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PubMed2003

Intestinal lipoprotein assembly in apobec-1-/- mice reveals subtle alterations in triglyceride secretion coupled with a shift to larger lipoproteins.

Mammalian enterocytes express apolipoprotein (apo)B-48, which is produced after posttranscriptional RNA editing of the nuclear apoB-100 transcript by the catalytic deaminase apobec-1. Earlier studies in apobec-1-/- mice revealed an apoB-100-only lipoprotein profile but no gross defects in triglyceride absorption. However, subtle defects may have been obscured by the mixed genetic background. In addition, the intrinsic susceptibility to proteolytic degradation of intestinal apoB-100 and apoB-48 has been questioned. Accordingly, we examined triglyceride absorption, intestinal apoB expression, and lipoprotein secretion in apobec-1-/- mice backcrossed into a C57BL/6 background. Inbred apobec-1-/- mice absorb triglyceride normally, yet secrete triglyceride-rich lipoproteins more slowly than wild-type congenic controls. There was comparable induction of apoB synthesis in response to fat feeding in both genotypes, but apoB-100 was preferentially retained and more extensively degraded than apoB-48. By contrast, synthesis, secretion, and content of apo A-IV were indistinguishable in apobec-1-/- and wild-type mice with 100% recovery, suggesting no degradation of this apoprotein in either genotype. Newly secreted lipoproteins from isolated enterocytes of wild-type mice revealed apoB-48 in both high-density lipoproteins and very low-density lipoproteins. By contrast, apobec-1-/- mice secreted apoB-100-containing particles that were almost exclusively in the low and very low-density lipoproteins range with no apoB-100-containing high-density lipoproteins. These studies establish the existence of preferential degradation of intestinal apoB-100 and subtle defects in triglyceride secretion in apobec-1-/- mice, coupled with a shift to the production of larger particles, findings that suggest an important divergence in intestinal lipoprotein assembly pathways with the different isoforms of apoB.

APOBEC-1 Deaminase↗
PubMed1987

Apolipoprotein A-IV synthesis in rat intestine: regulation by dietary triglyceride.

Apolipoprotein A-IV (apoA-IV) synthesis rates were measured in vivo in rat enterocytes by immunoprecipitation after administration of [3H]leucine into in situ loops of jejunum and ileum. Basal apoA-IV synthesis rates (percent total protein synthesis) were significantly higher in jejunal enterocytes (2.05 +/- 0.54%) compared with ileal enterocytes (0.48 +/- 0.32%) from the same fasted animals. After an acute triglyceride bolus, significant and sustained elevations of apoA-IV synthesis rates were seen in both jejunal and ileal enterocytes with maximal effects noted at 4-6 h. Animals fed diets containing 30% wt/wt triglyceride as saturated (SF) or polyunsaturated (UF) fats for 6 wk had similarly increased rates of apoA-IV synthesis in jejunal enterocytes with both SF (3.73 +/- 0.83%) and UF (3.33 +/- 0.64%) but no change in ileal enterocytes. By contrast, animals consuming a fat-free diet for 3 wk had jejunal apoA-IV synthesis rates indistinguishable from basal values (2.40 +/- 0.45%). Translatable intestinal mRNA levels for pre-apoA-IV after triglyceride increased in parallel to synthesis rates with a 50% increase in jejunum and a 350% increase in ileum observed at 4-6 h. These results suggest that apoA-IV synthesis by rat small intestine increases in response to acute and chronic dietary triglyceride, is maintained in the absence of dietary triglyceride, and may be under pretranslational control.

Animals↗
PubMed1995

Intestinal digestion, absorption, and transport of structured triglycerides and cholesterol in rats.

We compared the intestinal absorption of trilinolein (1,2,3-tri-[1-14C]linoleyl-sn-glycerol) with two different structured triglycerides containing one linoleic acid (C18:2) and two octanoic acids (C8:0), 1,3-dioctanoyl-2-[1-14C]linoleyl-sn-glycerol (2-linoleate) and 1,2-di[1-14C]octanoyl-3-linoleyl-sn-glycerol (1,2-octanoate), respectively. Lymphatic radioactive lipid output of 2-linoleate resembled that of trilinolein rats but remained significantly lower during the lipid infusion. Radioactive lipid was recovered along the entire small intestinal lumen, with a significantly higher amount of [14C]lipid recovered in the lower small intestine and cecum in the 2-linoleate group. Delayed uptake of radioactive 2-linoleate was not due to poor digestion. In contrast, 1,2-octanoate was efficiently digested, and both the free fatty acid (FFA) and the monoacylglycerol (MG) containing octanoate were rapidly absorbed. Irrespective of its position on the triglyceride molecule, 14C-labeled octanoate was poorly transported into lymph. In addition, intestinal luminal and mucosal recovery of [14C]octanoate was significantly lower in the 1,2-octanoate group compared with [14C]linoleate recovery in the 2-linoleate or trilinolein groups. Total recovery of infused radioactive lipid was significantly less in the 1,2-octanoate group than in the 2-linoleate or trilinolein groups. Thus radioactive octanoate in the form of FFA or 2-MG was rapidly absorbed and transported via the portal vein. The infusion of either 2-linoleate or 1,2-octanoate did not affect the absorption and lymphatic transport of cholesterol compared with trilinolein. In summary, the type of the fatty acid on the structured triglyceride molecule affects its digestion, absorption, and lymphatic transport. Structured triglycerides containing octanoic acid in the 1- and 3-positions and linoleic acid in the 2-position may not be advantageous to use as a sole source of dietary lipid, but should be supplemented with long-chain triglycerides.

Absorption↗
PubMed1999

Lymphatic absorption of structured triglycerides vs. physical mix in a rat model of fat malabsorption.

Comparison was made between the intestinal absorption and lymphatic transport of a randomly interesterified fish oil and medium-chain triglyceride (MCT) structured triglycerides (STG) vs. the physical mix in rat small intestine following ischemia and reperfusion (I/R) injury. Under halothane anesthesia, the superior mesenteric artery (SMA) was occluded for 20 min and then reperfused in I/R rats. The SMA was isolated but not occluded in control rats. In both treatment groups, the mesenteric lymph duct was cannulated and a gastric tube was inserted. Each treatment group received 1 ml of the fish oil-MCT STG or physical mix (7 rats/group) through the gastric tube followed by an infusion of PBS at 3 ml/h for 8 h. Lymph was collected hourly for 8 h. Lymph triglyceride, cholesterol, and decanoic and eicosapentaenoic acids increased rapidly and maintained a significantly higher output (P < 0.01) with STG compared with physical mix in control rats over 8 h. After I/R, lymphatic triglyceride output decreased 50% compared with control. Gastric infusion of STG significantly improved lipid transport by having a twofold higher triglyceride, cholesterol, and decanoic and eicosapentaenoic acids output to lymph compared with its physical mix (P < 0.01). We conclude that STG is absorbed into lymph significantly better than physical mix by both the normal intestine and the intestine injured by I/R.

Animals↗
PubMed2001

Corticosterone and insulin interact to regulate glucose and triglyceride levels during stress in a bird.

Captive European starlings (Sturnus vulgaris) were exposed to the stress of handling and restraint while corticosterone, glucose, and triglyceride concentrations were monitored in blood plasma. In saline-injected controls, basal samples were taken within 3 min of disturbance with subsequent samples taken at 40, 70, and 150 min. This was repeated at two times during the daily cycle (day and night) on two different photoperiods: short and long days. During both photoperiods, corticosterone concentrations approximately tripled (compared with a sixfold increase in free-living starlings) and triglyceride concentrations decreased 25-45% in response to stress at both times of the day, whereas an approximately 25% stress-induced hyperglycemia occurred only at night. Exogenous corticosterone (200 microg), 1.0 or 4.0 IU/kg of insulin, or a combination of corticosterone with each insulin dose was then separately administered to alter the above responses. Insulin did not affect corticosterone or triglyceride concentrations but resulted in a dose-dependent hypoglycemia of 10-40%. Injected corticosterone resulted in supraphysiological corticosterone concentrations (three- to fivefold higher than normal), yet it did not affect the already altered plasma glucose or triglyceride concentrations. This suggests that glucose output and triglyceride decreases were already maximal in response to handling and restraint. However, the low glucose concentrations resulting from exogenous insulin returned to basal quicker with exogenous corticosterone but only during the day. No response to either hormone showed photoperiodic differences. These data suggest that corticosterone's role in metabolism changes to meet varying energetic demands throughout the day.

Animals↗
PubMed1985

Endurance training and glucose conversion into triglycerides in human fat cells.

To study the influence of endurance training on glucose conversion into fat cell triglycerides, 24 (13 women, 11 men) inactive subjects (25.0 +/- 3.8 yr of age) took part in a 20-wk ergocycle training program 4 days and increasing to 5 days/wk, 40-45 min/day, starting at 60% and increasing to 85% of the heart rate reserve. Several body fatness indicators were measured before and after the training program: seven skinfold thicknesses, percent fat, and mean fat cell weight. Fat cell basal and maximal insulin-stimulated glucose conversion into triglycerides were also determined using [14C]glucose. Body fatness indicators decreased significantly after training only in male subjects (P less than 0.05). Basal and maximal insulin-stimulated glucose conversion into triglycerides increased significantly with training (P less than 0.05): pretest values (nanomoles glucose per hour per 10(6) cells) being 24.9 +/- 2.1 and 28.7 +/- 2.5, while post-test values were 30.1 +/- 3.2 and 33.0 +/- 3.4 for basal and insulin-stimulated values, respectively. However, this lipogenic increase was only observed in male subjects (P less than 0.01). Changes in body fatness indicators induced by training were negatively correlated with changes induced in fat cell glucose conversion into triglycerides (-0.24 less than or equal to r less than or equal to -0.45). These results demonstrate that endurance training increases fat cell glucose conversion into triglycerides and suggest that adipose tissue metabolism is part of the adaptive response to training. Moreover, it appears that adipose tissue response to aerobic training is more efficient in males than in females.

Adipose Tissue↗
PubMed1997

Effects of diet on muscle triglyceride and endurance performance.

The purpose of this investigation was to examine the effects of diet on muscle triglyceride and endurance performance. Seven endurance-trained men completed a 120-min cycling bout at 65% of maximal oxygen uptake. Each subject then ingested an isocaloric high-carbohydrate (Hi-CHO; 83% of energy) or a high-fat (Hi-Fat; 68% of energy) diet for the ensuing 12 h. After a 12-h overnight fast, a 1,600-kJ self-paced cycling bout was completed. Muscle triglyceride measured before (33.0 +/- 2.3 vs. 37.0 +/- 2.1 mmol/kg dry wt) and after (30.9 +/- 2.4 vs. 32.8 +/- 1.6 mmol/kg dry wt) the 120-min cycling bout was not different between the Hi-CHO and Hi-Fat trials, respectively. After the 24-h dietary-fasting period, muscle triglyceride was significantly higher for the Hi-Fat (44.7 +/- 2.4 mmol/kg dry wt) vs. the Hi-CHO (27.5 +/- 2.1 mmol/kg dry wt) trial. Furthermore, self-paced cycling time was significantly greater for the Hi-Fat (139.3 +/- 7.1 min) compared with the Hi-CHO (117.1 +/- 3.2 min) trial. These data demonstrate that there was not a significant difference in muscle triglyceride concentration before and after a prolonged moderate-intensity cycling bout. Nevertheless, a high-fat diet increased muscle triglyceride concentration and reduced self-paced cycling performance 24 h after the exercise compared with a high-carbohydrate diet.

Adult↗
PubMed2004

Menstrual cycle phase and oral contraceptive effects on triglyceride mobilization during exercise.

We examined the effects of menstrual cycle phase and oral contraceptive (OC) use on triglyceride mobilization during 90 min of rest and 60 min of leg ergometry exercise at 45 and 65% peak O(2) uptake (Vo(2 peak)) in eight moderately physically active, eumenorrheic women (24.8 +/- 1.2 yr). Subjects were tested during the follicular phase (FP) and the luteal phase (LP) before OC use and during the inactive phase (IP) and high-dose phase (HP) after 4 complete mo of OC use. Glycerol rate of appearance (R(a)), a measure of triglyceride mobilization, was determined in a 3-h postabsorptive state using a primed constant infusion of [1,1,2,3,3-(2)H]glycerol. Before OC use (BOC), there were no significant differences between FP and LP in any of the variables studied. Dietary composition, exercise patterns, plasma glycerol concentrations, growth hormone concentrations, and exercise respiratory exchange ratio did not change with OC use. However, 4 mo of OC use significantly (P < 0.05) increased glycerol R(a) in HP during exercise at 45% Vo(2 peak) (6.2 +/- 0.2, 6.5 +/- 0.4, and 7.7 +/- 1.1 micromol.kg(-1).min(-1) for BOC, IP, and HP, respectively) and in IP and HP at 65% Vo(2 peak) (6.6 +/- 0.1, 8.2 +/- 0.6, and 8.1 +/- 0.7 micromol.kg(-1).min(-1) for BOC, IP, and HP, respectively). Plasma cortisol concentrations were significantly higher with OC use at rest and during exercise at 45 and 65% Vo(2 peak). In summary, although fluctuations of endogenous ovarian steroids have little effect on triglyceride mobilization, the synthetic ovarian steroids found in OCs increase triglyceride mobilization and plasma cortisol concentrations in exercising women. We conclude that the hierarchy of effects of ovarian steroids and their analogs on triglyceride mobilization in exercising women is as follows: energy flux > OC use > recent carbohydrate nutrition, menstrual cycle effects.

Adult↗
PubMed2001

Supplementation of Areca catechu L. extract alters triglyceride absorption and cholesterol metabolism in rats.

Areca extracts have already been found to exhibit a strong inhibitory activity on cholesterol absorption in high-cholesterol-fed rats. Accordingly, this study was performed to determine whether Areca extracts also exert an inhibitory activity on triglyceride absorption in triglyceride-fed rats. Male rats were fed a diet containing corn oil (10%, w/w) with or without an Areca nut extract supplement (0.5%, w/w). The supplementation of the Areca extract significantly lowered the absorption of triglyceride and the plasma lipid concentration. The absorbed triglyceride that appeared in the blood after an oral dose of [9,10(n)-(3)H] triglyceride was significantly lower in the rats supplemented with the Areca nut extract, compared with the control group. The supplementation also significantly lowered the small intestinal pCEase (pancreatic cholesterol esterase) activity by 22.5% compared to the control group. The hepatic and intestinal ACAT (acyl-CoA:cholesterol acyltransferase) activities were significantly decreased in the Areca group compared with the control group. Hence, further studies are needed to elucidate the structure and chemical properties of the active compound in the water-soluble Areca extract that lowers cholesterol absorption.

Animals↗
PubMed2001

CSF collection time at lumbar puncture is influenced by plasma cholesterol and triglycerides.

It is a fairly well-known fact that the CSF collection time (tapping time) at lumbar puncture may influence CSF levels of monoamine compounds (e.g. the serotonin metabolite 5-hydroxyindoleacetic acid, 5-HIAA) and some neuropeptides. Since serum levels of cholesterol and triglycerides and low CSF levels of 5-HIAA have been linked to violent behaviour and impulsivity, we investigated retrospectively whether serum cholesterol and triglycerides affect CSF collection time. The series consists of 14 healthy males lumbar punctured at the L(4-5) level. We found that both serum cholesterol and serum triglycerides influenced the CSF collection time for 12 ml of CSF (R = 0.77; p = 0.0067). There was no correlation between cholesterol in serum and CSF, nor between cholesterol in the CSF and collection time. However, we accidentally found a correlation between cholesterol in the CSF and age. The proposed hypothesis tries to explain why cholesterol- and triglyceride-rich lipoprotein particles modify the CSF collection time and influence endothelial function with a subsequent effect on CSF production and/or intraspinal pressure. Thus, it may be of interest to pay attention to serum cholesterol and triglycerides, their effect on CSF collection time and, in the next step, their putative impact on levels of various compounds in the CSF.

Adult↗
PubMedDate not supplied

Apolipoprotein C-III, hypertriglyceridemia and triglyceride-rich lipoproteins in uremia.

Apolipoprotein C-III (ApoC-III) plays an important role in the metabolism of triglyceride-rich lipoproteins and is known to be elevated in patients with uremia. To investigate the role of apoC-III in uremic dyslipidemia, we examined apoC-III, triglyceride levels and lipoprotein particles containing both apoB and apoC-III (LP-Bc) in 27 uremic patients prior to dialysis (predialysis), 30 patients on hemodialysis (HD) and 31 patients on peritoneal dialysis (PD). All three groups of patients had elevated levels of plasma apoC-III (20+/-7 mg/dl for predialysis, 18+/-5 for HD and 22+/-8 for PD, compared to 11+/-3 mg/dl for control subjects [p<0/01 for all comparisons]). ApoC-III was positively correlated with plasma triglycerides in PD patients (r = 0.86, p<0.0001), HD patients (r = 0.67, p<0.0001) and predialysis patients (r = 0.60, p<0.001) as well as in all patients combined (r = 0.75, p<0.0001). ApoC-III was also positively correlated with levels of LP-Bc in all three groups of patients, although this correlation was less strong (r = 0.46, p<0.0001 for all patients combined). In predialysis and PD patients, the majority of apoC-III was found in heparin precipitable lipoproteins, whereas the majority of apoC-III in HD patients was found in HDL, indicating less efficient lipolysis in predialysis and PD patients in comparison with HD. These data support the hypothesis that the elevation of apoC-III in uremia can alter the metabolism of triglyceride-rich lipoproteins, leading to an elevation in triglycerides and LP-Bc. Understanding the mechanism(s) of elevated apoC-III in uremia may help to clarify the causes of uremic dyslipidemia.

Adult↗
PubMed2004

Quantitative trait loci for apolipoprotein B, cholesterol, and triglycerides in familial combined hyperlipidemia pedigrees.

OBJECTIVE: Familial combined hyperlipidemia (FCHL) is a genetically complex lipid disorder that is diagnosed in families by combinations of increased cholesterol, triglycerides, and/or apolipoprotein B (apoB) levels in patients and their first-degree relatives. Identifying the predisposing genes promises to reveal the primary risk factors and susceptibility pathways and suggest methods of prevention and treatment. As with most genetically complex disorders, a clinical definition of disease may not be the most useful phenotype for finding the complement of predisposing genes, and the quantitative traits used to define the disorder can provide important information. This is a report of a quantitative trait loci (QTL) analysis of FCHL. METHODS AND RESULTS: A full genome scan of 377 multi-allelic markers genotyped at approximately 10 centimorgan (cM) intervals was conducted in 150 sibling pairs from 22 nuclear families in FCHL pedigrees. These data were analyzed by 2 multipoint QTL linkage methods using the nonparametric and Haseman-Elston procedures of the Genehunter software. Using a criterion of P<0.001 by the nonparametric analysis, we found evidence of 2 apoB QTL at 1p21-31 (P<0.000009) and 17p11-q21 (P<0.000009), a total serum cholesterol QTL at 12p13 (P<0.0001), and a serum triglycerides QTL at 4p15-16 (P<0.0002). Using the criterion of P<0.03 for at least 2 traits at the same locus, additional evidence for cholesterol (P<0.01) and a triglycerides P<0.02) was observed at 17p11-21, as well as suggestive evidence for apoB (P<0.02) and triglycerides (P<0.01) at 4q34-35, and cholesterol (P<0.01) and triglycerides (P<0.02) and a binary FCHL trait (lod=1.5) at 16p12-13. CONCLUSIONS: QTL analyses of the traits that define FCHL are effective for localizing disease-predisposing genes.

Apolipoproteins B↗
PubMed2006

Hypoxia converts human macrophages into triglyceride-loaded foam cells.

OBJECTIVE: Atherosclerotic lesions have regions that are hypoxic. Because the lesion contains macrophages that are loaded with lipid, we investigated whether hypoxia can influence the accumulation of lipids in these cells. METHODS AND RESULTS: Exposure of human macrophages to hypoxia for 24 hours resulted in an increased formation of cytosolic lipid droplets and an increased accumulation of triglycerides. Exposure of the macrophages to oxidized low-density lipoprotein (oxLDL) increased the accumulation of cytosolic lipid droplets because of an increase in cellular cholesterol esters. The accumulation of lipid droplets in oxLDL-treated cells was further increased after hypoxia, caused by an increased level of triglycerides. Expression analyses combined with immunoblot or RT-PCR demonstrated that hypoxia increased the expression of several genes that could promote the accumulation of lipid droplets. Hypoxia increased the mRNA and protein levels of adipocyte differentiation-related protein (ADRP). It is well known that an increased expression of ADRP increases the formation of lipid droplets. Hypoxia decreased the expression of enzymes involved in beta-oxidation (acyl-coenzyme A synthetase and acyl-coenzyme A dehydrogenase) and increased the expression of stearoyl-coenzyme A desaturase, an important enzyme in the fatty acid biosynthesis. Moreover, exposure to hypoxia decreased the rate of beta-oxidation, whereas the accumulation of triglycerides increased. CONCLUSIONS: The results demonstrate that exposure of human macrophages to hypoxia causes an accumulation of triglyceride-containing cytosolic lipid droplets. This indicates that the hypoxia present in atherosclerotic lesions can contribute to the formation of the lipid-loaded macrophages that characterize the lesion and to the accumulation of triglycerides in such lesions.

Acyl-CoA Dehydrogenase↗
PubMed1992

Influence of insulin resistance, secretion, and clearance on serum cholesterol, triglycerides, lipoprotein cholesterol, and blood pressure in healthy men.

Relations between serum lipids, lipoproteins, blood pressure, and insulin metabolism were investigated in 158 healthy men aged 19-77 years and with body mass indexes (BMIs) of 19-41 kg.m-2. Mathematical modeling analysis of glucose, insulin, and C-peptide concentrations during an intravenous glucose tolerance test was used to measure parameters of insulin metabolism. In univariate analysis, both fasting and postglucose insulin concentrations showed significant positive associations with fasting serum triglyceride levels (r = 0.33 and 0.38, respectively) and systolic (r = 0.22 and 0.26) and diastolic (r = 0.21 and 0.24) blood pressure and negative associations with high density lipoprotein subfraction 2 cholesterol (HDL2; r = -0.21 and -0.25). In multivariate analysis, the associations between insulin and HDL2 cholesterol concentrations were found to depend on triglyceride levels. Insulin resistance and basal pancreatic insulin secretion showed significant positive associations with serum triglycerides, which were independent of the effects of age, BMI, and fat distribution. Hepatic insulin throughout was independently associated with HDL2 cholesterol. Associations of insulin-related variables with blood pressure were generally dependent on age and BMI. These results underline the importance of insulin sensitivity and insulin concentrations as determinants of triglyceride metabolism. They also indicate a close relation between hepatic insulin handling and HDL2 concentration that is independent of triglyceride metabolism.

Adult↗
PubMed1993

Stable isotopes show a direct relation between VLDL apoB overproduction and serum triglyceride levels and indicate a metabolically and biochemically coherent basis for familial combined hyperlipidemia.

Familial combined hyperlipidemia (FCHL) may be genetically and metabolically more heterogeneous than previously thought. A consistent feature is an increase in circulating very-low-density lipoprotein (VLDL) apolipoprotein (apo) B, which could be due to either an increase in apoB production or a decrease in its catabolism. Therefore, we directly measured VLDL apoB production in the postabsorptive state in seven FCHL subjects (four male, three female) and seven normal control subjects (three male, four female) by using L-[1-13C]leucine as an endogenous label. Mean age and body mass index did not differ significantly between the two groups. The mean total cholesterol levels were 4.7 +/- 0.8 and 8.8 +/- 1.6 mmol/L (+/- SD, P < .01) and the mean triglyceride levels were 0.84 +/- 0.14 and 3.30 +/- 1.10 mmol/L (+/- SD, P < .01) in the control and FCHL groups, respectively. Although the fractional production rate of VLDL apoB was 38% lower in the FCHL group than in the control subjects (0.11 +/- 0.03 versus 0.18 +/- 0.02 pool/h; mean +/- SD, P < .01), its absolute production rate was 2.7 times greater (534 +/- 193 micrograms/kg per hour in FCHL versus 196 +/- 71 micrograms/kg per hour in control subjects; mean +/- SD, P < .01). There was a linear relation (r = 0.8, P = .03) between triglyceride levels and the VLDL apoB production rate in FCHL, the slope of which indicated a similar VLDL triglyceride-to-apoB ratio in the FCHL and control groups. We conclude that FCHL is a metabolically coherent disorder and that the increase in circulating apoB and triglyceride levels in FCHL is due to secretion of an increased number of VLDL particles, each containing, on average, a normal amount of triglyceride and one molecule of apoB.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Mobilization of stored triglycerides from macrophages as free fatty acids.

Because many or most lipid-laden foam cells in atheromas and in xanthomas derive from macrophages, it is important to understand how they accumulate lipids and how they can divest themselves of lipids. The mobilization of stored triglycerides from macrophages was studied in cell cultures. Mouse resident peritoneal macrophages and J774 macrophages increased their triglyceride content six- to tenfold during a 24-hour incubation with free fatty acids complexed to albumin. Subsequent incubation in fresh medium containing free fatty acid-poor albumin was accompanied by a fall in cell triglyceride content (50% in 20 hours) and a corresponding increase in medium-free fatty acid. Release of free fatty acid was linear as a function of time, provided fresh medium was added hourly. When medium was not changed, release rates fell off rapidly, probably due to re-uptake of released free fatty acid. Chloroquine did not affect the rate of free fatty acid release. The results suggest that macrophages-foam cells can reduce their triglyceride stores via the action of a nonlysosomal (presumably cytoplasmic) neutral triglyceride lipase.

Animals↗
PubMed2004

Serum triglycerides as a risk factor for cardiovascular diseases in the Asia-Pacific region.

BACKGROUND: The importance of serum triglyceride levels as a risk factor for cardiovascular diseases is uncertain. METHODS AND RESULTS: We performed an individual participant data meta-analysis of prospective studies conducted in the Asia-Pacific region. Cox models were applied to the combined data from 26 studies to estimate the overall and region-, sex-, and age-specific hazard ratios for major cardiovascular diseases by fifths of triglyceride values. During 796,671 person-years of follow-up among 96,224 individuals, 670 and 667 deaths as a result of coronary heart disease (CHD) and stroke, respectively, were recorded. After adjustment for major cardiovascular risk factors, participants grouped in the highest fifth of triglyceride levels had a 70% (95% CI, 47 to 96) greater risk of CHD death, an 80% (95% CI, 49 to 119) higher risk of fatal or nonfatal CHD, and a 50% (95% CI, 29% to 76%) increased risk of fatal or nonfatal stroke compared with those belonging to the lowest fifth. The association between triglycerides and CHD death was similar across subgroups defined by ethnicity, age, and sex. CONCLUSIONS: Serum triglycerides are an important and independent predictor of CHD and stroke risk in the Asia-Pacific region. These results may have clinical implications for cardiovascular risk prediction and the use of lipid-lowering therapy.

Aged↗
PubMed1999

Elevated serum triglyceride levels and long-term mortality in patients with coronary heart disease: the Bezafibrate Infarction Prevention (BIP) Registry.

BACKGROUND: The association between elevated blood triglyceride levels and subsequent mortality risk in patients with established coronary heart disease (CHD) has been investigated rarely. The aim of the present study was to investigate this association. METHODS AND RESULTS: We evaluated mortality over a mean follow-up time of 5. 1 years among 9033 male and 2499 female CHD patients who were screened for participation in the Bezafibrate Infarction Prevention (BIP) Study. A stepwise increase in mortality with increasing serum triglyceride levels was observed in patients with desirable or elevated serum total cholesterol levels and in patients with either desirable or abnormally low HDL cholesterol levels. Multivariate adjustment for factors other than HDL cholesterol yielded a slightly increased adjusted mortality risk with a 1-natural-log-unit elevation of triglyceride levels in men (hazard ratio [HR] 1.14, 95% CI 1.00 to 1.30) and women (HR 1.37, 95% CI 1.04 to 1.88). Excess covariate-adjusted risk was noted among patients with elevated total and LDL cholesterol and in women with HDL cholesterol levels >45 mg/dL. After additional adjustment for HDL cholesterol, the risk of mortality with a 1-natural-log-unit elevation of triglycerides declined in men (HR 1.09, 95% CI 0.94 to 1.26) and in women (HR 1.10, 95% CI 0.80 to 1.50). A trend for increased mortality risk remained in patients with elevated total and LDL cholesterol and in women with HDL cholesterol >45 mg/dL. CONCLUSIONS: Elevated triglyceride levels were associated with a small, independent increased mortality risk in CHD patients. This risk may be increased among subgroups of patients with elevated total cholesterol and LDL cholesterol levels.

Aged↗