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At least 1,153 records · Page 64Linked to original sources
PubMed2001

Exercise training-induced triglyceride lowering negatively correlates with DHEA levels in men with type 2 diabetes.

OBJECTIVE: To investigate the effect of an exercise training program on lipid profile in correlation with DHEA level and body weight and body composition in type 2 diabetic men. DESIGN: Longitudinal, controlled clinical intervention study with exercise training consisting of an 8 week supervised program of aerobic exercise (75% VO(2) peak, 45 min), twice a week and intermittent exercise, once a week, on a bicycle ergometer. SUBJECTS: Sixteen men (age 45.4+/-7.2 y (mean+/-s.d.), HbA1c 8.15+/-1.7%, body mass index (BMI) 29.6+/-4.6 kg/m(2)) were randomly divided into two groups: trained group (n=8) and control group (n=8). MEASUREMENTS: Lipid, apo- and lipoprotein and DHEA concentrations. Cross-sectional areas of subcutaneous and visceral adipose tissue and mid-thigh muscle by magnetic resonance imaging. RESULTS: Training decreased visceral (153.25+/-38.55 vs 84.20+/-21.30 cm(2), P<0.001), subcutaneous (241.55+/-49.55 vs 198.00+/-39.99 cm(2), P<0.001) adipose tissue area and triglyceride levels (2.59+/-1.90 vs 1.79+/-1.08 nmol/l, P<0.05) and increased mid-thigh muscle cross-sectional area (148.30+/-36.10 vs 184.35+/-35.85 cm(2), P<0.001), and DHEA levels (11.00+/-3.10 vs 14.25+/-4.10 nmol/l, P<0.05) with no modification in body weight. Changes in triglycerides were negatively correlated with changes in DHEA (r=-0.81, P=0.03). This correlation was independent of changes in abdominal fat distribution. CONCLUSION: Training decreases abdominal fat depots, improves muscular mass and affects favourably triglyceride and DHEA levels. Changes in triglycerides and DHEA were inversely related.

Adipose Tissue↗
PubMed2002

Skeletal muscle triglycerides lowering is associated with net improvement of insulin sensitivity, TNF-alpha reduction and GLUT4 expression enhancement.

AIMS/HYPOTHESIS: The aim of the present study was to investigate the relationship between intramyocytic triglycerides levels, muscle TNF-alpha and GLUT4 expression and insulin resistance. METHODS: Insulin sensitivity was studied in 14 severely obese women (BMI>40 kg/m(2)), before and 6 months after low-dietary intake or bariatric malabsorptive surgery (bilio-pancreatic diversion, BPD), by the euglycaemic hyperinsulinaemic clamp technique, while the amount of intramyocytic triglycerides was chemically measured in needle muscle biopsies. Using reverse transcriptase-polymerase chain reaction analysis, the muscle mRNA expression of TNF-alpha and GLUT4 was also investigated. RESULTS: The weight loss after surgery was 25.98+/-5.81 kg (P<0.001), while that obtained with the diet was 5.07+/-5.99 kg (P=NS). Marked decrease in TNF-alpha mRNA levels (76.67+/-12.59 to 14.01+/-5.21 AU, P<0.001) were observed in comparison with pre-treatment, whereas GLUT4 was significantly increased (62.25+/-11.77-124.25+/-21.01 AU, P<0.001) only in BPD patients. Increased glucose uptake (M) was accompanied by a significant decrease of TNF-alpha mRNA (76.67+/-12.59-14.01+/-5.21 AU, P<0.01) and an increase of GLUT4. The amounts of TNF-alpha mRNAs in skeletal muscle correlated inversely with GLUT4 mRNAs and directly with intramyocytic triglycerides levels. In a step-down regression analysis (r(2)=0.95) TNFalpha mRNA (P=0.0014), muscular TG levels (P=0.018), and GLUT4 mRNA (P=0.028) resulted to be the most powerful independent variables for predicting M values. CONCLUSION/INTERPRETATION: These findings suggest that insulin resistance in morbidly obese patients is positively associated to the intramyocytic triglycerides content and to TNF-alpha gene expression and inversely correlated to GLUT4 expression.

Adult↗
PubMed1969

Triglyceride synthesis by the small-intestinal epithelium of the pig, sheep and chicken.

1. A comparative study was made of triglyceride synthesis by the intestinal epithelium of pigs, sheep and chickens. In pig and chicken tissue both the glycerol 3-phosphate and the monoglyceride pathway of triglyceride synthesis were operative, but the former pathway predominated in sheep tissue. 2. The fatty acid specificity of the glycerol 3-phosphate pathway was studied in pig and sheep total-homogenate preparations. Maximum incorporation was obtained with myristic acid and palmitic acid under optimum conditions for each fatty acid. Lauric acid, myristic acid, oleic acid, linoleic acid and linolenic acid were inhibitory at concentrations above their optimum, but octanoic acid, decanoic acid, palmitic acid and stearic acid did not show this effect. 3. Subcellular fractionation located the glycerol 3-phosphate and monoglyceride pathways of triglyceride synthesis in the microsomes in all instances. Phosphatidate phosphohydrolase was associated with both the microsomes and the particle-free supernatant. 4. Glycerol 1-mono-oleate was incorporated into triglycerides to a greater extent than glycerol 1-mono-palmitate or glycerol 1-monostearate by microsomal preparations from pig and chicken. 5. A lipase specific for monoglycerides was detected in the particle-free supernatant of all the species examined.

Animals↗
PubMed1975

Impaired hepatic release of triglycerides: a possible cause of acute alcoholic fatty liver in the Rhesus monkey.

1. The mechanism of development of acute alcoholic fatty liver in the Rhesus monkey was investigated by studying the effect of Triton WR-1339 on plasma triglycerides. 2. After ethanol infusion, the rise in plasma triglyceride produced by Triton was greatly reduced and there was an accumulation of triglyceride in the liver. 3. Thus findings suggest that acute alcoholic fatty liver in Rhesus monkeys is probably due to a defect in the release of triglyceride from the liver.

Alcoholism↗
PubMed2001

Effect of triglycerides with different fatty acid chain length on superior mesenteric artery blood flow.

Fat stimulates superior mesenteric artery (SMA) blood flow. Little is known, however, about the influence of fatty acid chain length on SMA flow. The present study was performed to compare the effect of long chain triglycerides (LCT, corn oil), very long chain triglycerides (VLCT, fish oil) and medium chain triglycerides (MCT) on SMA flow. A total of seven healthy volunteers (four men, three women; aged 26 +/- 4 years) participated in three experiments, performed in random order during 60 min continuous intra-duodenal infusion of either LCT (30 mL h(-1); 240 kcal h-1), equicaloric VLCT (30 mL h(-1); 240 kcal h(-1)) or MCT in equimolar (15 mL h(-1); 113 kcal h(-1)) and equicaloric amount (30 mL h(-1); 225 kcal h(-1)). Basal and stimulated SMA blood flow were measured by Doppler ultrasonography. At regular intervals blood samples were taken for measurement of plasma cholecystokinin (CCK) and plasma peptide YY (PYY). Basal SMA blood flow volumes were not significantly different among the LCT, VLCT and MCT experiments (426 +/- 135, 460 +/- 114 and 503 +/- 177 mL min(-1), respectively). The SMA flow increased significantly (P < 0.05) during fat infusion but was significantly higher during LCT (1460 +/- 692 mL min-1) compared with VLCT (1061 +/- 384 mL min-1), MCT 15 mL h(-1) (870 +/- 286 mL min(-1)) and MCT 30 mL h-1 (904 +/- 223 mL min(-1)). Plasma CCK levels increased significantly (P < 0.05) during LCT and VLCT but not during MCT infusion. No correlation was found between SMA flow and plasma CCK levels (r = 0.27; P = 0.2) The SMA blood flow in response to triglycerides is dependent on fatty acid chain length. This chain length-dependent blood flow response is, however, not linear and is not related to plasma CCK levels.

Adult↗
PubMed2003

Postprandial triglycerides in response to high fat: role of dietary carbohydrate.

BACKGROUND: The postprandial triglyceride response following a meal high in fat (HFM) has been related to atherogenesis and insulin resistance. We examined the influence of dietary carbohydrate and the accompanying insulin secretory response on the postprandial triglyceride response following a HFM. MATERIALS AND DESIGN: High-fat meals of equal fat content (fat 80 g) containing either 20 g (low) or 100 g (high) of carbohydrate (HFM-LC and HFM-HC, respectively), and therefore not isocaloric (4250 kJ of HFM-LC and 5450 kJ of HFM-HC), were consumed by seven (four male, three female) normolipidaemic subjects (aged 32.9 +/- 3.7 years, BMI 24.7 +/- 1.8 kg m-2). Blood and indirect calorimetry data were collected at 0-4 h. RESULTS: HFM-HC produced a significant rise in plasma glucose (Delta0.54 +/- 0.23 mmol L-1, P = 0.05) at 2 h, while a HFM-LC elicited no mean change from baseline. Following a HFM-LC, the plasma insulin incremental area under the curve (AUC) was significantly lower (31.3 +/- 6.7 vs. 83.2 +/- 11.9 mU l-1 h-1, P < 0.0003) and the postprandial triglyceride response AUC was significantly greater (1.66 +/- 0.36 vs. 1.24 +/- 0.31 mmol L-1 h-1, P < 0.006) compared with a HFM-HC. Plasma free fatty acids were suppressed by 44% (P = 0.04) and 66% (P < 0.0001) at 1 h following HFM-LC and HFM-HC, respectively, compared with baseline. There were no significant differences between the meals in energy expenditure, substrate oxidation rates, or respiratory quotient responses. CONCLUSIONS: By design, the HFMs were not isocaloric but the presence of carbohydrate in a HFM invoked an insulin response that significantly reduced the 4 h postprandial triglyceride response even in healthy, normolipidaemic subjects. This phenomenon may have clinical implications, particularly in relation to insulin sensitivity.

Blood Glucose↗
PubMed1999

Insulin-like growth factor-I lowers fasting and postprandial triglyceride levels without affecting chylomicron clearance in healthy men.

OBJECTIVES: To study whether IGF-I treatment alters the postprandial lipid and lipoprotein metabolism. DESIGN: Randomized, crossover study. SETTING: University Hospital, Zürich, Switzerland. SUBJECTS: Seven young healthy male subjects (aged 27+/-4 years, body mass index (BMI) 21.8+/-1.7 kg m(-2)). INTERVENTIONS: Each subject was studied two times at 2-week intervals, treated with saline 0.9% (S) and IGF-I (8 microg kg(-1) h(-1)) by a continuous subcutaneous infusion. 60 h after the start of treatment a vitamin A loading test was performed after an overnight 12-h fast. MAIN OUTCOME MEASURES: Glucose, insulin, total and free IGF-I, FFA, triglycerides and retinyl palmitate, total cholesterol, HDL and LDL cholesterol, lipoprotein (a) and apolipoprotein B were measured in serum before and after the fatty meal. RESULTS: Total IGF-I levels rose from 29.0+/-3.3 nmol L(-1) to 113.3+/-9.0 nmol L(-1) (P<0.02) and free IGF-I from 0.24+/-0.05 to 1.08+/-0.28 nmol L(-1) (P<0.02) during IGF-I treatment. IGF-I administration reduced insulin concentrations by 50% (P<0.02), as assessed by the area under the curve. Serum triglyceride levels were significantly lower at baseline and after the fat load during IGF-I treatment (P<0.02), whereas the retinyl palmitate concentrations in chylomicron and nonchylomicron lipoprotein fractions were similar during both treatment periods. CONCLUSIONS: IGF-I treatment reduces the triglyceride levels most probably by decreasing insulin secretion and the production of VLDL particles, and possibly by increasing their turnover. IGF-I treatment has no significant effect on the metabolism of intestine-derived triglyceride-rich lipoproteins after a high fat meal in healthy young men.

Adult↗
PubMed1997

A biometrical study of the relationship between sodium-lithium countertransport and triglycerides.

We addressed the question: Is there evidence that allelic variation in a single unmeasured gene that has a large effect on maximal activity of erythrocyte sodium-lithium countertransport (Na-Li CNT) also has pleiotropic effects on variation in plasma triglyceride levels? Complex segregation analysis models that included plasma triglyceride levels as a covariate were considered as explanations for interindividual variation in Na-Li CNT. A sample of 711 healthy adults from 254 pedigrees enrolled in the Rochester Family Heart Study was selected for this study. The majority of the pedigrees supported the hypothesis that variations in a single unmeasured non-transmitted environmental factor have large effects on the Na-Li CNT distribution. Only gender-specific first-order covariate parameters were necessary in the complex segregation models suggesting that the form of the relationship between Na-Li CNT and plasma triglyceride level was not influenced by variation in the inferred environmental factor with large effects. Stratification of the sample by this inferred environmental factor resulted in three classes of individuals with significant differences in the distributions of coronary heart disease risk factor traits, as well as interindividual variation in both Na-Li CNT and plasma triglyceride levels. These results, along with other observations from the Rochester Family Heart Study sample, emphasize the complex and multifactorial nature of the causes of interindividual variation in Na-Li CNT. Our study further suggests that new research strategies are needed for studying the relationships between genetic and environmental variation and variation in quantitative traits such as Na-Li CNT that have been identified as risk factors for hypertension.

Adult↗
PubMed2000

Effects of short-term leptin exposure on triglyceride deposition in rat liver.

Leptin has recently been suggested to play a role in the pathogenesis of hepatic steatosis. Consequently, this study was designed to examine the direct effects of portal leptin on the intrahepatic lipid contents in the postabsorptive state. Rat livers (n = 6 per group) were perfused in a recirculating system and portally infused with leptin (0.5 nmol/L, 5 nmol/L, and 25 nmol/L), insulin (10 nmol/L), leptin (5 nmol/L) plus insulin (10 nmol/L), glucagon (1 nmol/L), or vehicle (control). Intrahepatic contents of triglycerides, free cholesterol, cholesteryl esters, and free fatty acids were determined from the lipid extract of frozen livers by capillary gas chromatography. Short-term leptin infusion increased total triglycerides in a concentration-dependent (0.5 nmol/L: 2.8 +/- 0.4 mg/g, 5 nmol/L: 7.0 +/- 0.5 mg/g, 25 nmol/L: 8.3 +/- 1.0 mg/g) and time-dependent manner. Total triglycerides also rose during exposure to insulin plus leptin (7.2 +/- 0.6 mg/g) but fell during glucagon infusion (2.6 +/- 0.2 mg/g; control: 4.3 +/- 0.3 mg/g; P <.05). Leptin, insulin, and glucagon increased intrahepatic free cholesterol (P <.05). Free fatty acids were also higher during leptin exposure (0.5 nmol/L: 1.28 +/- 0.08 mg/g, 5 nmol/L: 0.47 +/- 0.01 mg/g, 25 nmol/L: 0.48 +/- 0.04 mg/g, control: 0.38 +/- 0.03 mg/g; P <.05). In conclusion, hyperleptinemia increases hepatic triglyceride content and may therefore contribute to hepatic steatosis in hyperleptinemic obese patients.

Animals↗
PubMed1984

Effects of ventromedial hypothalamic lesions on circadian rhythms in serum insulin, glucose, triglyceride and food intake in rats.

The effects of ventromedial hypothalamic (VMH) lesions on the circadian periodicity of serum insulin, glucose, triglyceride and food intake were studied in rats. The rhythms of serum insulin, glucose and triglyceride did not persist in VMH lesioned rats. The glucose level during the light period was reduced. The triglyceride and insulin levels were elevated. The VMH lesions markedly increased food intake during the later half part of the light cycle but kept it significantly less during the first half part. Thus, the VMH lesions abolished the circadian rhythmicity of serum insulin, glucose and triglyceride and attenuated the rhythmicity of eating through increase in daytime consumption.

Animals↗
PubMed1980

Epidemiology as a guide to clinical decisions. The association between triglyceride and coronary heart disease.

The hypothesis that triglyceride is a cause of coronary heart disease, although unconfirmed and never universally accepted, has nonetheless strongly influenced the practice of preventive medicine. We have examined the epidemiologic association between triglyceride and coronary heart disease to evaluate the validity of inferring that there is a causal relation between the two. Neither the evidence from published studies nor an analysis of data from the Western Collaborative Group Study provides strong support for the causal hypothesis. Information from other scientific disciplines is also meager, contrasting with the coherence of diverse evidence supporting the hypothesis that cholesterol is a cause of coronary heart disease. These arguments fall short of disproving the belief that lowering triglyceride will prevent coronary heart disease, especially since triglyceride and cholesterol are inextricably associated through mutual lipoprotein carriers. But we propose that the ethics of preventive medicine place the burden of proof on the proponents of intervention. We therefore recommend that widespread screening and treatment of healthy persons for hypertriglyceridemia be abandoned until more persuasive evidence becomes available.

Adult↗
PubMed1989

Effect of triglyceride levels on methyl and methylene envelope line widths in proton nuclear magnetic resonance spectroscopy of human plasma.

Recent studies have described a relation between the line widths of the methyl and methylene resonance envelopes in the proton nuclear magnetic resonance spectrum of human plasma and the occurrence of cancer. An average line width of less than 33 Hz has been reported to correlate with the presence of cancer, whereas greater line widths have not. In 26 normal volunteers, we found a significant inverse correlation between fasting triglyceride level and plasma spectral line width. We also observed that dietary lipids have measurable effects on spectral line widths. In another sample of seven normal persons (three of whom had elevated plasma triglyceride levels), the line widths of whole plasma varied widely (mean, 35.6 +/- 8.8 Hz); however, the mean line widths of the lipoprotein fractions isolated from those samples differed greatly, but the variance within each fraction was small (very-low-density lipoprotein, 22.0 +/- 1.9 Hz; low-density lipoprotein, 35.0 +/- 2.8; high-density lipoprotein, 28.8 +/- 1.9). The results of this study indicate that the plasma triglyceride level has a profound effect on the average spectral line width of plasma. This effect can be explained by the relative amounts of lipoprotein fractions in whole plasma. Plasma triglyceride concentrations of more than 1.24 mmol per liter (greater than 110 mg per deciliter), whatever the source, produce average plasma methyl and methylene line widths of less than 33 Hz.

Humans↗
PubMed1984

Metabolism of apolipoproteins B-48 and B-100 of triglyceride-rich lipoproteins in normal and lipoprotein lipase-deficient humans.

The metabolism of apolipoproteins B-48 and B-100 (apo B-48 and B-100) in large triglyceride-rich lipoproteins (300 to 1500 A in diameter) has been compared in three normal subjects and two subjects with genetically determined deficiency of lipoprotein lipase. The triglyceride-rich lipoproteins were obtained from a lipoprotein lipase-deficient donor 4 hr after a fat-rich meal in order to obtain chylomicrons (containing apo B-48) and very low density lipoproteins (VLDL) (containing apo B-100), whose properties had not been modified by the action of this enzyme. The triglyceride-rich lipoproteins were labeled with 125I and injected intravenously into recipients who had fasted overnight. In normal recipients, most of the apo B-48 was removed from the blood within 15 min, and most of the apo B-100 was removed within 30 min. In the lipoprotein lipase-deficient recipients, most of the injected apo B-100 remained in the blood for more than 8 hr; removal of apo B-48 was only slightly more rapid. In all subjects, only trace amounts of either protein were found in lipoproteins more dense than 1.006 g/ml. The results indicate that (i) the removal of the apo B of both chylomicrons and large VLDL from the blood is dependent upon the hydrolysis of their component triglycerides by lipoprotein lipase, and (ii) little or no apo B-48 of chylomicrons or apo B-100 of large VLDL is converted appreciably to low density lipoproteins (LDL). Our results suggest that the reported variability of the conversion of VLDL to LDL may be related to the size and composition of the particles secreted from the liver. The rapid production of remnant particles that are removed efficiently by the liver may minimize the opportunity for further reactions leading to the formation of LDL.

Apolipoprotein B-100↗
PubMed1993

Relationships between the responses of triglyceride-rich lipoproteins in blood plasma containing apolipoproteins B-48 and B-100 to a fat-containing meal in normolipidemic humans.

The concentration of triglyceride-rich lipoproteins containing apolipoprotein (apo) B-48 (chylomicrons) and apo B-100 (very low density lipoproteins) was measured in blood plasma of healthy young men after an ordinary meal containing one-third of daily energy and fat. Plasma obtained in the postabsorptive state and at intervals up to 12 hr after the meal was subjected to immunoaffinity chromatography against a monoclonal antibody to apo B-100 that does not bind apo B-48 and a minor fraction of apo B-100 rich in apo E. Measurements of the concentrations of components of the total and unbound triglyceride-rich lipoproteins separated from plasma by ultracentrifugation showed that about 80% of the increase in lipoprotein particle number was in very low density lipoproteins containing apo B-100 and only 20% was in chylomicrons containing apo B-48 that carry dietary fat from the intestine. The maximal increments and the average concentrations of apo B-48 and B-100 during the 12 hr were highly correlated (r2 = 0.80), suggesting that preferential clearance of chylomicron triglycerides by lipoprotein lipase leads to accumulation of hepatogenous very low density lipoproteins during the alimentary period. The composition of the bulk of very low density lipoproteins that were bound to the monoclonal antibody changed little and these particles contained about 90% of the cholesterol and most of the apo E that accumulated in triglyceride-rich lipoproteins. The predominant accumulation of very low density lipoprotein rather than chylomicron particles after ingestion of ordinary meals is relevant to the potential atherogenicity of postprandial lipoproteins.

Adult↗
PubMed1995

Enhancement of the binding of triglyceride-rich lipoproteins to the very low density lipoprotein receptor by apolipoprotein E and lipoprotein lipase.

The low-density lipoprotein (LDL) receptor plays a crucial role in cholesterol metabolism. A related protein, designated the very low density lipoprotein (VLDL) receptor, that specifically binds apolipoprotein (apo) E has recently been characterized and shown to be expressed in heart, muscle and adipose tissue and the human monocyte-macrophage cell line THP-1. The VLDL receptor binds and internalizes VLDL and intermediate density lipoprotein from Watanabe heritable hyperlipidemic (WHHL) rabbits as well as beta-migrating VLDL from cholesterol-fed rabbits but not LDL from WHHL rabbits. Chinese hamster ovary (CHO) cells transfected with the rabbit VLDL receptor cDNA have now been shown to bind or internalize VLDL (d < 1.006 g/ml) isolated from fasted normolipidemic human subjects with lower affinity than WHHL-VLDL or rabbit beta-VLDL. However, binding and internalization were markedly enhanced when fasted human VLDL was preincubated with either recombinant human apoE (3/3) or lipoprotein lipase (LPL) in CHO cells overexpressing the rabbit or human VLDL receptor. CHO cells transfected with both the rabbit VLDL receptor cDNA and the human LPL cDNA effectively bound, internalized, and degraded fasted human VLDL without pretreatment. Treatment of heparinase reduced the effect of LPL-mediated binding at 4 degrees C, but the inhibitory effect was lower at 37 degrees C. Pseudomonas LPL also enhanced the binding of human fasted VLDL to the VLDL receptor at 37 degrees C in CHO cells overexpressing the human VLDL receptor. Taken together, LPL causes the enhancement of triglyceride-rich lipoproteins binding to the VLDL receptor via both the formation of bridge between lipoproteins and heparan sulfate proteoglycans and its lipolytic effect. Ligand blot analysis showed that the apparent molecular mass of the VLDL receptor is 118 kDa, which is smaller than that of the LDL receptor. These results indicate that the VLDL receptor recognizes both triglyceride-rich lipoproteins that are also relatively rich in apoE, as well as the remnants of triglyceride-rich lipoproteins after catabolism and the interaction with heparan sulfate proteoglycans by LPL. The VLDL receptor may thus function as a receptor for remnants of triglyceride-rich lipoproteins in extrahepatic tissues.

Apolipoproteins E↗
PubMed1995

Effects of apoprotein E on intracellular metabolism of model triglyceride-rich particles are distinct from effects on cell particle uptake.

Apoprotein E (apoE) enhances uptake of triglyceride-rich lipoprotein particles (TGRP). We questioned whether apoE would also modulate intracellular metabolism of TGRP in addition to its effects on particle uptake. We prepared model TGRP with triolein and cholesteryl oleate (1:1, w/w) as the core lipids, emulsified by egg yolk phosphatidylcholine, and containing a non-degradable marker, [3H]cholesteryl hexadecyl ether. Particles were intermediate density lipoprotein-sized as determined by core lipid/phospholipid ratios (2.0-3.0/1) and gel filtration chromatography on Sepharose CL-2B. Emulsions were incubated with J774 macrophages for 5 min to 6 h at core lipid concentrations of 300-1200 micrograms/ml and 0-0.2 microgram recombinant apoE/mg core lipid. Particle uptake was determined by [3H]cholesteryl ether uptake and fluorescence microscopy in the absence and presence of apoE. Similar uptake of particles with and without apoE was achieved by utilizing a 4 times higher particle concentration in the absence of apoE. At equivalent levels of uptake, particles with apoE lead to one-half of the triglyceride mass accumulation and twice the triglyceride utilization as compared to particles without apoE. Further, apoE doubles cell cholesteryl ester hydrolysis and to a lesser extent (approximately 30%) increases cholesteryl ester resynthesis by acyl-CoA cholesterol acyltransferase. Particles, both with and without apoE, reach the lysosomal compartment as determined by colocalization with fluorescein-labeled alpha 2-macroglobulin. These results suggest that, in addition to its role in enhancing TGRP uptake, apoE has additional effects on modulating the cellular metabolism of both triglyceride and cholesteryl ester, after particle internalization.

Animals↗
PubMed2003

Decreased hepatic triglyceride accumulation and altered fatty acid uptake in mice with deletion of the liver fatty acid-binding protein gene.

Liver fatty acid-binding protein (L-Fabp) is an abundant cytosolic lipid-binding protein with broad substrate specificity, expressed in mammalian enterocytes and hepatocytes. We have generated mice with a targeted deletion of the endogenous L-Fabp gene and have characterized their response to alterations in hepatic fatty acid flux following prolonged fasting. Chow-fed L-Fabp-/- mice were indistinguishable from wild-type littermates with regard to growth, serum and tissue lipid profiles, and fatty acid distribution within hepatic complex lipid species. In response to 48-h fasting, however, wild-type mice demonstrated a approximately 10-fold increase in hepatic triglyceride content while L-Fabp-/- mice demonstrated only a 2-fold increase. Hepatic VLDL secretion was decreased in L-Fabp-/- mice suggesting that the decreased accumulation of hepatic triglyceride was not the result of increased secretion. Fatty acid oxidation, as inferred from serum beta-hydroxybutyrate levels, was increased in response to fasting, although the increase in L-Fabp-/- mice was significantly reduced in comparison to wild-type controls, despite comparable induction of PPAR alpha target genes. Studies in primary hepatocytes revealed indistinguishable initial rates of oleate uptake, but longer intervals revealed reduced rates of uptake in fasted L-Fabp-/- mice. Oleate incorporation into cellular triglyceride and diacylglycerol was reduced in L-Fabp-/- mice although incorporation into phospholipid and cholesterol ester was no different than wild-type controls. These data point to an inducible defect in fatty acid utilization in fasted L-Fabp-/- mice that involves targeting of substrate for use in triglyceride metabolism.

Adaptation, Physiological↗
PubMed1993

Proliferation and triglyceride synthesizing activities of fibroblast-like cells derived from epididymal and subcutaneous adipose tissues of rats.

Fibroblast-like cells from subcutaneous adipose tissue and epididymal adipose tissue were prepared from rats and their proliferation and [14C]deoxy-glucose uptake and triglyceride synthesis from [14C]palmitate were investigated. The proliferation of fibroblast-like cells from subcutaneous adipose tissue was greater than that from epididymal adipose tissue. Insulin enhanced the proliferation of fibroblast-like cells derived from subcutaneous adipose tissue, but not from epididymal adipose tissue. The uptake of [14C]deoxy-glucose by fibroblast-like cells from the two sources was similar. Triglyceride synthesis from [14C]palmitate by epididymal fibroblast-like cells was higher than that by subcutaneous fibroblast-like cells. The [14C]deoxy-glucose uptake and triglyceride synthesis from [14C]palmitate by fibroblast-like cells from the two sources were not enhanced by the addition of insulin. These findings suggest the existence of different types of adipocytes in subcutaneous and epididymal adipose tissues in terms of proliferation, and show that the proliferation of fibroblast-like cells from subcutaneous adipose tissue is regulated by insulin. The triglyceride synthesis by immature adipocytes from both adipose tissues was not affected by insulin.

Adipose Tissue↗