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PubMed2006

Does visual turbidity correlate with serum triglyceride levels in babies on total parenteral nutrition?

INTRODUCTION: Intravenous lipid is commonly used as part of total parenteral nutrition (TPN) in premature babies. The gold standard of measuring lipid tolerance involves measuring serum triglyceride levels. Many hospitals in Asia do not have this facility and rely on visual turbidity to titrate the rate of lipid infusion. The aim of this study was to determine if visual turbidity correlates with serum triglyceride levels. MATERIALS AND METHODS: Twenty-seven samples were taken from 8 babies on intravenous (IV) lipid infusion for the analysis of serum triglyceride levels and visual turbidity (assessed by 2 senior neonatologists independently). Serum turbidity was classified either as clear or turbid. Lipid intolerance was defined as triglyceride levels greater than 200 mg/dL (2.25 mmol/L). RESULTS: Both neonatologists similarly classified 20 out of 27 specimens. Serum triglyceride levels for clear samples (n = 10) were significantly lower than those for turbid samples (n = 10) (P <0.01). The clear specimens all had normal serum triglyceride levels (mean, 1.16 mmol/L; range, 0.43 to 1.96). Not all turbid specimens had unacceptable serum triglyceride levels (mean, 2.37 mmol/L; range, 1.37 to 5.75). In the remaining 7 specimens, there was a difference in opinion regarding serum turbidity. The triglyceride levels for these 7 samples were all normal (mean, 1.17 mmol/L; range, 0.66 to 1.72). CONCLUSION: Serum turbidity may be used as a screening tool in assessing lipid tolerance in babies on TPN as all clear samples had acceptable serum triglyceride level if we set the maximum cutoff at 2.25 mmol/L. Patients with turbid samples should ideally have their serum triglyceride taken to confirm lipid intolerance before altering their lipid infusion rate as they may have acceptable triglyceride levels.

Drug Combinations↗
PubMed1976

Effect of an anti-lipoprotein lipase serum on plasma triglyceride removal.

Anti-lipoprotein lipase sera injected intravenously in roosters blocked quantitatively the catabolism of very low density lipoprotein (VLDL) triglyceride. Antibodies were produced in rabbits immunized with highly purified lipoprotein lipase (LPL, glycerol ester hydrolase, E C 3.1.1.3) prepared from chicken adipose tissue. Following anti-LPL serum injection there was a linear increase in plasma triglyceride concentration. The rate of entry of triglyceride in plasma was estimated from the rate of triglyceride accumulation in the plasma of animals injected with anti-LPL serum, or from the disappearance curve of biologically labelled VLDL. In instances where both measurements were conducted in the same animals there was very close agreement between the two procedures. Inhibition of VLDL triglyceride catabolism of anti-LPL serum provided a way to characterize newly secreted VLDL that exhibited a broad spectrum of particle sizes with a median of 625 A degrees. They contained 76.2 +/- 1.2% triglyceride and had a high ratio of free to ester cholesterol (2.46 +/- 0.45). In control VLDL samples there was 46.1% triglyceride, and the ratio of free to ester cholesterol was 1.19. The complete inhibition of triglyceride removal by an antiserum prepared against adipose tissue LPL demonstrates that the NaCl-inhibited, serum-activated lipase prepared by affinity chromatography on heparin-Sepharose and concanavalin A-Sepharose columns is the enzyme responsible in vivo for the catabolism of VLDL triglyceride. Further, the kinetics of triglyceride accumulation in the plasma provide evidence that the site of degradation of VLDL triglyceride is within the plasma compartment.

Adipose Tissue↗
PubMed1977

Uptake of very low density lipoprotein triglyceride by bovine aortic endothelial cells in culture.

Primary monolayers of calf aortic endothelial cells were presented with isolated human very low density lipoproteins that had been labeled with radioactive triglyceride. The cells were observed to take up triglyceride over a 24 hr period; incorporation increased with exogenous lipoprotein concentrations, and up to 60% of the triglyceride taken up was converted to other cell lipids within 24 hr. When [2-3H]glyceryl tri[1-14C]oleate-labeled very low density lipoprotein was used, the 3H/14C ratio in the cell triglyceride was always similar to that of the exogenous lipoprotein triglyceride. Moreover, no significant hydrolysis of the exogenous very low density lipoprotein triglyceride was observed during the time of exposure to the cells. Similar experiments using doubly-labeled triglyceride exposed to endothelial cells in triglyceride-phospholipid liposome preparations also resulted in incorporation of the exogenous triglyceride without evidence of extracellular hydrolysis. The results indicate that primary monolayers of endothelial cells in culture are able to incorporate and metabolize very low density lipoprotein triglyceride. However, triglyceride does not appear to be significantly hydrolyzed during uptake, suggesting an absence of lipoprotein lipase activity in these cells.

Adipose Tissue↗
PubMed1974

Utilization of ascites plasma very low density lipoprotein triglycerides by Ehrlich cells.

Much of the lipid present in the ascites plasma in which Ehrlich cells grow is contained in very low density lipoproteins (VLDL). Chemical measurements indicated that triglycerides were taken up by the cells during in vitro incubation with ascites VLDL. When tracer amounts of radioactive triolein were incorporated into the ascites VLDL, the percentage uptakes of glyceryl tri[1-(14)C]oleate and triglycerides measured chemically were similar. The cells also took up [2-(3)H]glyceryl trioleate that was added to VLDL, but the percentage of available (3)H recovered in the cell lipids was 30-40% less than that of (1 4)C from glyceryl tri[1-(1 4)C]oleate. This difference was accounted for by water-soluble (3)H that accumulated in the incubation medium, suggesting that extensive hydrolysis accompanied the uptake of VLDL triglycerides. Radioactive fatty acids derived from the VLDL triglycerides were incorporated into cell phospholipids, glycerides, and free fatty acids, and they also were oxidized to CO(2). Triglyceride utilization increased as the VLDL concentration was raised. These results suggest that one function of the ascites plasma VLDL may be to supply fatty acid to the Ehrlich cells and that the availability of fatty acid to this tumor is determined in part by the ascites plasma VLDL concentration. Although Ehrlich cells incorporate almost no free glycerol into triglycerides, considerable amounts of [2-(3)H]glyceryl trioleate radioactivity were recovered in cell triglycerides. This indicates that at least some VLDL triglycerides were taken up intact. The net uptake of VLDL protein and cholesterol was very small relative to the triglyceride uptake, suggesting that intact triglycerides are transferred from the ascites VLDL to the Ehrlich cells and that hydrolysis occurs after the triglyceride is associated with the cells.

Animals↗
PubMed1984

Hepatic uptake of chylomicrons and triglyceride emulsions in rats fed diets of differing fat content.

The hepatic removal of plasma chylomicrons was determined for rats fed the following diets: a) containing no triglyceride, b) regular chow diet with 4.5% of its mass as lipid and, c) a corn oil-supplemented chow with triglyceride accounting for 20% of the mass. The fractional hepatic uptake of either radiolabeled chylomicrons or a triglyceride emulsion was reciprocally related to the amount of lipid in the diet. The animals receiving only carbohydrate and protein calories had the most active hepatic uptake of particulate triglyceride and were observed to have a significant decrease in the plasma concentration of the C apolipoproteins. The addition of either C-I, C-II, or C-III apoproteins to the triglyceride emulsion prior to intravenous injection produced a significantly lower hepatic triglyceride recovery of emulsions containing apoC-III. When the plasma of animals fed a fat-free diet was supplemented with human C-III-1 apolipoprotein, the distribution into the liver of either enterally administered fatty acid or parenteral triglyceride was diminished. The triglyceride content in the liver of the rats fed fat-free or corn oil-supplemented diets was significantly greater than that of the control rats and composition was somewhat similar to that of lymph triglyceride. The studies indicate an important influence of dietary lipid on both the partition of plasma triglyceride into the liver and the steady state hepatic triglyceride content.

Animals↗
PubMed1984

Interactions between fatty acid synthesis, oxidation, and esterification in the production of triglyceride-rich lipoproteins by the liver.

In a series of experiments with male rat livers perfused with or without 5-tetradecyloxy-2-furoic acid (TOFA) in the presence and absence of oleate, the relationships between fatty acid synthesis, oxidation, and esterification from newly synthesized and exogenous fatty acid substrates have been examined. When livers from fed rats were perfused without exogenous fatty acid substrate, 20% of the triglyceride secreted was derived from de novo fatty acid synthesis. Addition of TOFA caused immediate and nearly complete inhibition of fatty acid synthesis, measured by incorporation of 3H2O into fatty acids. Concurrently, ketone body production increased 140% and triglyceride secretion decreased 84%. These marked reciprocal alterations in fatty acid synthesis and oxidation in the liver almost completely abolished the production of very low density lipoproteins (VLDL). Cholesterol synthesis was also depressed by TOFA, suggesting that this drug also inhibited lipid synthesis at a site other than acetyl-CoA carboxylase. When livers from fed rats were supplied with a continuous infusion of [1-14C]oleate as exogenous substrate, similar proportions, about 45-47%, of both ketone bodies and triglyceride in the perfusate were derived from the infused [1-14C]oleate. The production of ketone bodies was markedly increased by TOFA; the secretion of triglyceride and cholesterol were decreased. Altered conversion of [1-14C]oleate into these products occurred in parallel. While TOFA decreased esterification of oleate into triglyceride, incorporation of [1-14C]oleate into liver phospholipid was increased, indicating that TOFA also affected glycerolipid synthesis at the stage of diglyceride processing. The decreased secretion of triglyceride and cholesterol following TOFA treatment was localized almost exclusively in VLDL. The specific activities of 3H and of 14C fatty acids in triglyceride of the perfusate were greater than those of liver triglyceride, indicating preferential secretion of triglyceride produced from both de novo fatty acid synthesis and from infused free fatty acid substrate. These observations suggest the following chain of events in the liver following TOFA treatment: inhibition of fatty acid and cholesterol synthesis; increased fatty acid oxidation and ketogenesis; decreased triglyceride synthesis as a result of inhibition of fatty acid synthesis, stimulation of fatty acid oxidation, and altered partition of diglyceride between triglyceride and phospholipid synthesis; and decreased production of VLDL. These comparative rat liver perfusion experiments indicate that free fatty acids provide the major source of substrate for the hepatic production of triglyceri

Animals↗
PubMed1981

Mechanism of triglyceride accumulation in rat preadipocyte cultures exposed to very low density lipoprotein.

Cultured preadipocytes derived from the stromal-vascular fraction of adipose tissue have been shown to accumulate sufficient triglycerides to assume adipocyte morphology when exposed to high concentrations of very low density lipoprotein. Since these cells synthesize and secrete lipoprotein lipase it was of interest to determine whether the accumulation of intracellular triglyceride originated from the uptake of products of the lipase reaction or whether the cells were utilizing intact lipoprotein particles. Upon incubation of preadipocytes with very low density lipoprotein, the triglyceride disappeared from the medium and accumulated in the cells. This response was accentuated by the addition of heparin to the culture medium. Balance studies conducted in the presence of heparin demonstrated that the loss of medium triglyceride could account for the increase in cell stores. Quantitative studies demonstrated that the increase in cellular triglyceride was a result of the cellular uptake and reesterification of the fatty acids liberated from very low density lipoprotein triglycerides by the action of cellular lipoprotein lipase. The magnitude of the cellular response was dependent on the concentration of fetal bovine serum in the incubation medium and increased as the serum level decreased. Likewise, when albumin was substituted for the serum, increasing amounts of albumin decreased the cellular triglyceride accumulation. It was concluded that the presence of albumin in the culture medium modulated cellular triglyceride accumulation by 1) influencing the extent of triglyceride lipolysis and 2) by regulating the uptake of liberated fatty acid into the cells. Experiments using very low density lipoprotein containing radiolabeled triglyceride and cholesteryl esters demonstrated that the uptake of the very low density lipoprotein or the remnant particle produced by the action of lipase did not significantly contribute to the accumulation of triglyceride in the cells.

Adipose Tissue↗
PubMed1996

Low rates of apoB secretion from HepG2 cells result from reduced delivery of newly synthesized triglyceride to a "secretion-coupled" pool.

The present study was aimed at defining the roles of intracellular triglyceride pools in apolipoprotein B secretion from HepG2 cells. Oleic acid (0.2 mmol/L) in the medium stimulated both triglyceride synthesis and apolipoprotein B secretion. Stimulation of apolipoprotein B secretion was lost about 30-40 min after oleic acid was removed from the medium, despite the finding that most newly synthesized triglyceride was still present in the cells. This suggested that only a small fraction of newly synthesized triglyceride was transferred to a pool available for assembly of nascent apoB into lipoproteins. Using cell fractionation, we analyzed two triglyceride pools in HepG2 cells: a microsomal pool and a cytoplasmic pool. Oleic acid-induced increases in the microsomal pool were small and short-lived due to secretion; this pool, therefore, is a "secretion-coupled" pool. The large majority of newly synthesized triglyceride was in a cytosolic pool that was not associated with secretion of apoB. Dibutyryl cAMP treatment was associated with a 3-fold increase in the mobilization of the triglyceride droplets. Apolipoprotein B secretion, however, was not increased, suggesting that the amount of triglyceride that entered the "secretion-coupled" pool after hydrolysis and re-esterification of cytoplasmic triglyceride was inadequate to stimulate apolipoprotein B secretion. In summary, the majority of newly synthesized triglyceride, whether derived from exogenous or endogenous fatty acids, is rapidly shifted to a cytoplasmic pool that does not play a regulatory role in apolipoprotein B secretion. The presence of a very small "secretion-coupled" pool of triglyceride in HepG2 cells likely explains the high rates of degradation of nascent apolipoprotein B, and the low rates of secretion of lipid-poor lipoproteins.

Apolipoproteins B↗
PubMed1996

Inhibition of apolipoprotein B and triglyceride secretion in human hepatoma cells (HepG2).

Apolipoprotein B (apoB), the major protein component of triglyceride-rich lipoproteins, is assembled into a lipoprotein particle via a complex, multistep process. Recent studies indicate that triglyceride-rich lipoprotein assembly requires the activity of the heterodimeric protein, microsomal triglyceride transfer protein (MTP). We identified a novel inhibitor of apolipoprotein B secretion using the human hepatoma cell line, HepG2. CP-10447, a derivative of the hypnotic drug methaqualone (Quaalude), inhibited apoB secretion from HepG2 cells with an IC50 of approximately 5 microM. CP-10447 also inhibited apoB secretion from Caco-2 cells, a model of intestinal lipoprotein production. In experiments using [3H]glycerol as a precursor for triglyceride synthesis, CP-10447 (20 microM) inhibited radiolabeled triglyceride secretion by approximately 83% (P < 0.0001) in HepG2 cells and 76% (P < 0.05) in Caco-2 cells with no effect on radiolabel incorporation into cellular triglyceride, indicating that CP-10447 inhibited triglyceride secretion without affecting triglyceride synthesis. RNA solution hybridization assay indicated that CP-10447 did not affect apoB or apoA-I mRNA levels. Pulse-chase experiments in HepG2 cells confirmed that CP-10447 inhibited the secretion of apoB (not its synthesis) without affecting secretion of total proteins or albumin and suggested that CP-10447 stimulates the early intracellular degradation of apoB in the endoplasmic reticulum (ER). Further studies demonstrated that CP-10447 is a potent inhibitor of human liver microsomal triglyceride transfer activity (IC50 approximately 1.7 microM) in an in vitro assay containing artificial liposomes and partially purified human MTP. These data suggest that CP-10447 may inhibit apoB and triglyceride secretion by inhibiting MTP activity and stimulating the early ER degradation of apoB. CP-10447 should provide a useful tool for further study of the mechanisms of apoB secretion and triglyceride-rich lipoprotein assembly.

Apolipoproteins B↗
PubMed1997

Triglycerides and coronary risk in women and the elderly.

There seems little doubt that triglycerides are causally related to the progress of atherogenesis. Mechanisms for this effect include adverse quantitative and qualitative changes in circulating lipoproteins. In particular, the effects of lower high-density lipoprotein levels and the production by hypertriglyceridemia of small, dense low-density lipoproteins are of great significance. The role of triglyceride-rich remnant particles in atherogenesis is likely important. These remnants, which are lipoproteins rich in both cholesterol and triglycerides, can be shown to produce cholesteryl ester-laden macrophages in vitro and are probably atherogenic in vivo. Triglyceride levels are a significant risk factor for coronary artery disease in women, more so than in men. Triglyceride levels also increase in older patients and continue to be predictors of coronary risk in both men and women older than 65 years. It is unclear whether triglyceride intervention efforts should be directed at lowering triglyceride levels (such as is accomplished with niacin or fibric acid derivatives) or lowering low-density lipoprotein levels in patients with high triglyceride levels, assuming triglyceride levels are only a passive marker of atherosclerotic risk. Until more is known about the precise role of hypertriglyceridemia in atherogenesis in women and older patients, use of triglyceride-lowering drugs should be conservative and limited to those individuals with high triglyceride levels (> 4.5 mmol/L [> 400 mg/dL]) who do not respond to diet modifications and who are at risk of coronary disease either because of a history of vascular disease or the presence of other risk factors.

Aged↗
PubMed1971

Diurnal fluctuations in triglyceride, free fatty acids, and insulin during sucrose consumption and insulin infusion in man.

Serial changes in circulating triglyceride, free fatty acids (FFA), insulin, and glucose have been measured in human subjects fed sucrose as the sole source of calories for 2- or 3-day periods. The sucrose was given either during the day with overnight fasting (19 subjects) or as continual 3-hour meals during the day and night (seven subjects). Insulin was infused overnight in five additional subjects on the day-feeding regimen to determine the effect on triglyceride concentration. The concentration of triglyceride increased during the study in all subjects, but there was a clear diurnal pattern in the response which was present even in the continual feeding studies. The rise in triglyceride occurred mainly overnight, and during the day there was frequently a fall in the concentration. The overnight increase was significantly less when insulin was infused. There were also diurnal fluctuations in FFA and insulin in both daytime and continual feeding regimens. The plasma FFA, like triglyceride, rose during the night and fell during the day while the insulin rose during the day and fell overnight. Separate statistical analysis of the daytime and overnight changes revealed that the changes in triglyceride were significantly but negatively correlated with changes in insulin during both periods. The changes in triglyceride and FFA were positively correlated during the day but not significantly related during the night. The data show that when sucrose is eaten for 2 or 3 days, there is a general increase in triglyceride concentration upon which are superimposed major diurnal fluctuations in the concentrations of triglyceride, insulin, and FFA. It is suggested that the highly significant inverse relationship between changes in triglyceride and insulin may be mediated through an effect of insulin on triglyceride removal.

Adolescent↗
PubMed1997

Is an exaggerated postprandial triglyceride response associated with the component features of the insulin resistance syndrome?

To investigate whether individual component features of the insulin resistance syndrome were associated with the postprandial triglyceride response, 57 healthy Caucasian men between 57 and 70 years of age underwent a fat tolerance test lasting 8 h. Fasting triglyceride concentrations were associated with the total unfractionated postprandial triglyceride response (r(s) = 0.54, p < 0.001) and the triglyceride-rich lipoprotein (TGRLP) fraction (d < 1.006) at 8 h was associated with the maximum non-esterified fatty acid concentration (NEFA) (r(s) = 0.33, p = 0.01). Measures of obesity (BMI and WHR) were not associated with the postprandial triglyceride response but were inversely related to NEFA suppression (NEFA nadir and BMI, r(s) = 0.31, p = 0.02; and NEFA nadir and WHR, r(s) = 0.36, p = 0.006). Other component features of the IRS, including glucose tolerance and two proxy measures of insulin resistance (fasting insulin concentration and HOMA measurement) were not associated with the postprandial triglyceride response despite being strongly associated with fasting triglyceride concentration. Current smoking habit, chronic alcohol consumption and birth weight were also not associated with an altered postprandial triglyceride response. In conclusion these results show that although component features of the IRS were associated with increased fasting triglyceride concentrations many of these features, including two proxy measures of insulin sensitivity were not associated with an exaggerated postprandial triglyceride response.

Aged↗
PubMed1991

Transport of free fatty acid and triglyceride in anhepatic rats.

Without a liver the fractional plasma removal of free fatty acid is one third and chylomicron triglyceride one half of that in the intact rat. The intestine of the anhepatic rat converted enteral fatty acid to plasma triglyceride but was unable to do the same for plasma free fatty acid. This decrease in plasma free fatty acid removal and the inability to recycle the acid as triglyceride were, in part, responsible for the conversion of large fractions of plasma triglyceride flux to the plasma free acid in hepatectomized rats. Increased intravascular triglyceride lipolysis resulting from high circulating lipoprotein lipase concentrations and reduced plasma triglyceride removal were other factors shifting the partition of anhepatic plasma fatty-acid transport from the ester to the free. After the anhepatic plasma clearance of either free fatty acid or triglyceride, relatively more of both compounds was recovered in the lipid of actively metabolizing (heart and muscle) as opposed to storage (adipose) tissue when compared with controls. Sequential evaluations of the recovery of plasma free fatty acid and triglyceride in tissues of anhepatic rats demonstrated accumulation or storage solely in adipose tissue and only when the plasma fatty acid was in triglyceride. This observation and the large conversion of anhepatic circulating triglyceride to the free acid may, in part, explain the lack of an increase in adipose lipid with reduced hepatic mass. The data help explain the preferential use of a lipid fuel in liver disease and the difficulties in obtaining carbon storage in this condition.

Animals↗
PubMed1975

Sterospecific analysis of hepatoma, host liver, and normal rat liver triglycerides from animals on chow and fat free diets.

Triglycerides from normal liver, host liver, and heptoma of rats maintained on chow and fat-free diets were subjected to sterospecific analysis. Normal and host liver triglycerides from animals on the same diet did not exhibit significant differences. Fat-free diet reduced polyunsaturated fatty acids in normal and in host liver triglycerides. Each position of hepatoma and liver triglyceride glycerol exhibited a characteristic fatty acid composition. Palmitate concentrations were reduced dramatically and stearate levels were increased significantly at the 1 position of hepatoma triglycerides, relative to the corresponding position of liver triglycerides which were affected little by diet ot tumor. Except for higher percentages of C-20 and higher fatty acids, common to all three positions, the composition of hepatoma triglycerides at the 2 position appeared normal. The 3 position of hepatoma triglycerides contained significantly higher percentages of stearate than liver. Data obtained previously for Ehrlich ascites cell triglycerides were in good agreement with this hepatoma. Data from these two neoplasms suggest that the metabolic system that regulates or controls the fatty acid composition at the 1 and 3 positions of normal tissue triglycerides does not function normally in neoplasms.

Animals↗
PubMed1995

Absorption of triglycerides with defined or random structure by rats with biliary and pancreatic diversion.

Fat absorption may be compromised by pancreatic or bile insufficiency, resulting in low uptake of essential fatty acid and energy. Using a rat model of malabsorption, we examined the absorption of defined triglycerides with medium-chain fatty acids (MCFA) in the sn-1,3 positions and essential fatty acids in the sn-2 position (MLM) compared to other fats. The thoracic duct was cannulated for collection of lymph, and the common bile and pancreatic duct was cannulated to divert both the pancreatic juice and bile. The rats were given a single bolus of triglyceride as a taurocholate emulsion. Fat absorption was measured from collected lymph samples. The triglycerides administered were a defined triglyceride, MLM [mainly (8:0/10:0)-(18:2n-6)-(8:0/10:0)], a similar triglyceride subjected to chemical randomization, a mixture of medium-chain triglycerides and soybean oil, and soybean oil, respectively. The first three triglycerides had approximately 36 wt% linoleic acid (18:2n-6) content. Administration of defined triglyceride was followed by significantly higher lymphatic level (wt%) of 18:2n-6 (P < 0.01) as well as a relative enhancement in mol% of 18:2n-6 (P < 0.05) compared to the other triglycerides. Lymphatic absorption of MCFA was similar in the three first groups but not as efficient as for long-chain fatty acids. Our results indicate that defined triglycerides thus may provide a means to increase absorption of essential fatty acids in fat malabsorption, such as that seen in cystic fibrosis, or for pre-term infants.

Absorption↗
PubMed2006

Plasma apolipoprotein A5 and triglycerides in type 2 diabetes.

AIMS/HYPOTHESIS: Variation in the human apolipoprotein (APO) A5 gene (APOA5) is associated with elevated plasma triglycerides. However, data on the exact role of plasma concentrations of APOA5 in human triglyceride homeostasis are lacking. In the present study, we estimated plasma APOA5 levels in patients with type 2 diabetes at baseline and during atorvastatin treatment, a lipid-lowering treatment that results in a reduction in plasma triglycerides and APOC3. SUBJECTS, MATERIALS AND METHODS: Plasma APOA5 concentration was measured by ELISA in 215 subjects with type 2 diabetes, who were taken from the Diabetes Atorvastatin Lipid-lowering Intervention (DALI) study, a 30-week randomised, double-blind, placebo-controlled study, and given atorvastatin 10 mg or 80 mg daily. RESULTS: At baseline, average plasma APOA5 concentration was 25.7+/-15.6 mug/100 ml. Plasma APOA5 (R (s)=0.40), APOC3 (R (s)=0.72) and APOE (R (s)=0.45) were positively correlated with plasma triglyceride levels (all p<0.001). In multiple linear regression analysis, adjusted for age and sex, the variation in plasma triglycerides was explained mostly by APOC3 (52%) and only to a small extent by APOA5 (6%) and APOE (1%). Atorvastatin treatment decreased plasma triglycerides, APOA5, APOC3 and APOE (all p<0.0001). After treatment, APOC3 remained the major determinant of plasma triglyceride levels (59%), while the contributions of APOA5 and APOE were insignificant (2 and 3%). CONCLUSIONS/INTERPRETATION: Our findings reveal a positive association between plasma APOA5 and triglycerides in patients with type 2 diabetes. Treatment with atorvastatin decreased plasma APOA5, APOC3, APOE and triglycerides. In contrast to APOC3, APOA5 is not a major determinant of triglyceride metabolism in these patients.

Aged↗
PubMed2001

Postprandial triglyceride-rich lipoprotein metabolism and insulin sensitivity in nonalcoholic steatohepatitis patients.

Nonalcoholic steatohepatitis (NASH) is a syndrome frequently associated with obesity, diabetes mellitus, and dyslipidemia. Increased fasting insulinemia and blood glucose levels may trigger a reduced catabolism of lipoproteins rich in triglycerides by lipoprotein lipase (LPL) and an increase in their fasting and postprandial levels. An association between postprandial lipemia and coronary heart disease has been observed, and many studies now support this concept. The most important result of our study is the increase in triglyceride-rich lipoproteins response after a fat load in NASH patients, the increase of incremental area under the postprandial curve, and the duration of the hypertriglyceridemic peaks. The persisting postprandial plasma triglyceride elevation in NASH patients was mostly due to the elevated plasma level of large triglyceride-rich particles. These data are coupled with lower plasma HDL2-cholesterol levels. As for lipoprotein analyses, the number of apolipoprotein B100 (ApoB100) particles is not significantly different between the two groups, and the higher content of triglycerides in NASH very low density lipoproteins (VLDL) increases the triglyceride-to-ApoB ratio and the particle size. A decreased enzymatic activity of LPL or a defective assembly and secretion of VLDL from hepatocytes due to a moderate reduction in microsomal triglyceride transfer protein could be involved in the overloading of VLDL. Moreover, the undetectable levels of ApoB48 in triglyceride-rich lipoproteins fraction A could be related to the synthesis of smaller and denser chylomicrons. NASH patients not only are insulin resistant but also tend to present alterations in fatty meal delivery, suggesting that an increase in fasting plasma insulin and glucose, with insulin resistance, joins with depressed metabolism of triglyceride-rich lipoproteins. An increase in postprandial triglyceride levels with production of large VLDL suggests an atherogenic behavior of lipid metabolism, in accordance with the high prevalence of the metabolic syndrome in NASH patients. This paper suggests that a fat load may be useful in early detection of atherogenic risk in the presence of otherwise normal fasting plasma lipids.

Adult↗
PubMed1988

Role of lipoprotein lipase activity on lipoprotein metabolism and the fate of circulating triglycerides in pregnancy.

The mechanism that induces maternal hypertriglyceridemia in late normal pregnancy, and its physiologic significance are reviewed as a model of the effects of sex steroids on lipoprotein metabolism. In the pregnant rat, maternal carcass fat content progressively increases up to day 19 of gestation, then declines at day 21. The decline may be explained by the augmented lipolytic activity in adipose tissue that is seen in late pregnancy in the rat. This change causes maternal circulating free fatty acids and glycerol levels to rise. Although the liver is the main receptor organ for these metabolites, liver triglyceride content is reduced. Circulating triglycerides and very-low-density lipoprotein (VLDL)-triglyceride levels are highly augmented in the pregnant rat, indicating that liver-synthesized triglycerides are rapidly released into the circulation. Similar increments in circulating VLDL-triglycerides are seen in pregnant women during the third trimester of gestation. This increase is coincident with a decrease in plasma postheparin lipoprotein lipase activity, indicating a reduced removal of circulating triglycerides by maternal tissues or a redistribution in their use among the different tissues. During late gestation in the rat, tissue lipoprotein lipase activity varies in different directions; it decreases in adipose tissue, the liver, and to a smaller extent the heart, but increases in placental and mammary gland tissue. These changes play an important role in the fate of circulating triglycerides, which are diverted from uptake by adipose tissue to uptake by the mammary gland for milk synthesis, and probably by the placenta for hydrolysis and transfer of released nonesterified fatty acids to the fetus. After 24 hours of starvation, lipoprotein lipase activity in the liver greatly increases in the rat in late pregnancy; this change is not seen in virgin animals. This alteration is similar to that seen in liver triglyceride content and plasma ketone body concentration in the fasted pregnant rat. In the fasting condition during late gestation, heightened lipoprotein lipase activity is the proposed mechanism through which the liver becomes an acceptor of circulating triglycerides, allowing their use as ketogenic substrates, so that both maternal and fetal tissues may indirectly benefit from maternal hypertriglyceridemia. Changes in the magnitude and direction of lipoprotein lipase activity in different tissues during gestation actively contribute both to the development of hypertriglyceridemia and to the metabolic fate of circulating triglycerides.(ABSTRACT TRUNCATED AT 400 WORDS)

Adipose Tissue↗