. The three other mAb interacted with hepatic triglyceride lipase only after denaturation of the enzyme with detergents. The relatedness of these two enzymes was examined by comparing under the same conditions the thermal inactivation, the sensitivity to sulfhydryl and reducing agents, amino acid composition, and the mobility of peptide fragments generated by cyanogen bromide cleavage. The results of these studies strongly support the view that the two enzymes are different proteins. Immunological studies confirm this conclusion. Four mAb to hepatic triglyceride lipase did not interact with lipoprotein lipase in Western blots, enzyme-linked immunosorbent assay, and immunoprecipitation experiments. These immunological studies demonstrate that several epitopes of the hepatic triglyceride lipase protein moiety are not present in the lipoprotein lipase molecule.

Amino Acids↗
PubMed1979

Triglyceride removal from very low density lipoproteins in vivo as a function of their triglyceride content.

Rabbit very low density lipoproteins (VLDL) were fractionated in 3 subfractions differing in density and triglyceride (TG) content. The fraction of total weight represented by triglycerides was: VLDL1 TG = 71%, VLDL2 TG = 62%, VLDL3 TG = 55%. No other difference in composition was observed. After intravenous administration of radioglycerol all subfractions were labelled and the distribution of radioactivity in their glycerolipids was the same. In 5 rabbits, a biologically labelled triglyceride-rich VLDL1 subfraction preparation was administered and the specific activity of triglyceride was determined in all 3 subfractions in serial samples. A precursor--product relationship between VLDL1 TG and VLDL TG in other subfractions was not observed. In another set of experiments the disappearance rates of VLDL TG from subfractions were determined in recipient rabbits. The half-lives were: VLDL1 TG = 9.5 +/- 1.3 min, VLDL2 TG : 16.0 +/- 1.3 min, VLDL3 TG: 26.9 +/- 1.3 min. It is concluded that triglyceride removal from a VLDL subfraction varies inversely with its triglyceride content. A role for partial VLDL lipolysis in this metabolic heterogeneity was not established.

Animals↗
PubMed1992

Postprandial pattern of triglyceride-rich lipoprotein in normal-weight humans after an oral lipid load: exaggerated triglycerides and altered insulin response in some subjects.

In 13 healthy, male nonsmokers (mean age: 25.7 +/- 2.4 years) with normal fasting triglycerides we investigated postprandial changes of triglycerides in several lipoprotein fractions. After a 12-hour overnight fast they ingested a standardized lipid load (1,017 kcal) including 30,000 IU retinyl palmitate. Postprandially, total triglycerides increased significantly (p < 0.001) to a peak value of 221 +/- 81 mg/dl at 5 h. Two subjects had an exceptionally strong triglyceride response (peak values: 363 and 390 mg/dl). They had the highest levels of retinyl palmitate in the chylomicron and the nonchylomicron fraction, and one of them showed elevated intermediate-density lipoprotein values throughout the test period. In addition, they showed an altered early and an increased late postprandial insulin response. Thus, our data provide evidence that an exaggerated postprandial triglyceride response may point to an increased atherogenic risk even in healthy subjects with normal fasting triglycerides.

Adult↗