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PubMed2003

Effect of atorvastatin on lipid parameters, LDL subtype distribution, hemorrheological parameters and adhesion molecule concentrations in patients with hypertriglyceridemia.

BACKGROUND AND AIM: Hypertriglyceridemia is a risk factor for atherosclerosis that is typically associated with high concentrations of adhesion molecules, impaired hemorrheology and an unfavourable low-density lipoprotein (LDL) subtype distribution. We hypothesised that some of these risk markers might be beneficially influenced by lipid-lowering therapy with atorvastatin in hypertriglyceridemic patients. METHODS AND RESULTS: Nineteen patents with primary hypertriglyceridemia were given 10 mg of atorvastatin per day for four weeks. Their cholesterol, triglyceride, LDL and high-density lipoprotein cholesterol (HDL-C) levels, LDL subtype profile, hemorrheological parameters and E-selectin, vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 concentrations were measured before and at the end of atorvastatin therapy. The levels of total and LDL cholesterol respectively decreased by 25% and 24% (both p < 0.001). Furthermore, cholesterol was reduced by 8-29% in all seven LDL subfractions (density range: 1.020-1.066 g/mL) (p < 0.05). The reduction in triglyceride concentrations was of marginal significance (9%, p = 0.1), but its degree positively correlated with the reduction of small-dense LDL (r = 0.5, p < 0.025). Plasma viscosity and blood viscosity at low shear rates were respectively reduced by 2% and 16% (both p < 0.05). The effect of the treatment on the concentrations of HDL-C, fibrinogen and adhesion molecules was not significant. CONCLUSIONS: Atorvastatin (10 mg/day) not only reduced the plasma concentrations of atherogenic lipoproteins but also improved the LDL-subtype profile and reduced plasma and blood viscosity in patients with hypertriglyceridemia; however, it failed to significantly lower triglyceride concentrations.

Anticholesteremic Agents↗
PubMed1997

Effects of fructose-induced hypertriglyceridemia on hepatorenal toxicity of acetaminophen in rats. II. Role of enhancement of fructose metabolism and overproduction of triglyceride in the liver and kidney on hepatorenal toxicity of acetaminophen.

Fructose-induced hypertriglyceridemic rats are resistant to hepatoxicity and susceptible to nephrotoxicity of acetaminophen (APAP) as compared with normal ones. The present studied were designed to evaluate how fructose-treatment affects the developmental mode of hepatorenal toxicity of APAP. First, following fructose-pretreatment for various durations (1 day, 1 week or 3 weeks), 1-day-fructose-pretreatment induced hypertriglyceridemia and enhancement of APAP-nephrectoxicity simultaneously. However, it took at least 3 weeks for fructose-pretreatment to reduce APAP-hepatotoxicity. Second, following fructose, sucrose or glucose-pretreatment for 3 weeks, fructose-pretreated rats showed marked hypertriglyceridemia and modification of APAP-hepatorenal toxicity. Sucrose-pretreated rats showed less effects than fructose-pretreated rats. Glucose-pretreated rats showed no changes in plasma triglyceride and APAP-hepatorenal toxicity. Third, rats with hypertriglyceridemia induced by olive oil or Triton WR-1339 which did not produce enhanced metabolism and triglyceride-overproduction in the liver and kidney showed no modification of APAP-hepatorenal toxicity. Pretreatment of glycerol which was metabolized in liver and kidney and induced an overproduction of triglyceride resulted in an enhancement of APAP-nephrotoxicity. These results indicate that an enhancement of fructose metabolism and an overproduction of triglyceride in liver and kidney are responsible for the modification of APAP-hepatorenal toxicity in fructose-induced hypertriglyceridemic rats.

Acetaminophen↗
PubMedDate not supplied

Diabetic hypertriglyceridemia-induced acute pancreatitis masquerading as biliary pancreatitis.

Diabetes mellitus has a profound effect on plasma lipid metabolism especially triglycerides. One complication of hypertriglyceridemia is acute pancreatitis. Here, we report a case of diabetic hypertriglyceridemia-induced recurrent acute pancreatitis that masquerades as biliary pancreatitis. Institution of insulin therapy caused a resolution of the hypertriglyceridemia and a cessation of the episodes of acute pancreatitis.

Acute Disease↗
PubMed2002

Severe hypertriglyceridemia and pancreatitis following hormone replacement prior to cryothaw transfer.

PURPOSE: A case of acute pancreatitis with severe hypertriglyceridemia occurred following use of intramuscular estradiol valerate during endometrial preparation for cryopreserved embryos. METHODS: A 30-year-old woman with primary infertility and a past history of well-controlled hypothyroidism, underwent endometrial development with intramuscular estradiol valerate in preparation for the transfer of cryopreservred embryos. RESULTS: Initial hospitalization, discontinuation of all estrogens, aggressive intravenous fluid hydration, and initiation of low-fat diet with additional gemfibrozil treatment resulted in complete resolution of all symptoms related to the pancreatitis including the hyperlipidemia. A subsequent cryothaw cycle using oral estradiol resulted in a viable pregnancy with only mild increases in the patient's triglyceride and cholesterol levels noted throughout her 38-week gestation. CONCLUSION(S): Estradiol valerate, a commonly used form of estrogen for endometrial preparation during cryothaw cycles, may cause severe hypertriglyceridemia and acute pancreatitis in certain predisposed individuals. Oral and transdermal estrogens should be the preferred method of endometrial preparation in patients at high risk for lipid metabolism disorders, such as patients with polycystic ovarian syndrome and familial hypertriglyceridemia. These estrogens are more rapidly metabolized and have a shorter half life compared to that of estradiol valerate.

Cryopreservation↗
PubMed2003

Experimental model of postprandial hypertriglyceridemia in sucrose-fed rats and the effectiveness of atorvastatin in the model.

Although postprandial hypertriglyceridemia has drawn attention as an independent risk factor of cardiovascular disease, there is no established animal model that shows a physiological transitory change in lipoprotein metabolism after ingestion of a fatty meal. We developed an animal model of postprandial hypertriglyceridemia using sucrose-fed rats, and used this model to evaluate the effect of atorvastatin on this condition. Compared with normal rats, sucrose-fed rats orally loaded with olive oil showed a high and prolonged increase in plasma triglyceride (TG) concentration accompanied by both an increase in TG secretion and decrease in TG clearance. Atorvastatin (30 mg/kg orally) for 2 weeks reduced not only fasting plasma TG concentration, but also the postprandial TG concentration. Atorvastatin also suppressed rates of TG secretion in both chylomicron (CM)-rich (d < 0.96 g/mL) and very-low-density lipoprotein (VLDL) (d = 0.96 to 1.006 g/mL) fractions after oral fat loading. Further, atorvastatin improved the elimination time of exogenous TG emulsion only in the nonfasted, namely, high plasma TG condition. These results indicate that this animal model satisfactorily replicates the postprandial hypertriglyceridemia observed in humans and may therefore be useful in evaluation of lipid-lowering agents. Furthermore, atorvastatin not only improves fasting but also postprandial lipoprotein metabolism, presumably by reducing TG secretion from the liver or intestine or both, and by secondarily increasing TG-rich lipoprotein clearance by eliminating saturation.

Animals↗
PubMed2001

Effect of gemfibrozil on the composition and oxidation properties of very-low-density lipoprotein and high-density lipoprotein in patients with hypertriglyceridemia.

Recent studies suggest that both oxidized very-low-density lipoprotein (VLDL) and oxidized high-density lipoprotein (HDL) may play a role in the pathogenesis of atherosclerosis. Gemfibrozil is widely used and is reported to decrease VLDL levels and increase HDL levels. The aim of this study was to investigate the effect of gemfibrozil on the chemical composition and oxidative susceptibility of VLDL and HDL and their relationship with atherosclerosis. Twenty patients with hypertriglyceridemia were treated with 300 mg gemfibrozil, 3 times daily, for 12 weeks. Venous blood samples were collected before treatment, at the end of treatment, and 4 weeks after the end of treatment. Gemfibrozil effectively lowered concentrations of plasma lipid, apolipoprotein (apo) B, and apo E. The lipid and protein content of VLDL were also decreased, but not by the same extent. The surface-to-core ratio and apo E/apo B ratio of VLDL particles were increased after gemfibrozil treatment. HDL(2) cholesteryl ester and HDL(3) apo A-II content were also increased. Gemfibrozil treatment lowered levels of lipid peroxides in both VLDL and HDL particles. The susceptibility of VLDL to oxidation was unchanged, whereas maximal peroxide production was decreased. The oxidative susceptibility of both HDL(2) and HDL(3) decreased with gemfibrozil treatment. These results indicate that after gemfibrozil treatment, VLDL and HDL particles in patients with hypertriglyceridemia are less atherogenic, which may explain why gemfibrozil treatment is beneficial in terms of coronary heart disease in hypertriglyceridemia.

Adult↗
PubMed2002

Very low density lipoprotein (VLDL) receptor-deficient mice have reduced lipoprotein lipase activity. Possible causes of hypertriglyceridemia and reduced body mass with VLDL receptor deficiency.

Although very low density lipoprotein (VLDL) receptor (VLDLr) knockout mice have been reported to have no lipoprotein abnormalities, they develop less adipose tissue than control mice when fed a high calorie diet. Mice that are deficient in adipose tissue expression of lipoprotein lipase (LpL) also have less fat, but only when crossed with ob/ob mice. We hypothesized that the VLDLr, a protein that will bind and transport LpL, is required for optimal LpL actions in vivo and that hypertriglyceridemia due to VLDLr deficiency is exacerbated by either LpL deficiency or VLDL overproduction. Fasted VLDLr knockout (VLDLr0) mice were more hypertriglyceridemic than controls (2-fold greater triglyceride levels). The hypertriglyceridemia due to VLDLr0 was even more evident when VLDLr0 mice were crossed with heterozygous LpL-deficient (LpL1) and human apolipoprotein B (apoB) transgenic mice. This was due to an increase in apoB48-containing VLDL. [(3)H]VLDL turnover studies showed that VLDL-triglyceride clearance in VLDLr0/LpL1 mice was impaired by 50% compared with LpL1 mice. VLDLr0/LpL1 mice had less LpL activity in postheparin plasma, heart, and skeletal muscle. Infection of mice with an adenovirus-expressing receptor-associated protein, an inhibitor of the VLDLr, reduced LpL activity in wild type but not VLDLr0 mice. Therefore, the VLDLr is required for normal LpL regulation in vivo, and the disruption of VLDLr results in hypertriglyceridemia associated with decreased LpL activity.

Adipose Tissue↗
PubMed1998

Insulin therapy for a non-diabetic patient with severe hypertriglyceridemia.

OBJECTIVE: To compare the short and long term effectiveness of fish oil, insulin, and gemfibrozil in a non-diabetic patient with severe hypertriglyceridemia. METHOD: An adolescent male with hypertriglyceridemia (triglyceride level 4575 mg/dl) and abdominal pain was treated with the goal of immediate reduction and maintenance of triglyceride (TG) level below 1000 mg/dl. Fish oil, insulin and gemfibrozil were administered sequentially, in separate time blocks, for a duration of 3, 6, and 6 months, respectively. RESULTS: Fish oil took several weeks to lower TG level, and patient compliance during 3 months of therapy was inadequate. Insulin was effective in immediately lowering the TG level, but was unable to maintain the level below 1000 mg/dl. Gemfibrozil was ineffective in achieving the immediate reduction of TG level; however, it was adequate in maintaining the desired level in the long-term and patient compliance was better than with the fish oil. CONCLUSION: In patients with risk of pancreatitis due to severe hypertriglyceridemia, immediate reduction of the triglyceride level is achievable by using a single dose of regular insulin (0.1 unit/kg, subcutaneous) while long-term maintenance therapy can be provided by gemfibrozil.

Abdominal Pain↗
PubMed2003

Dietary flaxseed meal is more protective than soy protein concentrate against hypertriglyceridemia and steatosis of the liver in an animal model of obesity.

OBJECTIVE: Soy protein and flaxseed meal have been reported to have beneficial effects on many chronic diseases in humans and animals. The primary objective of the study was to evaluate the beneficial effects of soy protein and flaxseed meal on hypertriglyceridemia and liver steatosis associated with obesity and diabetes. We compared the effects of dietary soy protein and flaxseed meal with that of casein on plasma and liver lipids in a genetic model of obesity, type II diabetes and insulin resistance, namely the SHR/N-cp rat. METHODS: Lean and obese phenotypes of SHR/-cp rats were fed AIN 93 diets containing 20% of energy from casein (control), soy protein concentrate or flaxseed meal for six months. Plasma was analyzed for total cholesterol, LDL cholesterol, triglyceride and total protein. Liver was analyzed for steatosis by light microscopy after staining samples with Hematoxylin-Eosin and Oil-Red-O. RESULTS: In lean rats soy protein and flaxseed meal significantly decreased plasma total cholesterol (26.0% and 20.3% respectively) compared to casein. In obese rats flaxseed meal had significant cholesterol lowering effect compared to control rats (41%). Soy protein significantly lowered both plasma LDL-cholesterol and HDL-cholesterol in lean phenotypes while in obese phenotypes flaxseed meal significantly lowered LDL-cholesterol and HDL-cholesterol compared to casein-fed rats. Flaxseed meal also significantly lowered plasma triglyceride in both lean and obese rats compared to casein fed rats (33.7% and 37% respectively). There was significantly greater fat accumulation in livers of obese rats than lean rats (200%) regardless of dietary protein type. Flaxseed meal significantly lowered fat deposition in livers of both lean and obese rats compared to rats fed casein or soy protein. Dietary component(s) present in flaxseed meal or soy protein responsible for hypolipidemic effects is not clear. CONCLUSIONS: The marked hypotriglyceridemic and hypocholesterolemic effects of flaxseed meal may have important therapeutic implications in patients with hypertriglyceridemia and hypercholesterolemia and deserve further study in humans with these disorders. Flaxseed meal supplementation may provide a new therapeutic strategy to reduce hypertriglyceridemia and fatty liver.

Animals↗
PubMed1997

Hypertriglyceridemia during long-term interferon-alpha therapy in a series of hematologic patients.

Adverse reactions to interferon-alpha (IFN-alpha) therapy include flu-like syndrome, bone marrow suppression, neurotoxic effects, and autoimmunity. A slight increase in triglyceride levels has been described less frequently during IFN-alpha administration. The incidence of IFN-alpha-induced hypertriglyceridemia seems variable, and there are no clear data on how to treat it. We report the effect of long-term (more than 12 months) IFN-alpha treatment on triglyceride levels in 43 patients suffering from hairy cell leukemia (18), multiple myeloma (10), chronic myelogenous leukemia (6), cryoglobulinemia (5), non-Hodgkin's lymphoma (3), and Sezary syndrome (1). Hypertriglyceridemia was found in 6 patients (15%). In 3 patients, gemfibrozil restored normal triglyceride values. This study suggests that hypertriglyceridemia is a minor side effect of long-term IFN-alpha therapy and that gemfibrozil might be considered the treatment of choice.

Adult↗
PubMed2003

A novel genetic variant in the apolipoprotein A5 gene is associated with hypertriglyceridemia.

The apolipoprotein A5 gene (APOA5 ) has been shown to play an important role in determining plasma triglyceride concentrations in humans. We describe here a novel variant, c.553G>T, in the apolipoprotein A5 gene that is associated with hypertriglyceridemia. In contrast to some other polymorphisms, which occur in non-coding regions of the gene, this variant occurs within the coding region and causes the change of amino acid sequence (a substitution of a cysteine for a glycine residue). The minor allele frequencies were 0.042 and 0.27 (P<0.001) for control and hypertriglyceridemic patients, respectively. The serum triglyceride level was significantly different among the genotypic groups (G/G 92.5+/-37.8 mg/dl, G/T 106.6+/-34.8 mg/dl, T/T 183.0 mg/dl, P=0.014) in control subjects. Multiple logistic regression revealed individuals carrying the minor allele had age, gender and BMI (body mass index)-adjusted odds ratio of 11.73 (95% confidence interval of 6.617-20.793; P<0.0001) for developing hypertriglyceridemia in comparison to individuals without that allele. These findings suggest the possible use of c.553G>T polymorphisms in APOA5 as prognostic indicators for hypertriglyceridemia susceptibility in Chinese.

Age Factors↗
PubMed1992

The role of the cytokines, interferon alpha and tumor necrosis factor in the hypertriglyceridemia and wasting of AIDs.

The hypertriglyceridemia of infection is mediated by many of the cytokines that regulate the immune response, including the tumor necrosis factors, the interleukins and the interferons. In the acquired immunodeficiency syndrome (AIDS), hypertriglyceridemia is most likely due to increased circulating levels of interferon alpha. Both in AIDS and in animal models there is no direct association between the presence of hypertriglyceridemia and the syndrome of wasting. Rather, circulating lipoproteins may neutralize infectious organisms and therefore contribute to host defense.

Acquired Immunodeficiency Syndrome↗
PubMed2001

Reduced hepatic triglyceride secretion in rats fed docosahexaenoic acid-rich fish oil suppresses postprandial hypertriglyceridemia.

To evaluate the mechanisms of suppression of postprandial hypertriglyceridemia by fish oil rich in docosahexaenoic acid, the effect on the intestinal absorption of triglyceride, activities of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) and metabolism of chylomicrons (CM) and CM remnants were compared with that of safflower oil in Sprague-Dawley rats in a series of studies. The feeding of fish oil for 3 wk suppressed postprandial hypertriglyceridemia (study 1). Dietary fish oil did not alter the rate of lymphatic absorption of triglyceride (study 2). The activities of LPL and HTGL were measured at 5 h after the beginning of feeding, when serum triglyceride concentrations were highest in both dietary groups. The activities of LPL in adipose tissue and heart were greater (P < 0.05) and those of HTGL were lower (P < 0.05) in the rats fed fish oil (study 3). In contrast, there were no differences in the activities of LPL and HTGL in postheparin plasma between the fish and safflower oil groups (study 4). The clearance rates of CM and CM remnants were measured by injecting intravenously CM collected from rats fed safflower or fish oils with [14C]triolein and [3H]cholesterol (study 5). Dietary oil did not influence the half-lives of CM or CM remnants. The secretion of triglyceride from the liver of rats injected with Triton WR-1339 was lower (P < 0.05) in the rats fed docosahexaenoic acid, a major component of fish oil, than those fed linoleic acid, a major component of safflower oil (study 6). These observations strongly support the hypothesis that in rats, the principal cause of the suppression of postprandial hypertriglyceridemia by fish oil is the depression of triglyceride secretion from the liver.

Absorption↗
PubMed2004

Ingestion of guar gum hydrolysate, a soluble and fermentable nondigestible saccharide, improves glucose intolerance and prevents hypertriglyceridemia in rats fed fructose.

Fructose feeding provides a dietary model of insulin resistance accompanied by hypertriglyceridemia. We examined the effects of guar gum hydrolysate (GGH), a soluble and fermentable nondigestible saccharide with low viscosity, on glucose intolerance and hypertriglyceridemia in rats fed high-fructose diets. Rats were fed either a dextrin-based or a fructose-based diet with or without GGH (75 g/kg) for 30 d. Oral glucose tolerance tests (OGTTs) were performed 0, 14, and 28 d after feeding. High-fructose feeding negatively affected glucose tolerance on d 14 and 28. The addition of GGH to the diets improved glucose intolerance on d 28. Fructose feeding induced hyperinsulinemia after an oral glucose load; this was also improved by GGH on d 28. The glycogen concentration in the gastrocnemius muscles of rats was lowered by dietary fructose, and GGH supplementation abolished this decrease. Triglycerides in the plasma and livers of rats fed fructose diets were elevated, and the increases were ameliorated by supplemental GGH. Regardless of the type of carbohydrate, GGH enlarged the cecum and increased the cecal SCFA pools. In conclusion, supplemental feeding of GGH to rats improved the glucose intolerance and hypertriglyceridemia induced by a high-fructose diet. Possible mediators of these beneficial effects of GGH are the SCFAs produced by microbial fermentation of GGH in the large intestine.

Animals↗
PubMed2004

Fenofibrate is effective in treating hypertriglyceridemia associated with HIV lipodystrophy.

OBJECTIVE: To determine the effectiveness of fenofibrate in treating hypertriglyceridemia associated with highly active antiretroviral therapy-associated HIV lipodystrophy syndrome (HLS). METHODS: The authors recruited from their HIV metabolic clinic 55 adult patients with anthropomorphic changes consistent with HLS together with hypertriglyceridemia. The patients had no prior history of taking lipid-lowering medications and were free of liver and renal disease. They were on various highly active antiretroviral therapy regimens, and these regimens were not altered during the course of the study. Fenofibrate was started at 54 mg a day and the dose increased every 2 weeks to a maximum of 162 mg/day. Fasting lipid concentrations were measured at baseline and 6 months after the intervention. RESULTS: At baseline, the fasting plasma concentrations of total cholesterol, triglyceride, and high-density lipoprotein (HDL) cholesterol were 259 +/- 11, 886 +/- 172, and 35.7 +/- 2.3 (mean +/- SEM) mg/dL, respectively. After 6 months of fenofibrate treatment, the fasting plasma concentrations were as follows: total cholesterol, 243 +/- 13; triglycerides, 552 +/- 104, and HDL cholesterol, 35.7 +/- 1.8 mg/dL. The decrease in fasting plasma triglyceride concentration was statistically significant (P < 0.05). Fenofibrate was well tolerated, and no subjects dropped out of the study. CONCLUSION: Fenofibrate is an effective, well-tolerated treatment for hypertriglyceridemia associated with HLS.

Adult↗
PubMed2002

Long-term follow-up of patients with acute hypertriglyceridemia-induced pancreatitis.

BACKGROUND: An acute and potentially life-threatening complication of hypertriglyceridemia (HTG) is acute pancreatitis (AP). Hypertriglyceridemia, usually severe, may be primary in origin or secondary to alcohol abuse, diabetes mellitus, pregnancy, and use of drugs. STUDY: The efficacy of treatment to prevent relapses in 17 patients with AP attributed to HTG was investigated in the current prospective study. The mean follow-up period of patients was 42 months. Hypertriglyceridemia-induced AP comprised 6.9% of all patients with AP (n = 246) hospitalized in our clinic during the study (6 years). RESULTS: Causative conditions of HTG-induced AP were familial HTG in eight patients, HTG caused by uncontrolled diabetes mellitus in five, HTG aggravated by drugs in two (one by tamoxifen and one by fluvastatin), familial hyperchylomicronemia (HCM) in one, and lipemia of pregnancy in one. During the acute phase of pancreatitis, patients underwent standard treatment. Thereafter, HTG was efficiently controlled with high dosages of fibrates or a fibrate plus acipimox, except for the patient with HCM, who was on a specific diet (the only source of fat was a special oil consisting of medium chain triglyceride) and taking a high dosage of acipimox. One of the patients died during the acute phase of pancreatitis with acute respiratory distress syndrome. During follow-up, maintenance treatment was successful and only one patient relapsed, because he discontinued diet and drug treatment. CONCLUSION: Appropriate diet and drug treatment, including dose titration, of severe HTG is very effective in preventing relapses of HTG-induced AP.

Acute Disease↗
PubMed1998

Sequential alterations in tissue lipoprotein lipase, triglyceride secretion rates, and serum tumor necrosis factor alpha during Escherichia coli bacteremic sepsis in relation to the development of hypertriglyceridemia.

The time sequence and the mechanisms leading to the development of the hypertriglyceridemia of bacteremic sepsis are not fully understood. This study was conducted to determine the mechanisms leading to the early rise in serum triglycerides (TG). Bacteremic sepsis was induced in fasted and parenterally fed rats by intravenous infusion of live Escherichia coli colonies over a 1 h period every 24 h up to 96 h. Body temperature was elevated from 12 to 48 h after E. coli infusion in fasted rats and from 24 to 72 h after E. coli infusion in fed rats. The initial rise in serum TG was observed at 3 h after E. coli infusion; in fasted rats this elevation was maintained over 72 h. In the parenterally fed rats, hypertriglyceridemia was evident only at the 3 h time point. Serum concentrations of tumor necrosis factor alpha (TNF-alpha) were elevated significantly at 60 min after initiating the E. coli infusion, peaked at 90 min, and declined by 120 min. Immunization with neutralizing goat anti-TNF-alpha IgG did not block the initial increase in serum TG induced by E. coli. This early rise in TG in fasted E. coli-treated rats was accompanied by a 33% increase in TG secretion in comparison with control rats. TG secretion declined by 27% at 9 h and remained depressed at 12 and 24 h in comparison with time-matched control rats. By 24 h lipid accumulation was evident in the livers of the fasted and fed E. coli-treated rats. Most of the fasted E. coli-treated rats died by 72 h. Parenteral feeding extended survival of E. coli-treated rats until 120 h. These findings along with the observation that two mechanisms are involved in maintaining the elevation of serum TG during E. coli sepsis suggests that the hypertriglyceridemia may be important in host survival.

Adipose Tissue↗
PubMed2000

Hypertriglyceridemia and the fibrate trials.

Epidemiological studies published since 1996 have established that hypertriglyceridemia can predict risk of cardiovascular disease in a manner statistically independent of HDL cholesterol. Nevertheless, the relationship of concentrations of plasma triglycerides to risk of cardiovascular disease remains less than straightforward, partly because triglycerides are carried in lipoproteins of different atherogenicity, partly because hypertriglyceridemia is associated with non-lipid atherogenic and thrombogenic processes. For example, the association of highest risk of cardiovascular disease to moderate rather than to severe hypertriglyceridemia can be understood in terms of the distribution of triglycerides between different classes of plasma lipoproteins. It is counter-intuitive to most clinicians, however, and hence it can result in the misdirection of clinical efforts including drug therapy. Fibrates lower plasma triglycerides, and raise HDL, efficiently and with few immediate side-effects. Central to their mode of action is activation of certain nuclear receptors in cells. There is no necessary connection, however, between that fascinating biochemistry and clinical benefit as defined by reductions in rates of death by coronary artery disease. A review of trials of cholesterol-lowering by diet and drugs, published between 1966 and 1996, included 12 trials of therapy with fibrates or placebo in more than 21000 patients. Overall, these trials indicated no benefit in terms of reduction in risk of coronary deaths. The period since 1996 has seen the publication of four additional trials of treatment of 6144 patients with fibrates or placebo. Two of them were major trials. The VA-HIT was very encouraging, because treatment with gemfibrozil produced a signficant reduction in the combined incidence of fatal and non-fatal coronary events. There was no significant reduction in coronary deaths, however. The results of BIP were frankly disappointing, because they demonstrated no significant effect of treatment with bezafibrate on either the primary end-point of the trial or on rates of coronary death. Clinical indications for the use of fibrates can obviously not be based on biochemical insights, however intriguing in their own right, but they have also not been satisfactorily defined by the randomized clinical trials published to date. Hope remains, however, that some clarification will result from ongoing trials of fibrate treatment of patients with type II diabetes.

Bezafibrate↗