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PubMed2002

Opposite effects of background genotype on muscle and liver insulin sensitivity of lipoatrophic mice. Role of triglyceride clearance.

The metabolic phenotype of the A-ZIP/F-1 (AZIP) lipoatrophic mouse is different depending on its genetic background. On both the FVB/N (FVB) and C57BL/6J (B6) backgrounds, AZIP mice have a similarly severe lack of white adipose tissue and comparably increased insulin levels and triglyceride secretion rates. However, on the B6 background, the AZIP mice have less hyperglycemia, lower circulating triglyceride and fatty acid levels, and lower mortality. AZIP characteristics that are more severe on the B6 background include increased liver size and liver triglyceride content. A unifying hypothesis is that the B6 strain has higher triglyceride clearance into the liver, with lower triglyceride levels elsewhere. This may account for the observation that the B6 AZIP mice have less insulin-resistant muscles and more insulin-resistant livers, than do the FVB AZIP mice. B6 wild type, as well as B6 AZIP, mice have increased triglyceride clearance relative to FVB, which may be explained in part by higher serum lipase levels and liver CD36/fatty acid translocase mRNA levels. Thus, it is likely that increased triglyceride clearance in B6, as compared with FVB, mice contributes to the strain differences in insulin resistance and lipid metabolism.

Adipose Tissue↗

PubMed2005

Obese yeast: triglyceride lipolysis is functionally conserved from mammals to yeast.

Storage and degradation of triglycerides are essential processes to ensure energy homeostasis and availability of precursors for membrane lipid synthesis. Recent evidence suggests that an emerging class of enzymes containing a conserved patatin domain are centrally important players in lipid degradation. Here we describe the identification and characterization of a major triglyceride lipase of the adipose triglyceride lipase/Brummer family, Tgl4, in the yeast Saccharomyces cerevisiae. Elimination of Tgl4 in a tgl3 background led to fat yeast, rendering growing cells unable to degrade triglycerides. Tgl4 and Tgl3 lipases localized to lipid droplets, independent of each other. Serine 315 in the GXSXG lipase active site consensus sequence of the patatin domain of Tgl4 is essential for catalytic activity. Mouse adipose triglyceride lipase (which also contains a patatin domain but is otherwise highly divergent in primary structure from any yeast protein) localized to lipid droplets when expressed in yeast, and significantly restored triglyceride breakdown in tgl4 mutants in vivo. Our data identify yeast Tgl4 as a functional ortholog of mammalian adipose triglyceride lipase.

Amino Acid Sequence↗

PubMed1998

Comparative clinical evaluation of the 13C-mixed triglyceride breath test as an indirect pancreatic function test.

BACKGROUND: Breath tests using stable isotopes of carbon or hydrogen are increasingly becoming established for the evaluation of various gastrointestinal functions, including measurement of exocrine pancreatic insufficiency. We wanted to evaluate the clinical relevance of the non-invasive, non-radioactive 13C-mixed triglyceride breath test in comparison with the secretin-caerulein test as the 'gold standard' of pancreatic function testing and with faecal chymotrypsin and elastase 1 in patients with mild and severe exocrine pancreatic insufficiency. METHODS: The secretin-caerulein test, faecal fat analysis, 13C-mixed triglyceride breath test, faecal elastase 1, and chymotrypsin and various morphologic investigations were done in 26 patients with mild (n = 13) or severe (n = 13) exocrine pancreatic insufficiency and 25 patients with gastrointestinal diseases of non-pancreatic origin. Twenty-seven healthy volunteers served as normal controls. After a 12-h fast 200 mg mixed triglyceride (1,3-distearyl,2(carboxyl-13C)octanoyl glycerol) were orally administered with a test meal, and breath samples were taken before and at 30-min intervals for 5 h thereafter, and the increase in 13C/12C isotopic ratio in breath was analysed by mass spectrometry. Various modifications of the test procedure were investigated. RESULTS: Specificity for impaired pancreatic function was higher for faecal elastase (90%) and equal for faecal chymotrypsin (82%) as compared with the various variables of the 13C-mixed triglyceride breath test (69-85%). The sensitivity of the 13C-mixed triglyceride breath test for total and separately for mild and severe exocrine pancreatic insufficiency was higher (total, 69-81%) than that of faecal chymotrypsin (total, 56%) but lower than faecal elastase (total, 92%). CONCLUSION: The 13C-mixed triglyceride breath test very sensitively reflects severe exocrine pancreatic insufficiency (steatorrhoea) but has limited sensitivity for the detection of mild cases. With regard to the higher sensitivity and specificity, the higher practicability, and the much lower cost, determination of faecal elastase 1 concentrations is superior to the 13C-mixed triglyceride breath test and therefore remains the most reliable indirect pancreatic function test available today.

Adult↗

PubMed2002

The plasma and lipoprotein triglyceride postprandial response to a carbohydrate tolerance test differs in lean and massively obese normolipidemic women.

The goal of the present study was to compare the plasma lipid responses of massively obese and lean women to a fat load and a carbohydrate load. For this purpose, 11 lean [body mass index (BMI), 21.6 +/- 2 kg/m(2)] and 8 obese (BMI, 50.8 +/- 7 kg/m(2)) normolipidemic women were given, in random order, either a dietary carbohydrate load (3.43 MJ, 166 g carbohydrates, 38 g proteins) or a dietary fat load (3.35 MJ, 70 g fat, 36 g proteins). Blood samples were collected hourly for 9 h after the test meal for measurements of triglyceride-rich lipoprotein (TRL)-lipid, apolipoprotein (apo)B-48 and apoB-100. Triglycerides (P < 0.0001), TRL triglycerides (P < 0.0001), TRL cholesterol (P < 0.04) and apoB-48 (P < 0.0001) peaked 3 h after the fat meal and returned progressively to baseline values in both obese women and lean controls. These lipid and apolipoprotein changes did not differ between the two groups. In contrast, after the carbohydrate load, the plasma triglyceride (P < 0.0001) and TRL triglyceride (P < 0.0001) increments were significantly greater in obese women than in lean controls. This carbohydrate-induced TRL triglyceride increment was half of that following the isocaloric fat load. The carbohydrate load did not affect apoB-100 and apoB-48 levels. These findings suggest that postprandial triglyceride metabolism is impaired after a carbohydrate load in normolipidemic massively obese women.

Adult↗

PubMed1988

Relation of triglyceride levels to coronary artery disease: the Milwaukee Cardiovascular Data Registry.

Although levels of triglycerides have consistently shown a strong association with cardiovascular disease in both case-control and cohort studies, it remains controversial whether this relation exists independently of levels of cholesterol and other risk factors. The association of arteriographically documented coronary artery disease with plasma levels of triglycerides, total cholesterol, and high density lipoprotein (HDL) cholesterol was therefore examined in 5,216 white adults (81% were male) referred to two Milwaukee hospitals between 1972 and 1986. Elevated levels of triglycerides were related to the extent of coronary artery disease (estimated using the total number and severity of stenoses) in both sexes; this association existed independently of total cholesterol, age, obesity, hypertension, smoking, and alcohol consumption. In addition, the association between triglycerides and coronary artery occlusion was strongest at total cholesterol levels less than or equal to 250 mg/dl. However, both stratified and regression analyses indicated there was no residual association between triglyceride levels and occlusion after controlling for HDL cholesterol. (Levels of HDL cholesterol and triglycerides showed a moderate inverse association: r = -0.39 to -0.51.) These results indicate that the association between coronary artery occlusion and levels of triglycerides is indirect, and that the disparate findings of earlier studies may have resulted from not controlling for HDL cholesterol.

Aged↗

PubMed2001

Evaluation of serum cholesterol and triglyceride levels in 1-6-year-old Saudi children.

Estimations of cholesterol and triglyceride in serum are frequently requested tests due to the close association between elevated levels of these parameters and the risk of arteriosclerosis later leading to cardiovascular disease. Since lipid levels in children show considerable variations in different populations, this study was conducted with the aim of investigating levels of cholesterol and triglycerides in Saudi children less than 6 years old. The study group comprised 582 children with ages ranging from 1 to 6 years, randomly selected during a household screening programme. Fasting blood was used for the estimation of cholesterol and triglyceride using an autoanalyser. The overall range for cholesterol was 2.1-5.7 mmol/l and for triglyceride it was 0.1-1.84 mmol/l. The children were separated into five further groups depending on age, and the levels of cholesterol and triglycerides were obtained in each age group. Using published guidelines for cholesterol and triglyceride levels, to estimate 'borderline' and 'high risk' for arteriosclerosis and coronary artery disease, the prevalence of both risk groups were calculated in Saudi children. A total of 6.87 per cent of children fell in the borderline risk and 1.55 per cent in the high-risk group using cholesterol levels, while 1.89 per cent fell in the borderline-risk group and 1.2 per cent in the high-risk group using triglyceride levels. This paper presents the lipid values and discusses the need for lipid awareness programmes in the country.

Age Distribution↗

PubMed1999

Medium-chain triglycerides inhibit growth of Malassezia: implications for prevention of systemic infection.

OBJECTIVE: Lipophilic Malassezia species may induce catheter-associated sepsis in newborns and immunocompromised patients receiving parenteral lipids. Therefore, we tested whether M. furfur and six other Malassezia species can use commercially available infusions as a lipid source. DESIGN: Prospective in vitro study. SETTING: Research laboratory in a university hospital. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: With the exception of M. restricta, all Malassezia species grow on lipid infusions. There are no substantial differences among the different brands. The most rapid growth is shown by M. furfur, which grows better on agar containing a 20% rather than a 10% lipid infusion. Growth of M. furdur and M. sympodialis can be reduced by infusions containing medium-chain triglycerides. Incubated in triglycerides, M. furfur is strongly suppressed by 50% medium-chain triglycerides and M. sympodialis by 8% medium-chain triglycerides. When medium-chain free fatty acids are added to triglycerides, both species can be suppressed by about 1% free fatty acids. CONCLUSION: Medium-chain triglycerides and medium-chain free fatty acids are toxic for Malassezia species. Commercially available infusions containing medium-chain triglycerides might be used to prevent systemic Malassezia infections.

Catheterization↗

PubMed1998

Suppression of endothelin-3-induced nitric oxide synthesis by triglyceride in human endothelial cells.

Reduced endothelium-derived nitric oxide (NO) production characterizes several vascular diseases. This study examined the effect of triglyceride on NO production induced by endothelin-3 (ET-3) in cultured human umbilical vein endothelial cells. Triglyceride-rich human plasma obtained after a high-carbohydrate diet with white wine was used in an ex vivo study. The plasma triglyceride fraction was found to consist of large amounts of palmitic and oleic acids detected by gas-liquid chromatography. Therefore, the effect of synthetic tripalmitin and triolein emulsion on NO production was also examined. ET-3 stimulated NO and guanosine 3',5'-cyclic monophosphate production and increased cytosolic Ca2+ levels in the endothelial cells (ECs). After incubation of the ECs with the triglyceride-rich plasma for 2 h, these responses to ET-3 were ameliorated in a triglyceride concentration-dependent manner (50-200 mg/dl). A synthesized emulsion of tripalmitin (100 mg/dl) and triolein (100 mg/dl) also blunted the responses to ET-3. Neither endothelial constitutive NO synthase mRNA expression nor its protein level was affected by treatment with triglycerides. These results suggest that triglyceride suppresses ET-3-induced NO synthesis in human ECs by inhibiting cytosolic Ca2+ elevation.

Blotting, Northern↗

PubMed2000

Is abnormal postprandial lipemia a familial risk factor for coronary artery disease in individuals with normal fasting concentrations of triglycerides and cholesterol?

OBJECTIVE: To assess the postprandial response to a fat load in patients with coronary artery disease (CAD) and age-matched controls. METHODS: Postprandial lipemia was assessed in patients with CAD confirmed by angiography (study group, n = 44) and in patients without coronary lesions (control group, n = 20). Family members of patients with CAD were also included (spouses group, n = 22; progeny group, n = 33). Fasting triglyceride and cholesterol concentrations in the control and study groups were less than 2.3 and 6.47 mmol/l, respectively. After initial blood sampling, the patients consumed 30% cream (200 ml/m2 body area). Repeat measurements of triglycerides, total cholesterol and high-density lipoprotein were made after 2, 4, 6, and 8 h. RESULTS: Changes were most marked in triglyceride concentrations. Peak values were observed after 4 h in the spouses, progeny, and control groups, and after 6 h in the study group. To compensate for the large age span (8-40 years) of the progeny, two subgroups were formed, taking 25 years as the cut-off value. Triglycerides continued to increase until the 4th hour in both subgroups, but the subgroups differed as to the absolute concentration of triglycerides. During the first 6 h of the test, the concentrations were significantly greater in the subgroup of older progeny than in their fathers with CAD. CONCLUSIONS: These findings indicate that triglycerides are metabolized at a slower rate and remain longer in the circulation of patients with CAD, as compared with patients without CAD. A significantly greater level of postprandial lipemia has been observed in adult progeny of patients with CAD, suggesting a genetic disorder of triglyceride metabolism in these individuals.

Adult↗

PubMed2002

HDL and triglyceride as therapeutic targets.

PURPOSE OF REVIEW: Epidemiological studies have shown that plasma HDL-cholesterol is inversely related to coronary artery disease and that there is an inverse relationship between HDL-cholesterol and triglyceride levels, but it is now demonstrated that hypertriglyceridemia is an independent risk factor for coronary heart disease (CHD). The goal of this review is to discuss if triglycerides and HDL-cholesterol could be therapeutic targets to reduce cardiovascular risk. RECENT FINDINGS: Triglyceride measurement is not informative on the specificity of the triglyceride-rich lipoproteins present in the plasma because some of these are not atherogenic (chylomicrons, large VLDLs) while others are highly atherogenic (small VLDLs, remnants, IDL...). Statins, in addition to reducing LDL-cholesterol, significantly reduced atherogenic remnant lipoprotein cholesterol levels. 4S, CARE+LIPID, and AFCAPS/TexCAPS studies, suggested enhanced therapeutic potential of statins for improving triglyceride and HDL-cholesterol levels in patients with CHD. A fibrate (gemfibrozil) was shown to reduce death from CHD and non-fatal myocardial infarction in secondary prevention of CHD in men with low levels of HDL-cholesterol (VA-HIT); during the treatment these levels predicted the magnitude of reduction in risk for CHD events. SUMMARY: ATP III recommendations state, on triglycerides and HDL-cholesterol as targets to reduce cardiovascular risk: (1) that lowering LDL-cholesterol levels is the primary target of therapy, (2) a secondary target is to achieve a triglyceride level < 150 mg/dL and (3) clinical trial data are considered to be insufficient to support recommended a specific HDL-cholesterol goal even if HDL-cholesterol < 40 mg/dL is considered to be a major risk factor of CHD.

Cholesterol, HDL↗

PubMed2004

The role and mode of action of apolipoproteins CIII and AV: synergistic actors in triglyceride metabolism?

PURPOSE OF REVIEW: Apolipoprotein (apo)CIII and apoAV play an important role in triglyceride metabolism as evidenced by the unambiguous and opposing phenotypes of transgenic and knockout mouse models. In this review we discuss studies on the genetics, protein structure, and regulation of apoCIII and apoAV and compare their potential molecular mechanisms of action in triglyceride metabolism. We examine the hypothesis that apoCIII and apoAV synergistically affect triglyceride metabolism. RECENT FINDINGS: It has now been firmly established that variation in plasma triglyceride levels in a wide range of human populations is strongly associated with genetic variation at the chromosomal locus encoding both the APOC3 and APOA5 genes, the APOA1/C3/A4/A5 gene cluster. The close physical linkage of these genes and the frequent concurrence of genetic variants, however, complicate the assignment of specific metabolic defects to specific polymorphisms. Recent insight into the regulation of APOC3 and APOA5 gene expression and structural modeling studies on the apoAV protein have provided novel clues for the potential molecular mechanisms responsible for the effects of apoCIII and apoAV on triglyceride metabolism. SUMMARY: Hypertriglyceridemia is a major independent risk factor in the development of cardiovascular disease. Moreover, triglyceride-derived fatty acids are thought to play a key role in the development and progression of the metabolic syndrome. As modulators of triglyceride metabolism, apoCIII and apoAV are key players and potential therapeutic targets. However, little is known of their molecular mechanism and potential cooperativity. Rational therapeutic application will require the filling of this hiatus in our knowledge.

Animals↗

PubMed2006

Why do omega-3 fatty acids lower serum triglycerides?

PURPOSE OF REVIEW: Fish oils rich in n-3 fatty acids reduce serum triglyceride levels. This well known effect has been shown to be caused by decreased very low-density lipoprotein triglyceride secretion rates in kinetic studies in humans. Animal studies have explored the biochemical mechanisms underlying this effect. Triglyceride synthesis could be reduced by n-3 fatty acids in three general ways: reduced substrate (i.e. fatty acids) availability, which could be secondary to increase in beta-oxidation, decreased free fatty acids delivery to the liver, decreased hepatic fatty acids synthesis; increased phospholipid synthesis; or decreased activity of triglyceride-synthesizing enzymes (diacylgylcerol acyltranferase or phosphatidic acid phosphohydrolase). RECENT FINDINGS: Rarely were experimental conditions used in rat studies physiologically relevant to the human situation in which 1.2% energy as n-3 fatty acids lowers serum triglyceride levels. Nevertheless, the most consistent effect of n-3 fatty acids feeding in rats is to decrease lipogenesis. Increased beta-oxidation was frequently, but not consistently, reported with similar numbers of studies reporting increased mitochondrial compared with peroxisomal oxidation. Inhibition of triglyceride-synthesizing enzymes was only occasionally noted. SUMMARY: As the vast majority of studies fed unphysiologically high doses of n-3 fatty acids, these findings in rats must be considered tentative, and the mechanism by which n-3 fatty acids reduce triglyceride levels in humans remains speculative.

Animals↗

PubMed2002

Atorvastatin treatment induced peroxisome proliferator-activated receptor alpha expression and decreased plasma nonesterified fatty acids and liver triglyceride in fructose-fed rats.

We aimed to investigate the effect of atorvastatin (5 and 30 mg/kg/day for 2 weeks) on hepatic lipid metabolism in a well established model of dietary hypertriglyceridemia, the fructose-fed rat. Fructose feeding (10% fructose in drinking water for 2 weeks) induced hepatic lipogenesis and reduced peroxisome proliferator-activated receptor alpha (PPARalpha) expression and fatty acid oxidation. As a result, plasma and liver triglyceride and plasma apolipoprotein B (apoB) levels were increased. Atorvastatin, 5 and 30 mg/kg during 2 weeks, markedly reduced plasma triglyceride, but decreased apoB levels only at the highest dose tested (50%). Triglyceride biosynthetic enzymes and microsomal triglyceride transfer protein were unchanged, whereas liver PPARalpha, acyl-CoA oxidase, and carnitine palmitoyltransferase I mRNA levels (1.9-, 1.25-, and 3.4-fold, respectively) and hepatic fatty acid beta-oxidation activity (1.25-fold) were increased by atorvastatin at 30 mg/kg. Furthermore, hepatic triglyceride content (45%) and plasma nonesterified fatty acids (NEFAs) (49%) were reduced. These results show for the first time that liver triglyceride increase in fructose-fed rats is linked to decreased expression of PPARalpha, which is prevented by atorvastatin treatment. The increase in PPARalpha expression caused by atorvastatin was associated with reduced liver triglyceride and plasma NEFA levels.

Adipose Tissue↗

PubMed1981

Heterogeneity of VLDL triglyceride production by the liver and intestine.

These studies examine the mechanisms responsible for the heterogeneous nature of very low density lipoprotein (VLDL) triglyceride production. The fasting dog has been used as a model to follow the incorporation of [2-3H]glycerol and [1-14C]palmitate into the triglyceride of VLDL isolated from plasma and from mesenteric lymph. The former represents mainly hepatic VLDL, and the latter, intestinal VLDL. VLDL from each source has been subfractionated into Sf 100-400, Sf 60-100, and Sf 20-60 components. The plateau in triglyceride specific activity achieved during constant infusions of the labelled precursors was higher in small VLDL than in large VLDL. This indicates that the small VLDL triglyceride is not derived exclusively from that in large VLDL. This applies to both hepatic and intestinal VLDL. This contrasts with apolipoprotein B in small VLDL, which other studies show to be entirely derived from large VLDL. Thus both the liver and the intestine incorporate triglyceride into particles whose density extends through the entire VLDL spectrum. Unless triglyceride-rich lipoproteins with the density of VLDL but with no apolipoprotein B are produced, these data raise the possibility that triglyceride may enter VLDL directly.

Animals↗

PubMed1997

CT depiction of experimental liver tumors: contrast enhancement with hepatocyte-selective iodinated triglyceride versus conventional techniques.

PURPOSE: To compare findings at computed tomography (CT) enhanced with a hepatocyte-selective contrast agent (iodinated triglyceride) and/or iohexol and at CT during arterial portography (CTAP). MATERIALS AND METHODS: Rabbit livers were directly inoculated with VX2 carcinoma. Results were compared for five helical CT examinations: unenhanced CT, iohexol-enhanced CT (600 mg iodine per kilogram of body weight [mg I/kg]), CTAP (with iohexol [600 mg I/kg]), triglyceride-enhanced CT (126 mg I/kg), and dual-contrast-enhanced CT (triglyceride plus iohexol [425 mg I/kg]). Attenuation of normal liver and tumor were compared with analysis of variance techniques and blinded reader evaluations. RESULTS: Normal liver attenuation was greatest at CTAP (127.3 HU +/- 5.3 [mean +/- standard error of the mean]), followed by dual-contrast-enhanced CT (112.4 HU +/- 1.2), iohexol-enhanced CT (97.9 HU +/- 2.2), triglyceride-enhanced CT (82.3 HU +/- 1.1), and unenhanced CT (54.9 HU +/- 1.8). Liver-to-lesion attenuation difference at triglyceride-enhanced CT was significantly greater than at iohexol-enhanced CT (P < .05), and attenuation differences at dual-contrast-enhanced CT were comparable to those at CTAP. Tumors did not enhance at triglyceride-enhanced CT, which increased conspicuity. Sensitivity values for lesion detection at dual-contrast-enhanced CT were greater than those at iohexol-enhanced CT or at CTAP (P < .05). CONCLUSION: At CT enhanced with triglyceride (especially when combined with iohexol), sensitivity values and liver-to-lesion attenuation differences were greater with lower iodine doses than with iohexol or at CTAP.

Animals↗

PubMed1990

Medium-chain triglycerides induce alterations in carnitine metabolism.

Medium-chain triglycerides are generally assumed to be metabolized independently of carnitine. The effects of infusing medium-chain triglycerides on plasma concentrations of carnitine derivatives and beta-hydroxybutyrate were studied in four healthy male adults. Glucose and amino acids were infused alone for 3 h, then continued for another 5.5 h together with a lipid emulsion containing only long-chain triglycerides or a 50:50% (wt/wt) mixture of medium-chain and long-chain triglycerides. During the fat-free infusion, the concentration of free carnitine rose, whereas the level of acylcarnitines decreased. Infusion of the mixed emulsion over 5.5 h reduced free carnitine to lower values (32.4 +/- 4.7 mumols/l) than long-chain triglycerides infusion (44.4 +/- 2.7 mumol/l). By contrast, the plasma concentrations of short-chain acylcarnitine (12.1 +/- 3.3 vs. 5.4 +/- 1.9 mumols/l; P less than 0.01) and of beta-hydroxybutyrate (93 +/- 32 vs. 47 +/- 14 mumols/l; P less than 0.01) became significantly higher with the mixed emulsion than with long-chain triglycerides. This suggests that intravenous medium-chain triglycerides are not metabolized independently of carnitine. Carnitine may play an important role in removing acyl and acetyl groups from mitochondria and in restoring the intramitochondrial CoA level. Fat substrates are converted into compounds that might be utilized by tissues that do not normally oxidize fatty acids, creating an interorgan energy cycle.

3-Hydroxybutyric Acid↗

PubMed1990

Diet affects the mechanisms by which TNF stimulates hepatic triglyceride production.

Tumor necrosis factor (TNF) induces hyperlipidemia in rodents by increasing hepatic triglyceride production. We now explore the mechanism of this increase. TNF does not increase phosphatidate phosphohydrolase, glycerolphosphate acyltransferase, or diacylglycerol acyltransferase, which are enzymes of triglyceride synthesis. Rather, TNF increases triglyceride production by providing increased fatty acids (FA) as substrate. In chow-fed rats, TNF increases plasma free fatty acids (FFA). The antilipolytic drug, phenylisopropyl adenosine (PIA), prevents the TNF-induced increase in plasma FFA and, most importantly, inhibits the TNF-induced increase in plasma triglycerides. Thus increased lipolysis with delivery of FA to liver contributes to TNF-induced hyperlipidemia in chow-fed animals. In contrast, in rats fed a high-sucrose diet, TNF causes hyperlipidemia without increasing plasma FFA, and PIA has no effect on TNF-induced increases in plasma triglycerides. However, in sucrose-fed rats, TNF markedly stimulates hepatic de novo FA synthesis, which provides FA. This diet determines the mechanism by which TNF stimulates hepatic triglyceride production. The use of multiple mechanisms to increase plasma triglycerides suggests that this TNF action plays an important role in the response to infection or inflammation.

Acyltransferases↗

PubMed1984

Apoprotein C effect on triglyceride transport in tandem-perfused rat hind end and liver.

The metabolism of double-labeled triglyceride in a synthetic emulsion was defined in an in vitro perfusion system of rat hind end and liver described previously [Am. J. Physiol. 245 (Gastrointest. Liver Physiol. 8): G106-G112, 1983]. The metabolism of [3H]glycerol-[14C]triolein was defined in the absence of added apoproteins and with additions of human CII and both CII and CIII. Without apoprotein, a pronounced lipolysis of the triglyceride was recognized by high concentrations of radiolabeled glycerol and free fatty acid in the perfusate. The removal of an aliquot of hind-end venous effluent 5 min after adding the labeled triglyceride emulsion to the arterial inflow demonstrated a brisk lipolysis of the substrate when incubated outside the perfusion system. The addition of CII protein to the emulsion before its introduction into the tandem system eliminated perfusate lipolysis, both within the perfusion system and in incubations of aliquots withdrawn from the system. Intravascular lipolysis was not seen with triglyceride emulsions containing both CII and CIH or when an aliquot of hind-end venous effluent was incubated with triglycerides that had not been exposed to the perfusion system. The intravascular lipolysis observed for the [14C]triglyceride added to the tandem system without apoproteins was associated with relatively greater recoveries of 14C-fatty acyl in liver, fat, and muscle and relatively greater recoveries of 14CO2 than when CII alone or both CII and CIII were added with the triglyceride. The addition of CIII to CII in a 1:1 molar ratio increased the recovery of 14C-fatty acyl in muscle and the recovery as 14CO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗