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PubMed1979

Di-, mono- and nonphytanyl triglycerides in the serum: a sensitive parameter of the phytanic acid accumulation in Refsum's disease.

The relative proportions of the diphytanyl, monophytanyl and nonphytanyl triglycerides ("triglyceride pattern"), the phytanic acid content of the triglycerides and the phytanic acid levels in the serum of 3 patients with Refsum's disease (heredopathia atactica polyneuritiformis, phytanic acid storage disease) were estimated by thin-layer chromatography, densitometry and gas chromatography, respectively. The individual triglyceride patterns were clearly dependent on the phytanic acid content of the triglycerides: the more phytanic acid in the triglycerides, the higher the percentage of the diphytanyl and the lower the percentage of the nonphytanyl triglycerides. The monophytanyl triglycerides were also related to the phytanic acid content of the triglycerides, although in a complex manner. The triglyceride pattern can be taken as a parameter of the phytanic acid accumulation in Refsum's disease to be at least as sensitive as the serum phytanic acid level in the biochemical evaluation of the efficiency of the dietary treatment.

Eicosanoic Acids↗
PubMed1988

Triglyceride-rich lipoprotein metabolism during acute hyperinsulinemia in hypertriglyceridemic humans.

Chronic endogenous hyperinsulinemia is associated with increased rates of triglyceride production in humans. The effect of acute exogenous hyperinsulinemia on triglyceride production was studied in seven hypertriglyceridemic men before and during six hours of hyperinsulinemic-euglycemic clamping, and in two men before and during six hours of hyperinsulinemic-hyperglycemic clamping. Apparent triglyceride production rates were assessed qualitatively by examining the rate of decline of 3H-glycerol-labeled plasma triglyceride specific activity in the preclamp period, and again when a new steady state had occurred, during the final three hours of the clamp. During the euglycemic (91.2 +/- 3.0 mg glucose/dL plasma) clamps, plasma insulin levels were increased by 700% (0.76 +/- 0.12 to 5.3 +/- 0.29 ng/mL, P less than .001) and plasma glucagon levels decreased by 19%, compared with baseline. The apparent triglyceride production rate did not increase in five of six men during the euglycemic-hyperinsulinemic clamp, or in either man during the hyperglycemic-hyperinsulinemic clamp. During the clamp period the triglyceride declined in the plasma by 23.4 +/- 3.1%; and the apolipoprotein B by 10.5 +/- 1.5%. Hyperinsulinemia with euglycemia was also associated with a decline in the ratio of triglyceride to apolipoprotein B in the triglyceride-rich lipoproteins. This was more pronounced in very low density lipoprotein (VLDL) than in intermediate density lipoprotein (IDL). In this study, hyperinsulinemia led to a decrease in the plasma glucagon concentration. This decrease was positively correlated with the decrease in the slope of the triglyceride specific activity v time curve. Hence, the changes in triglyceride production were not due to an increase in plasma glucagon concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed2002

Triglyceride-lowering effect of pitavastatin [corrected] in a rat model of postprandial lipemia.

The triglyceride-lowering effect of pitavastatin, a potent 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, was investigated in a rat model of postprandial lipemia. Plasma triglyceride levels started to increase 4 h after the fat load, reached the maximum at 6 h and then gradually decreased. A single dose of pitavastatin (1 mg/kg) significantly suppressed chylomicron-triglyceride secretion into the lymph by 40% and delayed the elevation of plasma triglyceride. Pitavastatin at 1 mg/kg decreased the 6-h plasma triglyceride levels by 53% and at 0.5 mg/kg decreased the 0-12 h area under the curve (AUC) of triglyceride levels by 56%. Atorvastatin also caused decreases, but to a lesser extent. Pitavastatin, and atorvastatin to a lesser extent, reduced the activity of the intestinal microsomal triglyceride transfer protein (MTP) at 6 h. These results suggested that a single dose of pitavastatin lowered postprandial triglyceride levels in rats by decreasing chylomicron-triglyceride secretion, probably through a reduction of intestinal MTP activity and triglyceride droplet formation in the endoplasmic reticulum.

Animals↗
PubMed1999

Triglyceride-lowering effect of a novel insulin-sensitizing agent, JTT-501.

JTT-501, 4-[4-[2-(5-methyl-2-phenyl-4-oxazolyl)ethoxy]benzyl]-3, 5-isoxazolidinedione, is a novel insulin-sensitizing agent. We investigated the triglyceride-lowering activity of JTT-501 in a high-fat (HF) rat model. The HF rats showed insulin resistance with elevation of fasting insulin levels and reduction of insulin-stimulated glucose oxidation. There was also a tendency towards increased basal insulin and triglyceride levels. Oral administration of JTT-501 (3-30 mg kg(-1) day(-1) for 7 days) reduced basal triglyceride levels dose dependently with a minimum effective dose of 3 mg kg(-1) day(-1). Furthermore, regarding triglyceride metabolism, JTT-501 (30 mg kg(-1) day(-1) for 15 days, p.o.) decreased hepatic triglyceride output rate and serum triglyceride half-life (T1/2). In contrast, pioglitazone (30 mg kg(-1) day(-1) for 15 days, p.o.) reduced T1/2, but did not affect hepatic triglyceride output rate. We conclude that JTT-501 possesses potent triglyceride-lowering activity due to its inhibition of triglyceride secretion from the liver and enhancement of triglyceride disposal in peripheral tissues.

Animals↗
PubMed2003

APOA5-1131T>C polymorphism is associated with triglyceride levels in Chinese men.

A new apolipoprotein gene, APOA5, was recently discovered near the APOA1/C3/A4 gene cluster. Transgenic mice overexpressing the homologous gene, apoa5, showed reduced plasma triglyceride levels, while knockout mice had greatly increased triglycerides, suggesting that human genetic variants affecting expression of the protein product, APOAV, might affect triglyceride levels. Polymorphisms in the APOA5 gene were indeed found to be associated with triglyceride levels in men, though not in women. We sought to confirm the association of the APOA5-1131T>C polymorphism with triglyceride levels in 167 Chinese men chosen for having either high (>/=1.7 mm, n = 82) or low (</=1.2 mm, n = 85) triglycerides. More subjects with high triglycerides had one or two copies of the minor (C) allele of the polymorphism (67%) than did low triglyceride subjects (48%), and combining all subjects showed that those with one or two C alleles had higher triglyceride levels [1.67 +/- 2.20 (geometric mean +/- SD)] than those without (1.22 +/- 2.08 mm, p = 0.01), confirming the reported effect in a different ethnic group. The C allele is more common in Chinese than in Caucasians (26-40% vs. 8% of alleles), suggesting that the impact of this polymorphism on triglyceride levels in the population and therefore on public health is greater among Chinese.

Adult↗
PubMed1997

Dietary triglycerides, up to 40 g/meal, do not affect preformed vitamin A bioavailability in humans.

OBJECTIVE: Assessing the effect of the dose of dietary triglycerides on preformed vitamin A (retinyl esters) bioavailability in humans. DESIGN: Four test meals containing 15,000 RE retinyl-palmitate and either 0, 15, 30 or 40 g added triglycerides were ingested by eight healthy volunteers, at different days and in a randomized order. SETTING: The study was done in the Hospital Sainte Marguerite, Marseille, France. SUBJECTS: Eight healthy male volunteers were recruited by advertisement. INTERVENTION: Blood samples were collected every hour for seven hours after the test meals intake. Serum and chylomicron (Svedberg flotation unit > 1000) were prepared by centrifugation and retinyl esters were measured by HPLC. RESULTS: The serum retinyl ester response was not significantly lower after the intake of the meal without added triglycerides (7944 +/- 3262 nmol/L h) than after the intake of the fat meals (10012 +/- 2182, 7869 +/- 3157 and 10777 +/- 2067 nmol/L h for the 15, 30 and 40 g-fat meal, respectively), indicating that the serum retinyl ester response was not related to the amount of meal triglycerides. Chylomicron retinyl linoleate response stepwise increased when the amount of meal triglycerides increased while retinyl palmitate and retinyl stearate responses reached a maximum since 15 g triglycerides. Postprandial serum retinol concentration did not change whatever the meal ingested. CONCLUSIONS: (i) a significant amount of preformed vitamin A is apparently absorbed when ingested with trace amount of meal triglycerides only; (ii) meal triglycerides, up to 40 g/meal, do not increase preformed vitamin A bioavailability; (iii) the retinyl ester pattern recovered in the chylomicrons, and probably the esterification process of retinol, is affected by the amount of meal triglycerides; (iv) postprandial retinol homeostasis is not affected by dietary triglycerides.

Adult↗
PubMed1983

Insulin-induced glucose utilization influences triglyceride metabolism.

1. We have investigated the possibility that the effect of insulin on triglyceride metabolism is related to the individual's responsiveness to insulin-mediated glucose utilization. Changes in plasma triglyceride levels were determined during 2 h infusions of insulin with glucose that maintained euglycaemia in 17 subjects, some of whom were overweight and/or hypertriglyceridaemic. 2. Plasma triglyceride concentrations fell in most subjects (mean +/- SD: 19.9 +/- 13.0%). The percentage fall in plasma triglyceride was inversely related to body mass index (r = -0.64, P less than 0.01) and to basal triglyceride concentration (r = -0.69, P less than 0.005), but directly to insulin sensitivity (r = +0.48, P less than 0.05), and was unrelated to plasma free fatty acid concentration. 3. Since insulin sensitivity was also related to body mass index and basal triglyceride level stepwise regression analysis was carried out to determine the influence of these three variables on insulin-mediated lowering of plasma triglyceride. The percentage fall in plasma triglyceride remained independently related to insulin sensitivity (P less than 0.05) and to body mass index (P less than 0.05), and these two variables accounted for 44% of the fall in triglyceride. 4. Resistance to insulin (in terms of glucose utilization) may therefore be one significant, independent factor determining the plasma triglyceride concentration.

Adult↗
PubMed1996

Impaired suppression of plasma free fatty acids and triglycerides by acute hyperglycaemia-induced hyperinsulinaemia and alterations in high density lipoproteins in essential hypertension.

OBJECTIVES: Essential hypertension may be associated with abnormalities in free fatty acids (FFA) and triglyceride metabolism, which could lead to alterations in high density lipoproteins (HDL). Lecithin: cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP) are key factors in the esterification of cholesterol and the subsequent transfer of cholesteryl ester from HDL towards triglyceride-rich lipoproteins. We compared baseline plasma lipids, HDL lipids, plasma LCAT and CETP activity as well as the lowering of plasma FFA and triglycerides by acute hyperglycaemia-induced hyperinsulinaemia in patients with essential hypertension and control subjects. SETTING: University Hospital, Groningen. SUBJECTS AND DESIGN: Eight patients with essential hypertension and eight control subjects were studied during a 3-h hyperglycaemic glucose clamp (blood glucose, 10 mmol L-1). MAIN OUTCOME MEASURES: Plasma insulin, FFA, triglycerides and HDL lipids, plasma LCAT and CETP. RESULTS: Baseline plasma FFA, total cholesterol and HDL cholesterol were not different between the groups, but plasma triglycerides tended to be higher in the hypertensive patients (P < 0.10). The baseline HDL free cholesterol content and the HDL free cholesterol/cholesteryl ester ratio were lower (P < 0.05 for both) in the hypertensive than in the control group. Although baseline plasma LCAT and CETP activity were not significantly different between the groups, the plasma LCAT/CETP ratio, reflecting the amount of active LCAT compared to that of CETP, was higher in the hypertensive patients (P < 0.05). In the combined subjects and in the hypertensive group, the HDL free cholesterol content was negatively related to plasma triglycerides and to the LCAT/CETP ratio, whereas this ratio was positively correlated with plasma triglycerides (P < or = 0.01 for all correlations). During a 3-h hyperglycaemic clamp (blood glucose 10 mmol L-1) plasma FFA and triglycerides decreased to a lesser extent (P < 0.02 and P = 0.05) and remained higher (P < 0.05 for both) in the hypertensive patients, despite similar plasma insulin levels. CONCLUSION: The action of insulin on FFA metabolism is impaired which is likely to contribute to higher plasma triglycerides in essential hypertension. In turn, higher triglycerides influence the HDL lipid composition, either directly or via an effect on the plasma LCAT/CETP ratio.

Acute Disease↗
PubMed2001

Maximal post-prandial triglyceride increase reflects post-prandial hypertriglyceridaemia and is associated with the insulin resistance syndrome.

AIMS: To assess the value of maximal post-prandial triglyceride increase after a high fat, low carbohydrate (CHO) test meal, as index of post-prandial hypertriglyceridaemia and its relation with insulin resistance. METHODS: Fifty non-diabetic subjects, 22 male and 28 female, aged 52.1+/-4.5 and 56.9+/-3.8 years, were studied. Glucose, insulin and triglycerides were measured fasting and 1, 2, 3 and 4 h after a meal consisting of 40 g fat, 19 g protein and 10 g CHO. Insulin resistance was calculated according to the HOMA model. RESULTS: The maximal triglyceride increment occurred during the 4th hour. Its absolute value (delta-TG) and the per cent increase over the fasting value (PTI), were considered appropriate for the evaluation of the post-prandial triglyceride response. Both delta-TG and PTI were strongly correlated with triglycerides incremental area in males and females, r = 0.797 and r = 0.700, P<0.01 and r = 0.805 and r = 0.774, P<0.001, respectively, and thus they can be used as indices of the post-prandial triglyceride response. No correlation was found between fasting triglyceride and triglyceride incremental area or delta-TG. Thus, post-prandial hypertriglyceridaemia can occur irrespectively of the fasting triglyceride concentrations. A weak correlation was found between PTI and insulin resistance in females, r = 0.384, P<0.05, but not in males, r = 0.224, P>0.05. However further analysis by quartiles of PTI showed similar insulin resistance levels in the first three quartiles and a significant increase in the 4th, both for males and females, 4th vs. 3rd quartile 7.4+/-3.6 vs. 2.2+/-0.7 and 6.4+/-2.4 vs. 2.2+/-0.6, respectively. The 4th quartile corresponds to a PTI > or =80%. CONCLUSIONS: PTI after the high fat, low CHO test meal used, consistently reflects post-prandial hypertriglyceridaemia, is easily measured and it is not predicted by fasting triglycerides. A PTI > or = 80% is associated with a significant increase of insulin resistance, and might therefore be considered the cut-off point for an abnormal post-prandial hypertriglyceridaemic response, at least in relation with insulin resistance. Such response could be added to the abnormalities of the insulin resistance syndrome, as an independent parameter.

Blood Glucose↗
PubMed2004

Evaluation of the effect of tibolone and transdermal estradiol on triglyceride level in hypertriglyceridemic and normotriglyceridemic postmenopausal women.

The objective of the present study was to quantify the magnitude of the association between the change in triglycerides and high-density lipoprotein (HDL) cholesterol levels with the use of tibolone and transdermal estrogen in postmenopausal women with hypertriglyceridemia and normotriglyceridemia. This prospective randomized study enrolled 140 postmenopausal women who had all been hysterectomized for almost a year or more. All subjects completed the 3-month follow-up. The 140 patients were divided into two groups: 70 were given transdermal 17beta-estradiol 0.05 mg/day, and 70 were given tibolone 2.5 mg/day. We compared the effects of tibolone and transdermal 17beta-estradiol on lipids and dimacteric symptoms of the patients. To evaluate the effects of tibolone and transdermal estrogens on triglycerides and HDL cholesterol in postmenopausal women with normotriglyceridemia and hypertriglyceridemia, the women were assigned to five groups according to triglyceride levels (0-100, 101-200, 201-300, 301-400 and > or = 401 mg/dl). We compared changes in the triglyceride and HDL cholesterol levels of each group after treatment. All 140 postmenopausal women completed the trial. No significant differences were found in baseline characteristics of the patients. The tibolone group showed a 22.6% decrease whereas the transdermal estrogen group had a 10.9% decrease in the mean triglyceride levels after 3 months of treatment. The mean decrease of triglyceride level with transdermal estradiol was approximately 11% in normotriglyceridemic and hypertriglyceridemic postmenopausal women. The mean decrease of triglyceride level was 17% in the normotriglyceridemic group and 22-30% in the hypertriglyceridemic groups with tibolone. While the mean HDL cholesterol level increased in the transdermal estrogen group (3.6%), it decreased in the tibolone group (9.3%). We found that tibolone decreased triglyceride levels much more than did transdermal estradiol. However, HDL cholesterol was decreased by tibolone and increased by transdermal estradiol. Tibolone had a more marked decreasing effect in postmenopausal women who had higher initial triglyceride levels. It is suggested that the beneficial effect of tibolone on the cardiovascular system might be greater in women with a high level of triglycerides.

Administration, Cutaneous↗
PubMed2003

The influence of maternal triglyceride levels on infant birth weight in Peruvian women with pre-eclampsia.

OBJECTIVE: Hypertriglyceridemia is an important pathophysiological feature of pre-eclampsia, a complication associated with retarded fetal growth. We studied the relation between third-trimester maternal triglyceride levels and infant birth weight in 113 pre-eclamptic and 150 normotensive women. METHODS: Plasma triglyceride concentrations were determined using enzymatic methods. The relative risk of infant low birth weight (LBW, < 2500 g) was determined using logistic regression to calculate the odds ratio (OR) and 95% confidence interval (CI). RESULTS: Approximately 12% of normotensive and 32% of pre-eclamptic mothers delivered LBW infants. After adjusting for maternal age, parity, pre-pregnancy adiposity and gestational age at delivery, pre-eclamptics were 2.3 times more likely to deliver a LBW infant as compared with normotensive mothers (95% CI 1.1-5.0). There was no association between plasma triglyceride level and infant birth weight. Pearson correlation coefficients for birth weight and triglyceride were r = 0.10 (p = 0.24) and r = 0.06 (p = 0.49) for normotensive and pre-eclamptic women, respectively. The OR for LBW associated with high triglyceride level (> or = 233 mg/dl) was 0.8 (95% CI 0.2-3.1) and 0.9 (95% CI 0.4-2.0) for the two groups. Triglyceride levels did not modify the pre-eclampsia and LBW association. Compared to normotensive women with low triglyceride level (< 233 mg/dl), the ORs for LBW were 1.2 (95% CI 0.4-4.0), 3.6 (95% CI 1.0-12.5) and 2.8 (95% CI 1.0-8.0) for normotensive and high triglyceride, pre-eclamptic and low triglyceride, and pre-eclamptic and high triglyceride mothers, respectively. CONCLUSIONS: Hypertriglyceridemia in late pregnancy, considered a maternal adaptation to maintain stable fuel distribution to the fetus, was not related to birth weight.

Adult↗
PubMed1989

Plasma triglyceride as a risk factor for coronary heart disease. The epidemiologic evidence and beyond.

Elevated plasma triglyceride has been found to be a univariate risk factor for coronary heart disease in many epidemiologic studies, but this increased risk is not independent of other lipid and lipoprotein measures. Rather than dismiss triglyceride as a risk factor, we can see this disparity between univariate and multivariate results as a clue to better understanding of the potential role of triglyceride in atherosclerosis. From a statistical point of view, triglyceride often is not a significant predictor of coronary heart disease in multivariate statistical models because of the large variation in triglyceride measurements and the strong inverse relation between HDL cholesterol and triglyceride. Heterogeneity in both the biologic mechanisms producing hypertriglyceridemia and the manifestations of cardiovascular disease complicates the study of triglyceride as a risk factor. recently, subclasses of both HDL and LDL have been shown to be related to triglyceride metabolism and may provide more precise variables for predicting risk. However, none of this evidence precludes the involvement of triglyceride in the development of atherosclerosis. The final answer as to whether triglyceride is a causal risk factor for coronary heart disease must come from the biologic sciences, and the complexity of the epidemiologic results likely reflects the intricate metabolic processes involved.

Cholesterol↗
PubMed1998

Medium-chain triglyceride and n-3 polyunsaturated fatty acid-containing emulsions in intravenous nutrition.

Medium-chain triglycerides and n-3 polyunsaturated fatty acid emulsions as a physical mixture have attracted increasing interest for use in parenteral nutrition and may play an important role in the development of structured triglycerides in a future generation of new lipids. Over the past two decades, the clinical use of intravenous emulsion for the nutritional support of hospitalized patients has relied exclusively on long-chain triglycerides providing both a safe, calorically dense alternative to dextrose and a source of essential fatty acids needed for biological membranes and maintenance of the immune function. During the past decade, the development of new triglycerides (medium- and long-chain triglyceride emulsions and structured triglyceride emulsions) for parenteral use have provided useful advances and opportunities to enhance nutritional and metabolic support. Medium-chain triglycerides and n-3 polyunsaturated fatty acid emulsions possess unique physical, chemical, and metabolic properties that make them theoretically advantageous over the conventional long-chain triglycerides. The physical mixture of medium- and long-chain triglycerides have been used clinically in patients with critical illness, liver disease, immunosuppression, pulmonary disease, and in premature infants, with good tolerance and the avoidance of some of the problems encountered with long-chain triglycerides alone.

Animals↗
PubMed1986

Triglyceride kinetics: effects of dietary glucose, sucrose, or fructose alone or with hyperinsulinemia.

The effects of different dietary sugars, with or without exogenously induced hyperinsulinemia, on rat plasma triglyceride kinetics have been studied. Glucose, sucrose, or fructose were supplied as 10% drinking solutions. The sugar-supplemented groups were each divided into subgroups, one receiving 6 U of insulin per day for 2 wk from intraperitoneally implanted minipumps and the other receiving none. The same degree of hyperglycemia and of endogenous hyperinsulinemia was seen in each sugar-supplemented group. Infusing exogenous insulin restored normoglycemia and produced more pronounced but equal hyperinsulinemia in each subgroup. In those rats that received no exogenous insulin, triglyceride production increased 18% in the sucrose-supplemented group and 20% in the fructose supplemented subgroups, but not at all in the glucose-supplemented subgroup. This 20% increase in triglyceride production in the fructose-supplemented subgroup was accompanied by a six times greater (120%) increase in triglyceride concentration. This suggested that dietary fructose not only increased triglyceride production, but also impaired triglyceride removal. Exogenously induced hyperinsulinemia further increased triglyceride production in those rats receiving dietary fructose, either as the monosaccharide or as sucrose, but not in those receiving only glucose. Thus, in the presence of fructose, but not glucose, insulin stimulates triglyceride production. As exogenous insulin returned the triglyceride concentrations to normal in the fructose-supplemented rats, it also appeared to overcome any fructose-associated impairment of triglyceride removal.

Animals↗
PubMed1985

Intestinal triglycerides are derived from both endogenous and exogenous sources.

Although studies have indicated that the small intestine is capable of utilizing endogenous substrates for triglyceride synthesis in the absence of dietary lipid, the importance of the endogenous contribution to total intestinal triglyceride production during absorption has not yet been defined. In this study we have examined the quantitative contribution of endogenous triglyceride production during different luminal lipid loads. By use of a mesenteric lymph fistula rat model with total parenteral nutritional support, mesenteric lymphatic triglyceride transport was investigated. Our results indicate that, during absorption, a substantial fraction (greater than 50%) of total triglyceride is derived from endogenous sources. Increased luminal fatty acid loads lead to an increase in both endogenous and exogenous triglyceride production. Incorporation of luminally infused oleic acid into triglyceride carried by chylomicrons is dependent on the luminal fatty acid load, while incorporation of oleic acid into very low-density lipoprotein (VLDL) triglyceride is saturable. We conclude that both chylomicron and VLDL are involved in transporting triglyceride derived from both endogenous and exogenous sources. The different patterns in the partition of endogenous and exogenous triglyceride into chylomicrons and VLDL suggest that these two lipid-carrying lipoproteins are probably packaged differently in the small intestine.

Animals↗
PubMed1999

Independent effects of Apo E phenotype and plasma triglyceride on lipoprotein particle sizes in the fasting and postprandial states.

LDL particle sizes and Apo E phenotypes were determined in 212 subjects of whom 51 had angina. LDL diameter was significantly less in subjects with an epsilon2 allele (24.76+/-0.08 vs 24.94+/-0.02 nm, P=0.02), and this was evident for both E2/E3 (24.77+/-0.09 nm) and E2/E4 (24.69+/-0.08 nm) phenotypes. Although there was a negative relation between LDL diameter and plasma triglyceride, the effect of apo E2 was still evident with adjustment for triglyceride. In multiple regression analysis, the significant determinants of LDL diameter were gender (with females having larger particles than males), body mass index, and the presence (or absence) of E2. HDL particle sizes and compositions were determined on fasting samples and, additionally, 5 and 8 hours after a fat-rich meal for 48 coronary heart disease cases and 49 control subjects. Fasting HDL particle sizes were not related to the presence of E2 but were significantly smaller for subjects possessing an epsilon4 allele (8. 09+/-0.08 vs 8.39+/-0.05 nm, P=0.003) and were negatively related to plasma triglyceride. However, the effect of E4 persisted after adjustment for triglyceride. In a multiple regression analysis, the only significant determinant of fasting HDL diameter was the presence (or absence) of E4 with fasting plasma triglyceride just failing to reach significance (P=0.06). There was a postprandial increase in HDL diameter that was less marked in subjects with coronary heart disease. The postprandial increase in HDL diameter was of sufficient magnitude to result in size reclassification of HDL particles. The influence of E4 was also evident at both postprandial time points. Compositional analysis demonstrated that the increase in HDL diameters postprandially could be attributed to triglyceride enrichment, with an accompanying fall in cholesterol ester content. Phospholipid changes postprandially were biphasic with an initial fall followed by a rise in concentration. The increase in triglyceride content was significantly less in those subjects with angina despite an equivalent rise in plasma triglyceride. The present study demonstrates significant, but different, effects of variation in apo E phenotype on the particle sizes of both HDL and LDL. Such effects were still evident with adjustment for differences in plasma triglyceride and suggests that variation in apo E phenotype exerts effects on lipoprotein particle sizes by mechanisms additional to those dependent on change in plasma triglyceride.

Alleles↗
PubMed1973

Accelerated triglyceride secretion. A metabolic consequence of obesity.

A new animal model was developed to determine the effect of obesity upon endogenous triglyceride secretion. Desert sand rats (Psammomys obesus), rodents which become spontaneously obese and hyperinsulinemic when given ad lib. chow, were given intravenous Triton to allow in vivo measurement of triglyceride secretion rates (TGSR). In a group of 18 fasted animals of varying body weight and degrees of obesity, TGSR correlated significantly with body weight (r=0.68, P < 0.01) indicating that obesity was associated with accelerated endogenous release of triglyceride. In these same animals, basal plasma insulin levels correlated significantly with body weight (r=0.78, P < 0.001) and TGSR correlated significantly with mean plasma insulin levels (r=0.73, P < 0.001), suggesting that hyperinsulinemia may have been the mechanism through which obesity enhanced TGSR. No correlation was found between basal triglyceride level and either body weight, basal insulin, or TGSR which suggested that individual triglyceride removal rates among the animals may have been variable. To test this hypothesis, seven animals were studied prospectively before and after induction of obesity. There were significant increases (P < 0.02) in all parameters, i.e., weight, plasma insulin level, TGSR, and basal triglyceride level. Thus, when each animal was used as its own control, thereby minimizing the postulated factor of variable individual triglyceride removal, increments in basal triglyceride were shown to accompany the development of obesity, hyperinsulinemia, and accelerated triglyceride secretion. These data from studies in the sand rat offer in vivo evidence that obesity leads to accelerated triglyceride secretion, an effect which may be mediated by hyperinsulinemai, and which can be invoked as one possible mechanism to explain hypertriglyceridemia associated with obesity in man.

Animals↗
PubMed1973

The effect of high-carbohydrate diets on liver triglyceride formation in the rat.

The effect of feeding diets containing 75% glucose or fructose on liver triglyceride formation in the rat was studied by both in vivo and in vitro techniques. The results were compared with those from control rats fed laboratory chow. Both high-sugar diets increased the capacity for triglyceride formation from sn-glycerol-3-P by rat liver homogenates and correspondingly increased incorporation of [1,3-(14)C]glycerol into hepatic triglyceride by the intact animal. These independent measures of hepatic triglyceride production changed with a similar time-course characteristic for each diet. The 75% fructose diet produced a greater increase in both determinations, reaching a maximum after 11 days.Despite the increase in hepatic triglyceride formation by both high-sugar diets, only the 75% fructose diet resulted in a consistent and sustained increase in serum triglyceride. This results most probably from differences in the fractional rate of serum triglyceride removal between the two groups.When serum triglyceride removal was inhibited by administration of Triton WR-1339, both high-sugar diets increased incorporation of [1,3-(14)C]glycerol in serum triglyceride in vivo and increased serum triglyceride level above that in control rats.

Animals↗