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PubMed1990

Serum factors influencing cultured hepatocyte exogenous and endogenous triglyceride.

Rat hepatocyte monolayer triglyceride content was increased modestly by incubations with apolipoprotein E-containing triglyceride emulsions or chylomicrons (exogenous) and was increased substantially by increasing media free fatty acid concentrations (endogenous). The secretion of both endogenous and exogenous triglyceride into media was enhanced by additions of serum and serum components. These additions not only enhanced hepatocyte triglyceride secretion but also, because of the absence of media lipolysis, more triglyceride was recovered in the system. Lipoprotein-free serum replicated the effect of whole serum. Lipoprotein produced a more modest secretory response. The apolipoprotein C components were the only ones that enhanced hepatic triglyceride secretion. Both lipoprotein-free plasma and lipoprotein enhanced the in vitro transfer of hepatocyte exogenous triglyceride to fibroblast.

Animals↗
PubMed2001

Triglycerides impair postischemic recovery in isolated hearts: roles of endothelin-1 and trimetazidine.

There is growing evidence that hypertriglyceridemia exacerbates ischemic injury. We tested the hypothesis that triglycerides impair myocardial recovery from low-flow ischemia in an ex vivo model and that such an effect is related to endothelin-1. Hyperglycemic (glucose concentration = 12 mmol/l) and hyperinsulinemic (insulin concentration = 1.2 micromol/l) isolated rat hearts were perfused with Krebs-Henseleit buffer (PO(2) = 670 mmHg, pH 7.4, 37 degrees C) added with increasing triglycerides (0, 1,000, 2,000, and 4,000 mg/dl, n = 6-9 rats/group). Hearts were exposed to 60 min of low-flow ischemia (10% of basal coronary flow), followed by 30 min of reperfusion. We found that increasing triglycerides impaired both the diastolic (P < 0.005) and systolic (P < 0.02) recovery. The release of endothelin-1 during reperfusion increased linearly with triglyceride concentration (P = 0.0009). Elevated triglycerides also increased the release of nitrite and nitrate (NO(x)), the end products of nitric oxide, up to 6 micromol/min. Trimetazidine (1 micromol) further increased NO(x) release, blunted endothelin-1 release, and protected myocardial function during recovery. We conclude that high triglyceride levels impair myocardial recovery after low-flow ischemia in association with endothelin-1 release. The endothelium-mediated effect of triglycerides on both contractile recovery and endothelin-1 release is prevented by 1 microM trimetazidine.

Animals↗
PubMed2003

Low triglyceride, not low cholesterol concentration, independently predicts poor outcome following acute stroke.

BACKGROUND: Recent data have shown an unexpected association between poor outcome after acute stroke and lower serum cholesterol. Triglyceride concentration has been linked to coronary heart disease and stroke; however, there are currently no data on the relationship between triglyceride and stroke outcome. Such information may yield further mechanistic information on the relationship between lipids and stroke outcome. METHODS: We studied 1,310 nondiabetic patients presenting to our acute stroke unit with computed tomography-confirmed acute stroke. Fasting blood samples were drawn within 24 h of admission for glucose, lipids and a standard battery of biochemistry and hematological tests. Information on age, stroke type, admission blood pressure, smoking status, presence of atrial fibrillation, resolution time of symptoms and Oxfordshire Community Stroke Project clinical classification was collated. Stepwise proportional hazards regression was used to estimate the effect of the above variables on survival following stroke. RESULTS: Increased age (p < 0.0001), presence of atrial fibrillation (p = 0.009), hyperglycemia (p = 0.0005) and lower triglyceride level (p < 0.0001) independently predicted higher mortality; early resolution of symptoms (p = 0.005) independently predicted lower mortality. Although serum cholesterol level predicted outcome after adjusting for other prognostic factors, it did not remain significant when triglyceride level was entered into the model. The relative hazard per additional quartile of triglyceride was 0.84 (95% confidence interval 0.77-0.91). CONCLUSIONS: Low triglyceride concentration strongly predicts higher mortality following stroke, whereas serum cholesterol level is not an independent predictor. Outcome following stroke is thus related more strongly to triglyceride-rich than to cholesterol-rich lipoprotein concentrations. The mechanisms explaining this require further investigation.

Acute Disease↗
PubMed1989

Coagulation factor VII and plasma triglycerides. Decreased catabolism as a possible mechanism of factor VII hyperactivity.

High circulating levels of coagulation factor VII (FVII) are known to be associated with elevated concentrations of blood lipids. More specifically, hypertriglyceridemia is correlated with raised FVII coagulant activity (FVIIc). Recently, evidence has been described which suggests that elevation in FVIIc might reflect an increase in the total concentration of FVII, as evaluated by quantitation of FVII antigen (FVIIag). It is also known that FVIIc represents a risk factor for cardiovascular death, but the prediction of cardiovascular risk based on triglyceride estimation is the subject of conflicting results. Since dyslipidemia featuring abnormal triglyceride metabolism is pathophysiologically heterogeneous, we analyzed the possible relationships between FVII and triglyceride further and under standardized postprandial conditions. For this purpose we studied FVIIc and FVIIag in relation to triglyceridemia after a standardized test meal. Our results confirm that FVIIc and FVIIag levels are strongly correlated with each other (r = 0.714; p = 0.01). In addition, both were significantly increased (p less than 0.02) in patients who exhibited abnormal triglyceride levels 8 h after a standardized test meal, as compared to those who displayed normal triglyceridemia. Furthermore, we found that apolipoprotein B levels were also increased in such patients. The deficient postprandial catabolism of triglycerides, therefore, appears to be related to an increase in total FVII concentration, suggesting that some association between the metabolism of triglyceride-rich lipoproteins and FVII might underlie the mechanism of the elevation in FVII. Given the important contribution of FVII to hypercoagulability, then our results may be relevant to the understanding of the role of postprandial triglyceride in atherogenesis and in consideration of the circadian prevalence of cardiovascular thrombosis.

Adult↗
PubMed2004

Analysis of apolipoprotein A5, c3, and plasma triglyceride concentrations in genetically engineered mice.

OBJECTIVE: Both the apolipoprotein A5 and C3 genes have repeatedly been shown to play an important role in determining plasma triglyceride concentrations in humans and mice. In mice, transgenic and knockout experiments indicate that plasma triglyceride levels are strongly altered by changes in the expression of either of these 2 genes. In humans, common polymorphisms in both genes have also been associated with plasma triglyceride concentrations. These similar findings raised the issue of the relationship between these 2 genes and altered triglycerides. METHODS AND RESULTS: To address this issue, we generated independent lines of mice that either overexpressed ("double transgenic") or completely lacked ("double knockout") both apolipoprotein genes. We report that both "double transgenic" and "double knockout" mice display normal triglyceride concentrations compared with overexpression or deletion of either gene alone. Furthermore, we find that human ApoAV plasma protein levels in the "double transgenic" mice are approximately 500-fold lower than human ApoCIII levels, supporting ApoAV as a potent triglyceride modulator despite its low concentration. CONCLUSIONS: Together, these data support that APOA5 and APOC3 independently influence plasma triglyceride concentrations but in an opposing manner.

Animals↗
PubMedDate not supplied

Levels and interrelationships of serum and lipoprotein cholesterol and triglycerides. Association with adiposity and the consumption of ethanol, tobacco, and beverages containing caffeine.

We have carried out a cross-sectional multivariate analysis of serum and lipoprotein lipid levels in white persons from an industrial population. Very low density lipoprotein triglyceride level was independent of ethanol consumption but increased with adiposity and cigarette smoking and decreased with coffee-tea drinking. Concomitant age variation in indices of adiposity accounted for only a small part of the sex-specific age trends in triglyceride level. Very low density lipoprotein cholesterol level was independent of all variables considered when controlled for very low density lipoprotein triglyceride. Low density lipoprotein cholesterol covaried with very low density lipoprotein triglyceride among normotriglyceridemic persons. Small increases in low density lipoprotein cholesterol level with adiposity and cigarette smoking appeared to reflect associated increases in very low density lipoprotein triglyceride. Increased low density lipoprotein cholesterol level with age, however, was largely independent of concomitant age variation in very low density lipoprotein triglyceride. High density lipoprotein cholesterol level increased with ethanol consumption and decreased with adiposity and cigarette smoking even after adjustment for its inverse relationship with very low density lipoprotein triglyceride.

Adult↗
PubMed1997

Moderate genetic influences on plasma levels of plasminogen activator inhibitor-1 and evidence of genetic and environmental influences shared by plasminogen activator inhibitor-1, triglycerides, and body mass index.

Both genes and environmental factors have been reported to influence plasma levels of plasminogen activator inhibitor-1 (PAI-1). However, the relative importance of genetic influences (i.e., heritability) on plasma PAI-1 levels has not yet been investigated. Furthermore, PAI-1 levels are correlated with body mass index (BMI) and triglycerides. These correlations could reflect genetic and/or environmental factors in common to PAI-1, triglycerides, and BMI. We applied multivariate genetic analysis methods to assess the relative importance of genetic and environmental influences on plasma PAI-1 levels and to test the significance of genetic and/or environmental influences shared by PAI-1, triglycerides, and BMI in 217 pairs of middle-aged and elderly twins, of whom 113 pairs were reared apart and 121 pairs were women. The heritability estimate for PAI-1 levels was 42%. Individual-specific environmental factors explained 36% of the variance for PAI-1 levels. The remaining variance of PAI-1 was explained by rearing and residual-familial environmental factors. Furthermore, a genetic correlation of 1.00 between PAI-1 and triglycerides, a rearing environmental correlation of 1.00 between PAI-1 and BMI, a residual-familial environmental correlation of 1.00 between PAI-1 and triglycerides, and a genetic correlation of 0.63 between PAI-1 and BMI, were found. In conclusion, the present results suggest that genetic influences on plasma PAI-1 are moderate. Genetic and shared rearing or residual-familial environmental factors shared by PAI-1, BMI, and triglycerides explain the phenotypic association between these measures. It appears that all the genetic influences for PAI-1 are more or less shared with those for triglycerides and BMI.

Adoption↗
PubMed2000

HIV protease inhibitors stimulate hepatic triglyceride synthesis.

Hyperlipidemia may complicate the use of HIV protease inhibitors (PIs) in AIDS therapy. To determine the cause of hyperlipidemia, the effect of PIs on lipid metabolism was examined with HepG2 liver cells and AKR/J mice. In HepG2 cells, the PIs ABT-378, nelfinavir, ritonavir, and saquinavir stimulated triglyceride synthesis; ritonavir increased cholesterol synthesis; and amprenavir and indinavir had no effect. Moreover, nelfinavir increased mRNA expression of diacylglycerol acyltransferase and fatty acid synthase. The retinoid X receptor agonist LG100268, but not the antagonist LG100754, further increased PI-stimulated triglyceride synthesis and mRNA expression of fatty acid synthase in vitro. In fed mice, nelfinavir or ritonavir did not affect serum glucose and cholesterol, whereas triglyceride and fatty acids increased 57% to 108%. In fasted mice, ritonavir increased serum glucose by 29%, cholesterol by 40%, and triglyceride by 99%, whereas nelfinavir had no effect, suggesting these PIs have different effects on metabolism. Consistent with the in vitro results, nelfinavir and ritonavir increased triglyceride 2- to 3-fold in fasted mice injected with Triton WR-1339, an inhibitor of triglyceride clearance. We propose that PI-associated hyperlipidemia is due to increased hepatic triglyceride synthesis and suggest that retinoids or meal restriction influences the effects of select PIs on lipid metabolism.

Acyltransferases↗
PubMed2000

Apolipoprotein E2 (Lys146-->Gln) causes hypertriglyceridemia due to an apolipoprotein E variant-specific inhibition of lipolysis of very low density lipoproteins-triglycerides.

The apolipoprotein E2 (Lys146-->Gln) variant is associated with a dominant form of familial dysbetalipoproteinemia. Heterozygous carriers of this variant have elevated levels of plasma triglycerides, cholesterol, and apolipoprotein E (apoE). It was hypothesized that the high amounts of triglycerides in the very low density lipoprotein (VLDL) fraction are due to a disturbed lipolysis of VLDL. To test this hypothesis, apoE knockout mice were injected with an adenovirus containing the human APOE*2 (Lys146-->Gln) gene, Ad-E2(146), under the control of the cytomegalovirus promoter. ApoE knockout mice injected with an adenovirus vector encoding human apoE3 (Ad-E3) were used as controls. Five days after adenovirus injection, plasma cholesterol levels of mice injected with a high dose of Ad-E2(146) (2x10(9) plaque-forming units) were not changed compared with preinjection levels, whereas in the group who received a low dose of Ad-E2(146) (5x10(8) plaque-forming units) and in the groups injected with a low or a high dose of Ad-E3, plasma cholesterol levels were decreased 5-, 6-, and 12-fold, respectively. Plasma triglycerides were not affected in mice injected with Ad-E3. In contrast, a 7-fold increase in plasma triglycerides was observed in mice injected with the low dose of Ad-E2(146) compared with mice injected with Ad-E3. Injection with the high dose of Ad-E2(146) resulted in a dramatic increase of plasma triglycerides (50-fold compared with Ad-E3 injection). In vitro lipolysis experiments showed that the lipolysis rate of VLDLs containing normal amounts of apoE2 (Lys146-->Gln) was decreased by 54% compared with that of VLDLs containing comparable amounts of apoE3. The in vivo VLDL-triglyceride production rate of Ad-E2(146)-injected mice was not significantly different from that of Ad-E3-injected mice. These results demonstrate that expression of apoE2 (Lys146-->Gln) causes hypertriglyceridemia due to an apoE variant-specific inhibition of the hydrolysis of VLDL-triglycerides.

Adenoviridae↗
PubMed2001

Metabolic and lifestyle determinants of postprandial lipemia differ from those of fasting triglycerides: The Atherosclerosis Risk In Communities (ARIC) study.

Despite the reported association of lipoprotein responses to a fatty meal with atherosclerosis, little is known about the determinants of these responses. Plasma triglyceride, retinyl palmitate, and apolipoprotein B-48 responses to a standardized fatty meal containing a vitamin A marker were measured in 602 Atherosclerosis Risk in Communities (ARIC) study participants. To focus on postprandial responses specifically, which have been reported to be related to atherosclerosis independently of fasting triglycerides, analyses for determinants of postprandial responses were adjusted for fasting triglycerides. Major determinants of fasting triglycerides, namely, diabetes, obesity, other factors related to insulin resistance, and male sex, were not independently associated with postprandial responses. Fasting triglycerides were the strongest predictor of postprandial lipids, but independent of triglycerides, the predictors of postprandial responses were smoking, diet, creatinine, and alcohol. Smokers had substantially increased retinyl palmitate and apolipoprotein B-48 responses, indicators of chylomicrons and their remnants. Persons who consume more calories or omega3 fatty acids had reduced chylomicron responses. Triglyceride responses were associated positively with serum creatinine levels and negatively with moderate alcohol consumption. Thus, determinants of fasting and postprandial lipids differ. The independent atherogenic influence of postprandial lipids may relate more to smoking and diet than to obesity and insulin resistance.

Aged↗
PubMedDate not supplied

Triglyceride-lowering effect of marine polyunsaturates in patients with hypertriglyceridemia.

Twenty male patients with primary hypertriglyceridemia were treated for 4 weeks with daily supplements (15 g) of oil, which provided approximately 6 g of polyunsaturated fatty acid (PUFA) either of fish or of vegetable origin. Total plasma cholesterol concentrations were unaffected, but both types of supplement increased high density lipoprotein-3 (HDL3) cholesterol concentrations. The fish, but not the vegetable, oil supplement led to a decrease in plasma triglyceride concentrations. Very low density lipoprotein (VLDL), fatty acid composition, and VLDL triglyceride kinetics were subsequently studied in five patients (four male, one female) before and after 4 weeks of therapy with 15 g of the same fish oil. The fish oil led to increases in the proportion of eicosapentaenoic acid in both the VLDL triglyceride and phospholipid fractions, but the increase was greater in the latter. In contrast, the proportion of docosahexanoic acid was increased only in the VLDL triglycerides. The decrease in plasma triglyceride concentrations that occurred with fish-oil therapy was accompanied by a reduction in the absolute catabolic rate of VLDL triglyceride, implying a concomitant change in synthetic rate; the fractional catabolic rate of VLDL triglyceride was unaltered. It is suggested that polyunsaturated fatty acids of marine origin may be therapeutically useful for hypertriglyceridemia.

Adult↗
PubMed2000

Secondary prevention by raising HDL cholesterol and reducing triglycerides in patients with coronary artery disease.

BACKGROUND: Coronary heart disease patients with low high-density lipoprotein cholesterol (HDL-C) levels, high triglyceride levels, or both are at an increased risk of cardiovascular events, but the clinical impact of raising HDL-C or decreasing triglycerides remains to be confirmed. METHODS AND RESULTS: In a double-blind trial, 3090 patients with a previous myocardial infarction or stable angina, total cholesterol of 180 to 250 mg/dL, HDL-C < or =45 mg/dL, triglycerides < or =300 mg/dL, and low-density lipoprotein cholesterol < or =180 mg/dL were randomized to receive either 400 mg of bezafibrate per day or a placebo; they were followed for a mean of 6.2 years. The primary end point was fatal or nonfatal myocardial infarction or sudden death. Bezafibrate increased HDL-C by 18% and reduced triglycerides by 21%. The frequency of the primary end point was 13. 6% on bezafibrate versus 15.0% on placebo (P=0.26). After 6.2 years, the reduction in the cumulative probability of the primary end point was 7.3%, (P=0.24). In a post hoc analysis in the subgroup with high baseline triglycerides (> or =200 mg/dL), the reduction in the cumulative probability of the primary end point by bezafibrate was 39.5% (P=0.02). Total and noncardiac mortality rates were similar, and adverse events and cancer were equally distributed. CONCLUSIONS: Bezafibrate was safe and effective in elevating HDL-C levels and lowering triglycerides. An overall trend in a reduction of the incidence of primary end points was observed. The reduction in the primary end point in patients with high baseline triglycerides (> or =200 mg/dL) requires further confirmation.

Aged↗
PubMed1997

Fasting triglycerides, high-density lipoprotein, and risk of myocardial infarction.

BACKGROUND: Recent data suggest that triglyceride-rich lipoproteins may play a role in atherogenesis. However, whether triglycerides, as a marker for these lipoproteins, represent an independent risk factor for coronary heart disease remains unclear, despite extensive research. Several methodological issues have limited the interpretability of the existing data. METHODS AND RESULTS: We examined the interrelationships of fasting triglycerides, other lipid parameters, and nonlipid risk factors with risk of myocardial infarction among 340 cases and an equal number of age-, sex-, and community-matched control subjects. Cases were men or women of <76 years of age with no prior history of coronary disease who were discharged from one of six Boston area hospitals with the diagnosis of a confirmed myocardial infarction. In crude analyses, we observed a significant association of elevated fasting triglycerides with risk of myocardial infarction (relative risk [RR] in the highest compared with the lowest quartile=6.8; 95% confidence interval [CI]=3.8 to 12.1; P for trend <.001). Results were not materially altered after control for nonlipid coronary risk factors. As expected, the relationship was attenuated after adjustment for HDL but remained statistically significant (RR in the highest quartile=2.7; 95% confidence interval [CI]=1.4 to 5.5; P for trend=.016). Furthermore, the ratio of triglycerides to HDL was a strong predictor of myocardial infarction (RR in the highest compared with the lowest quartile=16.0; 95% CI=7.7 to 33.1; P for trend <.001). CONCLUSIONS: Our data indicate that fasting triglycerides, as a marker for triglyceride-rich lipoproteins, may provide valuable information about the atherogenic potential of the lipoprotein profile, particularly when considered in context of HDL levels.

Adult↗
PubMedDate not supplied

Echo-lucency of computerized ultrasound images of carotid atherosclerotic plaques are associated with increased levels of triglyceride-rich lipoproteins as well as increased plaque lipid content.

BACKGROUND: Echo-lucency of carotid atherosclerotic plaques on computerized ultrasound B-mode images has been associated with a high incidence of brain infarcts as evaluated on CT scans. We tested the hypotheses that triglyceride-rich lipoproteins in the fasting and postprandial state predict carotid plaque echo-lucency and that echo-lucency predicts a high plaque lipid content. METHODS AND RESULTS: The study included 137 patients with neurological symptoms and > or = 50% stenosis of the relevant carotid artery. High-resolution B-mode ultrasound images of carotid plaques were computer processed to yield a measure of echogenicity (gray-scale level). Lipoproteins were measured before and hourly for 4 hours after a standardized fatty meal. A subgroup of 58 patients underwent endarterectomy. On linear regression analysis, echo-lucency (low gray-scale level) was associated with elevated levels of fasting and postprandial plasma triglycerides (P=.0002 and P=.002), IDL cholesterol (P=.0009 and P=.006), and VLDL/chylomicron remnant cholesterol (P=.0003 and P=.0004) and triglycerides (P=.0003 and P=.003), the area under the plasma triglyceride curve 0 to 4 hours after a fatty meal (P=.001), and body mass index (P=.0001). On ANCOVA, body mass index, fasting IDL cholesterol, and fasting plasma triglycerides were independent predictors of echo-lucency. Echo-lucency was associated with increased relative plaque lipid content (P=.02). CONCLUSIONS: Increased plasma levels of triglyceride-rich lipoproteins predict echo-lucency of carotid plaques, which is associated with increased plaque lipid content. Because echo-lucency has been associated with a high incidence of brain infarcts on CT scans, triglyceride-rich lipoproteins may predict a plaque type particularly vulnerable to rupture.

Arteriosclerosis↗
PubMed2004

Lower serum triglyceride level is associated with increased stroke severity.

BACKGROUND AND PURPOSE: A previous study showed that low triglyceride concentration predicts higher mortality after stroke. The aim of our study was to determine whether serum triglyceride level is associated with stroke severity on admission. METHODS: 863 consecutive patients with acute ischemic stroke were included. Serum triglyceride level was measured within 36 hours after stroke onset. Stroke severity on admission was assessed using Scandinavian Stroke Scale (SSS). The patients were divided into 2 groups: those with severe stroke (SSS < or =25) and those with mild/moderate stroke (SSS >25). RESULTS: Patients with severe stroke had significantly lower serum triglyceride level than patients with mild/moderate stroke (1.4+/-0.6 versus 1.7+/-1.3 mmol/L). After adjusting for age, sex, atrial fibrillation, diabetes mellitus, obesity, and ischemic heart disease, patients with triglyceride >2.3 mmol/L had lower risk of severe stroke than those with triglyceride < or =2.3 mmol/L (OR: 0.58; 95% CI: 0.35 to 0.95). CONCLUSIONS: Our results suggest that lower level of triglyceride is associated with the more severe stroke.

Aged↗
PubMed1996

Echolucent carotid artery plaques are associated with elevated levels of fasting and postprandial triglyceride-rich lipoproteins.

BACKGROUND AND PURPOSE: Echolucent carotid atherosclerotic plaques are associated with an increased risk of neurological symptoms. Elevated plasma triglycerides is a risk factor for cerebral and coronary infarction. This study examined these individual pathogenetic risk factors to determine whether they were related. METHODS: We included 85 symptomatic patients with at least 40% carotid artery stenosis. Plaque morphology of the relevant artery was evaluated by high-resolution B-mode ultrasonography as echolucent, echo-rich, or intermediate. Fasting and postprandial lipids and lipoproteins were measured before and at hourly intervals for 4 hours after a fatty meal (1 g cream fat per kilogram body weight). RESULTS: When we compared patients with echolucent plaques to patients with echo-rich or intermediate plaques, the former had higher fasting and postprandial plasma triglycerides (P < or = .006), higher chylomicron remnants/VLDL cholesterol (P = .02) and triglycerides (P < or = .004), a larger area under the plasma triglyceride curve 0 to 4 hours after a fatty meal, with (AUCTG-TG oh) or without (AUCTG) subtraction of fasting levels (P = .007 and P = .003), a larger body mass index (P = .03), and were younger (P = .01). Multiple logistic regression analysis found that when age and body mass index were taken into account, fasting plasma and VLDL triglycerides, postprandial chylomicron remnants/VLDL triglycerides, AUCTG-TG oh and AUCTG with odds ratios of 4.1, 3.8, 3.0, 2.7, and 4.3, respectively, were independent predictors of an echolucent plaque. CONCLUSIONS: Echolucent carotid artery plaques are associated with elevated levels of triglyceride-rich lipoproteins in the fasting or postprandial state.

Adult↗
PubMed1975

Effect of elevated triglycerides on the diffusing capacity of man.

In view of the decreased diffusing capacity recently reported in man during lipid infusion, studies have now been made on the effects of hyperlipidemia on the diffusing capacity for carbon monoxide (DLco). In normal volunteers and patients with hyperlipidemias, DLco and plasma triglyceride concentrations were determined during fat tolerance tests and while the patients were on diets that increased or decreased triglyceride concentrations. During the fat tolerance tests, the largest triglyceride and DLco changes were from 346 mg per 100 ml with a DLco of 18.8 ml per min per mm Hg to 1,545 mg per 100 ml with a DLco of 23.4 ml per min per mm Hg. While patients were on speical diets, the largest triglyceride and DLco changes were from 5,102 mg per 100 ml and 29.0 ml per min per mm Hg to 492 mg per 100 ml and 26.4 ml per min per mm Hg, respectively. Sta tistical tests showed no significant change of DLco with change in triglyceride concentration. The data suggest that there is normally no association between change in triglyceride concentration and change in DLco, and that triglycerides normally transported in plasma, even when present in extreme amounts as chylomicrons or very-low-density lipoprotein, do not affect the DLco.

Adult↗
PubMed1971

Quantitative studies of the metabolism of chylomicron triglycerides and cholesterol by liver and extrahepatic tissues of sheep and dogs.

Unanesthetized sheep and dogs, previously fitted with indwelling catheters in the aorta, lower vena cava, mesenteric, portal, left hepatic and jugular veins, were given constant intravenous infusions of lymph in which the chylomicron lipids were variously labeled with (3)H or (14)C. Para-aminohippuric acid was infused into the mesenteric venous catheter for measurement of portal and hepatic venous blood flow. In some animals, alternately labeled free fatty acids bound to albumin were mixed with the lymph to be infused. In both species, chylomicron triglyceride fatty acids were taken up in the region drained by the lower vena cava and portal vein and free fatty acids derived from hydrolysis of these triglycerides were extensively recycled in the blood. Direct uptake of triglyceride fatty acids also occurred in liver and accounted for about 10% of the total triglyceride fatty acids removed from the blood in sheep and 22% in dogs. In sheep, 10% and, in dogs, about 40% of these triglyceride-fatty acids were released into the blood as free fatty acids. The free fatty acids recycled from various regions accounted for a substantial fraction of the chylomicron fat eventually deposited in each tissue. Uptake of chylomicron cholesterol from the blood of sheep occurred primarily in liver and to a small extent in certain tissues drained by the portal vein. The results obtained, together with other available data, demonstrate that chylomicron triglycerides are removed primarily in extrahepatic tissues of both species, while the liver removes cholesterol contained in chylomicron "skeletons" from which most of the triglycerides have been removed. The quantitative differences between transport of chylomicron lipid in sheep and dogs may be related to known differences in the structure of their hepatic sinusoids.

Animals↗