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PubMed1985

Reduced triglyceride formation from long-chain polyenoic fatty acids in rat hepatocytes.

The mechanism for the marked reduction in hepatic triglyceride secretion when rats are fed fish oils was explored in studies with isolated rat hepatocytes. Hepatocytes obtained from Sprague-Dawley rats fed either chow or fish oil or safflower oil were incubated in the presence of [3H]-glycerol to estimate triglyceride formation. In some experiments, various fatty acids, complexed to albumin, were added to the incubations. Similar experiments were carried out with hepatocytes from a genetic strain of hypertriglyceridemic, obese rats. In the absence of added fatty acid, hepatocytes from fish oil-fed rats produced and secreted substantially less triglyceride than cells from safflower oil-fed rats. However, the addition of 2 mmol/L Na oleate stimulated triglyceride formation similarly in both types of hepatocytes. When hepatocytes from chow fed rats were incubated with fatty acids of increasing chain length and unsaturation (oleate, linolenate, arachidonate, eicosapentaenoate, and docosahexaenoate), the latter two, which characterize the fish oil used, almost totally suppressed triglyceride formation. Coincubation with oleate partly reversed this effect. Hepatocytes from the hypertriglyceridemic rats synthesized significantly more triglyceride than hepatocytes from normal rats; however triglyceride formation was markedly reduced also in this strain of rat by feeding fish oil or by adding docosahexaenoate to hepatocytes in vitro. These studies confirm previous conclusions with perfused livers from fish oil-fed rats that showed diminished triglyceride production and secretion. These findings suggest that diversion of polyenoic acids from pathways of esterification is a major factor in the triglyceride lowering effect of fish oils.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effects of dietary sucrose on age-related changes in VLDL-triglyceride kinetics in the rat.

The effects of sucrose feeding on in vivo kinetics of triglyceride metabolism were compared in rats aged 2 and 12 months. Sucrose was supplied as a 10% solution in their drinking water for 2 weeks. Although plasma triglyceride concentrations doubled with age, total triglyceride secretion rates for the whole rat (mg/min/rat) increased by 40%, suggesting a decrease in the efficiency of triglyceride removal from plasma with aging. The rate of triglyceride secretion per unit body mass (mg/min/kg body weight), however, decreased by 40% as the rats grew to 12 months of age. These age-related differences were statistically significant only in rats receiving supplementary sucrose. Feeding sucrose to rats of both ages doubled the secretion rates of triglyceride not only for the whole rat but also per unit body mass. However, it tripled triglyceride concentrations, implying that the sugar decreases the removal efficiency of plasma triglyceride equally in rats at either age. Fasting hypertriglyceridemia induced by sucrose supplement was much greater in old rats than in young rats (162 +/- 30 vs. 80 +/- 8 mg/dl). The present studies demonstrate that dietary sucrose enhances age-related changes in triglyceride kinetics in the rat.

Aging↗
PubMed2006

Relationship of apolipoprotein A5 and apolipoprotein C3 levels to serum triglycerides in patients with type 2 diabetes.

BACKGROUND: The role of apolipoprotein A5 (ApoA5) in modulating triglyceride levels in humans is incompletely understood. Some researchers have reported modest positive correlations of ApoA5 with triglycerides while others have reported negative correlations. A recent report suggested that ApoA5 gene expression may be influenced by insulin. In type 2 diabetes, some groups have reported higher levels of ApoA5 compared to normals while others have reported lower levels. METHODS: To better understand the relationships between ApoA5, apolipoprotein C3 (ApoC3), and triglycerides in type 2 diabetes, ApoA5 levels were measured and correlated with triglyceride, insulin, and HbA1c levels. ApoC3 levels were measured and correlated with triglycerides. RESULTS: In patients with type 2 diabetes, ApoA5 levels were elevated compared to normals, with several patients having markedly increased levels confirmed by Western blotting. ApoA5 levels were positively correlated with triglycerides (r=0.60) but were not correlated with either HbA1c or serum insulin levels. ApoC3 levels were highly positively correlated with triglycerides (r=0.88). CONCLUSIONS: These data indicate that in patients with type 2 diabetes ApoA5 levels are positively correlated with triglycerides but are not correlated with HbA1c or insulin levels. ApoC3 levels are strongly positively correlated with triglycerides in these patients.

Adult↗
PubMed2003

An observational study of severe hypertriglyceridemia, hypertriglyceridemic acute pancreatitis, and failure of triglyceride-lowering therapy when estrogens are given to women with and without familial hypertriglyceridemia.

BACKGROUND: We assessed severe hypertriglyceridemia, hypertriglyceridemic acute pancreatitis, and failure of triglyceride-lowering therapy when estrogens were given to 56 women with and without familial hypertriglyceridemia. The 56 women had been consecutively referred to our center over a 3-year period because of triglycerides >400 mg/dl despite diet-drug treatment and/or a history of hypertriglyceridemic acute pancreatitis (AP). Of the 56 women, 17 had received estrogen replacement therapy (ERT), hormone replacement (HRT, n=6), or selective estrogen receptor modulators (SERM, n=1). METHODS: After study at entry, in 56 women (median age, 52 years), 36 with familial hypertriglyceridemia, to lower triglycerides, estrogens and SERMs (hormone treatment, HT) were stopped; a very low fat diet (<15% of calories), gemfibrozil (1.2-1.5 mg/day), and omega-3-fatty acid (4-12 g/day) were started, with restudy 2-4 weeks later. RESULTS: Of the 56 women, 24 (43%) were taking HT at entry, with median fasting triglycerides 1270 mg/dl in the HT group and 1087 mg/dl in the no-HT group. Seventeen women (30%) had a history of AP, nine of whom (53%) were/had been on HT at the development of AP. Significant positive correlates of triglycerides at entry in a stepwise regression model were hemoglobin A(1C) (partial r(2)=10.7%, p<0.05) and an interaction between estrogen use and familial hypertriglyceridemia (partial r(2)=15%, p=0.017). After 2-4 weeks on therapy, median triglycerides in the previous-HT group fell from 1270 to 284 mg/dl (p<0.0001) and in the no-HT group from 1087 to 326 mg/dl (p<0.0001). CONCLUSIONS: Before starting HT, to avoid HT induced hypertriglyceridemic AP and exacerbation of overt or covert familial hypertriglyceridemia, triglycerides must be measured. HT is contraindicated in women with preexisting hypertriglyceridemia (triglycerides> or =500 mg/dl). Triglyceride-lowering diets and drugs often fail in the presence of HT and/or poorly controlled diabetes mellitus, but commonly succeed when HT is stopped and diabetes mellitus is tightly controlled.

Adult↗
PubMed2001

Distribution and cardiovascular risk correlates of serum triglycerides in young adults from a biracial community: the Bogalusa Heart Study.

Elevated serum triglyceride level is increasingly being recognized as an important indicator of cardiovascular risk. The distribution and correlates of serum triglycerides were examined in a biracial (black-white) community-based sample of 1342 young adults (30% black) aged 20-37 years. Triglyceride levels showed significant race (white>black) and sex (male>female) differences. Black females, despite their relatively increased body fatness, had lowest triglyceride levels. In terms of conjoint trait of dyslipidemia based on the National Cholesterol Education Program cutpoints, 9% of white males displayed high triglyceride (> or =200 mg/dl) in combination with low high-density lipoprotein (HDL)-cholesterol (<35 mg/dl). In comparison, none of the black females fell into this category. Serum triglycerides even at levels between 100 and 150 mg/dl were significantly adversely associated with risk variables of insulin resistance syndrome such as adiposity and visceral fatness measures, HDL-cholesterol, insulin, and systolic blood pressure, especially among whites. Visceral fatness as measured by waist circumference (except black males) and insulin were the major predictors of triglyceride levels. Overall, triglyceride levels above 150 mg/dl were associated with increased risk of hypertension (odds ratio (OR)=1.8, 95% confidence interval (CI)=1.8-3.0), type 2 diabetes (OR=3.1, CI=1.4-6.9), parental history of hypertension (OR=1.3, CI=1.0-1.8) and parental history of type 2 diabetes (OR=1.7, CI=1.2-2.3). Thus, serum triglyceride levels may be valuable in the assessment of cardiovascular risk during young adulthood.

Adult↗
PubMed1998

Triglyceride metabolism in heterozygote of Watanabe heritable hyperlipidemic rabbit.

The present study was conducted in order to examine the role of low-density lipoprotein (LDL)-receptor activity in very-low-density lipoprotein (VLDL) triglyceride metabolism in vivo. Fructose-feeding (10% in drinking water) for 2 weeks resulted in elevated plasma triglyceride in heterozygote of Watanabe heritable hyperlipidemic (WHHL) rabbit (WHHLH) associated with suppressed fractional catabolic rate (FCR) of plasma triglyceride, whereas Japanese white (JW) rabbit with normal LDL receptor activity showed no remarkable change in plasma triglyceride turnover after fructose-feeding, suggesting an involvement of LDL receptor activity on triglyceride metabolism. Thereafter, in order to stimulate cellular LDL receptor activity, fluvastatin, a new 3-hydroxy-3-methylglutaryl-coenzyme-A (HMG-CoA) reductase inhibitor, was administered orally (1.52 +/- 0.26 mg/kg) to fructose-fed WHHLH. Significant suppression of triglyceride secretion rate (TGSR) was observed after treatment. However, since plasma triglyceride level was markedly suppressed, FCR of plasma triglyceride was significantly elevated by fluvastatin. Thus, it is speculated from the present data that LDL receptor activity is significantly involved in VLDL triglyceride metabolism in rabbits.

Animals↗
PubMed1999

Relationship between triglycerides and factor VIIc and plasminogen activator inhibitor type-1: lack of threshold value.

Increased factor VIIc (FVIIc) and plasminogen activator inhibitor type 1 (PAI-1) levels may lead to a thrombotic state and subsequently to a higher risk of myocardial infarction. The relationships between triglycerides and plasma levels of both PAI-1 and FVIIc were established in previous studies. However, there is no data assessing whether there is a threshold value of triglycerides above which FVIIc and PAI-1 levels increase or whether the relationship is continuous. Therefore, we measured triglycerides, FVIIc, and PAI-1 levels in a large group of 1254 asymptomatic patients with hyperlipoproteinemia. Our results showed that both FVIIc and PAI-1 levels increase linearly in parallel to triglyceride levels (p=0.0001). In the multiple regression analysis, the relationship between log triglycerides and FVIIc was significantly independent of total cholesterol, body mass index, fasting glycemia, gender, and age; the relationship between log triglycerides and PAI-1 was significantly independent of body mass index, fasting glycemia, gender, and age. Interestingly, we found that the correlation coefficients between triglycerides and the haemostatic parameters measured were almost identical in different subgroups of subjects: males, females, nonobese, and normoglycemic, as well as nonalcoholic. We conclude that the relationships between triglyceride levels and FVIIc, as well as PAI-1, are continuous without threshold value of triglycerides.

Adsorption↗
PubMed1998

Apolipoprotein E2 reduces the low density lipoprotein level in transgenic mice by impairing lipoprotein lipase-mediated lipolysis of triglyceride-rich lipoproteins.

Apolipoprotein (apo) E2 is often associated with low levels of low density lipoprotein (LDL) cholesterol and high levels of plasma triglycerides in humans. Mice expressing apoE2 also have low LDL levels. To evaluate the possible role of the LDL receptor in the cholesterol-lowering effect of apoE2, we bred transgenic mice expressing low levels of apoE2 with LDL receptor-null mice (hE2(+/0), LDLR-/-). Even in the absence of the LDL receptor, plasma total and LDL cholesterol levels decreased progressively with increasing levels of plasma apoE2. At plasma apoE2 levels >20 mg/dl, LDL cholesterol was approximately 45% lower than in LDLR-/- mice. Thus, the LDL cholesterol-lowering effect of apoE2 is independent of the LDL receptor. In contrast, plasma triglyceride levels increased (mostly in very low density lipoproteins (VLDL) and intermediate density lipoproteins (IDL)) progressively as apoE2 levels increased. At plasma apoE2 levels >20 mg/dl, triglycerides were approximately 150% higher than in LDLR-/- mice. Furthermore, in apoE-null mice (hE2(+/0), mE-/-), apoE2 levels also correlated positively with plasma triglyceride levels, suggesting impaired lipolysis in both hE2(+/0),LDLR-/- and hE2(+/0),mE-/- mice. Incubating VLDL or IDL from the hE2(+/0),LDLR-/- or the hE2(+/0),mE-/- mice with mouse postheparin plasma inhibited lipoprotein lipase-mediated lipolysis of apoE2-containing VLDL and IDL by approximately 80 and approximately 70%, respectively, versus normal VLDL and IDL. This observation was confirmed by studies with triglyceride-rich emulsion particles, apoE2, and purified lipoprotein lipase. Furthermore, apoE2-containing VLDL had much less apoC-II than normal VLDL. Adding apoC-II to the incubation partially corrected the apoE2-impaired lipolysis in apoE2-containing VLDL or IDL and corrected it completely in apoE2-containing emulsion particles. Thus, apoE2 lowers LDL cholesterol by impairing lipoprotein lipase-mediated lipolysis of triglyceride-rich lipoproteins (mostly by displacing or masking apoC-II). Furthermore, the effects of apoE2 on both plasma cholesterol and triglyceride levels are dose dependent and act via different mechanisms. The increase in plasma cholesterol caused by apoE2 is due mostly to impaired clearance, whereas the increase in plasma triglycerides is caused mainly by apoE2-impaired lipolysis of triglyceride-rich lipoproteins.

Animals↗
PubMed2002

Lipoprotein production by the heart: a novel pathway of triglyceride export from cardiomyocytes.

The current knowledge on lipoprotein secretion from the heart is examined in this article. The ability of cells to secrete apolipoprotein B (apo-B) containing lipoproteins depends on expression of the apo-B and microsomal triglyceride transfer protein (MTP) genes. Initially, it was shown that both genes are expressed in cardiac myocytes of mice and humans. Electron microscopy of human cardiac myocytes revealed lipoproteins in the secretory pathway and metabolic labelling studies demonstrated the secretion of LDL-like lipoproteins from minced heart biopsies. To examine the role of lipoprotein formation in the heart, we tested whether overexpression of a human apo-B transgene in the heart affects cardiac triglyceride accumulation. In wild-type mice, diabetes conferred an increase in heart triglycerides. In apo-B transgenic mice, diabetes did not affect heart triglycerides. Also, apo-B overexpression prevents fasting-induced heart triglyceride accumulation, whereas inhibition of MTP expression increases heart triglycerides in mice. In hypoxic human hearts, MTP mRNA expression was negatively associated with triglyceride contents. These findings suggest that lipoprotein formation rates affect cardiac triglyceride stores. The MTP mRNA levels are approximately 2-fold higher in hypoxic compared with normoxic human myocardium and in diabetic compared with non-diabetic mouse hearts. In both hypoxia and diabetes, the delivery of triglycerides to the heart exceeds their utilization for beta-oxidation. Thus, endogenous lipoprotein secretion rates might be upregulated to remove surplus fat from the heart. Diabetes negatively affected indexes of systolic and diastolic function in wild-type mice. However, the diabetogenic effects on the heart were absent or much less pronounced in apo-B transgenic mice. This suggests that accelerated lipoprotein formation by the heart attenuates development of diabetic cardiomyopathy in mice. In conclusion, current evidence suggests that lipoprotein secretion from the heart plays an integrated role in cardiac lipid homeostasis and that it can affect the biomechanical function of the heart.

Animals↗
PubMed2001

Low-density lipoprotein particle size, triglyceride-rich lipoproteins, and glucose tolerance in non-diabetic men with essential hypertension.

The aim of the study is to investigate serum lipoproteins abnormalities including low-density lipoprotein (LDL) particle size, and their relationship with other cardiovascular risk factors in men with essential hypertension. Plasma glucose and serum insulin levels during oral glucose tolerance test (OGTT), serum lipoprotein(a), apolipoprotein (apo) A-I. apo B. cholesterol and triglycerides in serum and in lipoproteins, and LDL particle diameter were measured in thirty-eight consecutive newly-diagnosed non-diabetic untreated hypertensive men and 38 healthy male controls. Plasma glucose at baseline, 60 and 120 min during OGTT was significantly higher in patients than controls whereas serum insulin levels did not differ between patients and controls. Serum apo B and triglycerides were significantly raised in patients compared with controls (1.08 +/- 0.17 g/L [mean +/- SD] vs 0.97 +/- 0.22 g/L. p < 0.05, and 1.56 +/- 0.90 mmol/L vs 1.15 +/- 0.57 mmol/L, p < 0.05, respectively). Very-low-density lipoprotein (VLDL) triglycerides and LDL-cholesterol were increased in patients compared with controls (0.89 +/- 0.79 mmol/L and 0.54 +/- 0.35 mmol/L, p < 0.05, and 4.08 +/- 0.85 mmol/L and 3.60 +/- 0.92 mmol/L, p < 0.05, respectively) whereas high-density lipoprotein (HDL) cholesterol was lower in patients compared with controls 0.95 +/- 0.22 mmol/L and 1.07 +/- 0.20 mmol/L, p < 0.05). Adjustment for body mass index, abdominal/hip perimeter ratio and area under the glucose curve did not attenuate the relationship between hypertension and VLDL-triglycerides. Six patients and two controls had a mean LDL diameter < or = 25.5 nm and in the former serum triglycerides ranged from 1.86 mmol/L to 2.37 mmol/L. Mean LDL particle diameter in both patients and controls showed an inverse relationship with log-transformed serum triglycerides (r = - 0.51, p < 0.001 and r = - 0.47, p < 0.005, respectively). Among patients, those with serum triglycerides > or = [corrected] 1.58 mmol/L had a lesser mean LDL diameter than those with triglycerides above this threshold (25.78 +/- 0.47 nm vs 26.30 +/- 0.35 nm, p < 0.001). Higher plasma glucose, serum apo B and LDL-cholesterol as well as the decrease in serum HDL-cholesterol in patients with hypertension are consistent with high coronary heart disease risk. Not only mild hypertriglyceridemia but also high-normal serum triglycerides in themselves or as a surrogate of a predominance of small dense LDL particles in plasma convey an additional risk for cardiovascular disease in hypertensive patients even though routine plasma lipids are within or near normal range.

Adult↗
PubMed1990

The triglyceride controversy: a review of the data.

Although some studies indicate that elevated triglyceride levels are an independent risk factor for coronary heart disease (CHD), the significance of hypertriglyceridaemia in atherosclerosis and CHD remains controversial. While many epidemiologic case-control studies show a significant association between triglyceride levels and CHD, these studies do not consider other variables that may affect the significance of triglycerides in their analysis of the data (e.g. triglycerides and high density lipoproteins). The absence of a consensus on the role of elevated triglycerides is balanced by the flaws in the currently available statistical approaches to analysing triglyceride levels. An association between hypertriglyceridaemia and abnormally high concentrations of apolipoprotein (apo) B has also been observed. Some researchers suggest that apo B is a better predictor of angiographically proven coronary atherosclerosis than total cholesterol or low density lipoprotein cholesterol and triglycerides. Although no consensus yet exists on the triglyceride question, available data strongly suggest that triglycerides warrant serious consideration.

Coronary Disease↗
PubMed1992

Lymph chylomicron composition and size are modified by level of intestinally infused cholesterol and triglyceride source in rats.

Mesenteric lymph chylomicrons were characterized following acute continuous intestinal infusion of triglyceride emulsions in rats. Emulsions were prepared using corn, olive or butter oils with graded doses of cholesterol (0, 3, 10, 20, 30, 60, 100 mg/g triglyceride) added to each. Chylomicron cholesterol content varied directly with dose of cholesterol infused, ranging from approximately 1.5% (by weight) with no added cholesterol to 5-10% at 100 mg cholesterol/g triglyceride. Minimum effective dose for increasing chylomicron cholesterol content (about twofold) was 20 mg/g triglyceride regardless of the triglyceride source. Esterified cholesterol accounted for most of the increase in chylomicron total cholesterol with corn oil infusion, whereas increases in the unesterified fraction accounted for 10-30% of the increase in total cholesterol during infusion of olive or butter oils. The effect of infused cholesterol on chylomicron lipid composition was dependent on triglyceride source: no effect on phospholipid:triglyceride ratio with corn and butter oils, but increased phospholipid:triglyceride ratio with olive oil at cholesterol doses greater than 20 mg/g triglyceride. Infusion of butter emulsions produced smaller chylomicrons than those produced during infusion of corn or olive oil emulsions.

Animals↗
PubMed1999

Triglyceride oxidation in cystic fibrosis: a comparison between different 13C-labeled tracer substances.

BACKGROUND: For indirect evaluation of pancreatic lipase activity in cystic fibrosis, different 13C-labeled triglycerides may be used. METHODS: Triglyceride oxidation in patients with cystic fibrosis was investigated after administration of different 13C-labeled triglycerides by comparing 13CO2 breath exhalation. In the comparative study, five patients with cystic fibrosis (age, 8-15 years; body weight, 22.5-39.8 kg) were treated with Pangrol (individual dosages: 1-3 capsules per morning meal; Berlin-Chemie, Berlin, Germany). [1,1,1-13C3]Glyceryl tripalmitate and [1,1,1-13C3]glyceryl trioleate were administered as a single oral pulse at 8:00 A.M. (dosage, 4 mg/kg each) with the standard diet Fresubin (dosage, 10 ml/kg; Fresenius, Bad Homburg, Germany). Alternately, the same subjects were given the synthetic mixed triglyceride 1,3-distearyl, 2[13C]octanoyl glycerol (dosage, 12.5 mg/kg) contained in the standard diet Nutri-Mix (dosage, 10 ml/kg; Nutricia, Zoetemeer, The Netherlands). Breath samples were taken in 15- and 30-minute intervals over 8 hours. The 13CO2 enrichment was measured by continuous-flow isotope ratio mass spectrometry. RESULTS: After administration of the 13C-labeled tripalmitin-triolein mixture and the mixed triglyceride, mean maximum 13CO2 enrichments were 4.70 and 7.37 delta over baseline, occurring at 7.0 and 3.5 hours, respectively. The corresponding percentage cumulative 13CO2 exhalations were 12.25% and 29.19%, respectively, and differed significantly in the five paired subjects (p = 0.003). CONCLUSIONS: After using different 13C-labeled triglycerides the resultant 13CO2 exhalation reflected the triglyceride hydrolysis and subsequent oxidation. It is concluded that the different cumulative 13CO2 exhalations were mainly caused by the rate-limiting step of triglyceride hydrolysis to free fatty acids and 2-monoglycerides and by fat deposition. Noninvasive 13C breath tests using different 13C-labeled triglycerides can be used for evaluation of pancreatic lipase activity before and during enzyme supplementation.

Adolescent↗
PubMed1978

Influence of chenodeoxycholic acid on the kinetics of endogenous triglyceride transport in man.

Plasma lipids and triglycerides kinetics were studied in ten subjects before and after 6-8 weeks treatment with 1 g/day chenodeoxycholic acid for radiolucent gallstones. Plasma triglyceride concentration fell by 20% and phospholipid concentration rose by 5% on average; there was no change in cholesterol or free fatty acids. Body weight remained constant. Triglyceride kinetics, studied by a precursor-labelling technique, revealed a reduction both of triglyceride plasma pool and turnover rate, accompanied by a decline of more than 35% both of plasma triglyceride precursor pool and of incorporation of plasma free fatty acids into newly synthesized plasma triglycerides. Fractional turnover rates in both pools remained unaltered. The appearance-time for newly synthesized plasma triglycerides after injection of label did not change. These results indicate that chenodeoxycholic acid lowers plasma triglyceride by reducing its synthesis, thereby precluding alternative, and possibly undesired, modes of action, such as impaired secretion or increased peripheral catabolism of endogenous triglyceride. Several biochemical mechanisms may be responsible for this effect, among which stimulation of phospholipid synthesis by bile acids could play a role.

Chenodeoxycholic Acid↗
PubMed1994

Studies in hypertriglyceridaemia. 1. Serum triglyceride distribution and its correlates in randomly selected Swedish middle-aged men.

OBJECTIVES: To obtain a randomly selected hypertriglyceridaemic population for detailed further characterization. DESIGN: Study of randomly selected males. SETTING: Subjects examined and blood sampled at Sollentuna Primary Health Care Centre. SUBJECTS: Men aged 40-50 years (n = 1564), living in the Stockholm area, who were screened for hypertriglyceridaemia, January 1990-June 1992. MAIN OUTCOME MEASURES: Fasting concentrations of serum triglycerides. RESULTS: The serum triglyceride concentration distribution showed the expected skew distribution with the 90th and the 95th percentile at 2.51 and 3.05 mmol L-1, respectively. The mean serum triglyceride level compared well with several population values reported from this laboratory over the last 30 years, indicating stable triglyceride levels over time. There was no significant age-trend for the triglyceride concentration. Lower mean values for triglyceride, insulin and waist-to-hip (W/H) ratio were observed during the summer, whilst apolipoprotein A-I levels were higher. There was a linear relation between the number of cigarettes smoked and the serum triglyceride concentration. In stepwise multiple linear regression analysis with the triglyceride concentration as the dependent variable the following variables appeared as significant (P < 0.01) contributors: insulin, cholesterol, glucose, apolipoprotein A-I, number of cigarettes smoked, BMI, W/H ratio and diastolic blood pressure. The regression coefficient for apolipoprotein A-I was negative; all the others were positive. The multiple regression (R) was 0.68, suggesting that up to 47% of the variation of the serum triglyceride concentration could be predicted by these factors. CONCLUSIONS: A group of randomly selected hypertriglyceridaemic men has been recruited for further clinical, metabolic and genetic studies. Basic characteristics of the population for their recruitment are described.

Adult↗
PubMed1981

Plasma lipids, lipoproteins, and triglyceride turnover in eu- and hypo-thyroid rats and rats on a hypocaloric diet.

Lipid and lipoprotein concentration, and triglyceride turnover were studied in control, thyroidectomized, and pair-fed control rats (pair-fed to match the food intake of the thyroidectomized rats). Thyroidectomy induced a significant increase in plasma cholesterol (and low density lipoprotein) concentrations and a decrease in plasma triglyceride (and very low density lipoprotein) concentrations. Changes in similar direction but of smaller magnitude were observed in the plasma of the pair-fed control rats. To further investigate triglyceride metabolism in these three groups of animals, triglyceride turnover was studied in fasted, unrestrained, and unanesthetized rats, following injection of [2-3H]glycerol. Peak incorporation of [2-3H]glycerol into plasma triglyceride occurred in all three groups of animals at 25 min after precursor administration, although the maximal incorporation was substantially lower in the thyroidectomized group than in either of the control groups. Thereafter, plasma triglyceride radioactivity decayed monoexponentially with a half-life of 24 +/- 1 min for both normal and pair-fed control rats, compared with the half-life of 41 +/- 3 min observed in the thyroidectomized rats. The calculated apparent fractional catabolic rates were thus 0.029 min-1 for both control groups and only 0.017 min-1 for the thyroidectomized animals. The apparent total catabolic rates of plasma triglyceride were 299 +/- 11, 138 +/- 11, and 48 +/- 4 micrograms triglyceride . min-1 for the normal controls, pair-fed controls, and thyroidectomized rats, respectively. These data further emphasize the importance of thyroid hormones in regulating plasma lipid and lipoprotein metabolism and, specifically, indicate that hypothyroidism results in a reduction of triglyceride secretion into, and the removal from, circulation. Furthermore, evidence was presented that the decreased caloric intake of the hypothyroid animals cannot, in itself, account for this observation.

Animals↗
PubMed1992

Muscle triglyceride metabolism during exercise.

Skeletal muscle cell contains a considerable amount of triglycerides. The amount stored depends on the animal species as well as on muscle fiber composition. It is well documented that triglycerides in the fast-twitch red muscle and to a lesser extent in the slow-twitch muscle, but not those in the fast-twitch white muscle, are mobilized during prolonged exercise. Yet, little is known about the regulation of the metabolism of muscle triglycerides either at rest or during exercise. This is well reflected by the fact that an enzyme responsible for the hydrolysis of muscle triglycerides has not been identified. Mobilization of muscle triglycerides during exercise seems to be under both adrenergic and noradrenergic control. Accumulation of lactic acid and reduction in muscle pH are likely to be strong inhibitors of muscle triglyceride lipolysis. Reduction of carbohydrate availability accelerates mobilization of muscle triglycerides during exercise. The relationship between the plasma free fatty acids and muscle triglyceride metabolism seems to be complex. It has been proposed that most free fatty acids entering the muscle cell is esterified before being oxidized, but this is arguable for contracting skeletal muscles. It is suggested that most free fatty acids entering contracting high oxidative myocytes are transported directly to the mitochondria. A much lesser portion is likely esterified. It is proposed that triglycerides stored in the contracting muscle cell are mobilized when the delivery of the blood-borne-free fatty acids to the mitochondria is insufficient.

Animals↗
PubMed1980

Essential fatty acid deficiency and plasma triglyceride turnover in rats.

Hepatic triglyceride secretion in essential fatty acid-deficient rats was examined by three separate techniques in an effort to resolve conflicting evidence on the question of whether essential fatty acid deficiency altered hepatic triglyceride secretion in vivo. First, plasma triglyceride turnover was measured by intravenous injection of [2-3H]glycerol trioleate. Equations of the kinetics were formulated based on a single, open pool model. Turnover rates and pool sizes of plasma triglyceride were calculated from these equations. Second, [2-3H]glycerol was injected, and apparent rate constants for plasma triglyceride secretion and clearance were calculated by kinetic analysis. Third, Triton WR-1339 was used to inhibit lipoprotein clearance from blood plasma, and rates of plasma triglyceride accumulation were measured. The results of these studies showed that the rate of hepatic triglyceride secretion was 2-3 times greater in essential fatty acid-deficient rats than in nondeficient controls. The increase in triglyceride secretion, as well as the higher level of liver triglyceride typical of essential fatty acid-deficient rats, could be caused by increased lipogenesis and increased mobilization of fatty acids from adipose tissues.

Animals↗