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PubMed1985

Metabolism of low-density lipoprotein from patients with diabetic hypertriglyceridemia by cultured human skin fibroblasts.

To test whether triglyceride-enriched low-density lipoprotein (LDL) obtained from subjects with diabetic hypertriglyceridemia is metabolized normally by cells, LDL was separated from seven healthy control subjects (fasting plasma glucose [FPG] 91 +/- 10 mg/dl [mean +/- SD], triglyceride [TG] 110 +/- 47 mg/dl), six diabetic normolipidemic patients (FPG 218 +/- 65 mg/dl; TG 139 +/- 75 mg/dl), six diabetic hypertriglyceridemic patients (FPG 214 +/- 71 mg/dl; TG 1915 +/- 1680 mg/dl), and five nondiabetic hypertriglyceridemic patients (FPG 92 +/- 8 mg/dl; TG 2013 +/- 1889 mg/dl). Binding of 125I-labeled LDL from hypertriglyceridemic subjects with and without diabetes to cultured skin fibroblasts was significantly decreased to 74 +/- 19% and 78 +/- 14% of that seen with LDL from normolipidemic nondiabetic subjects and diabetic normolipidemic controls (100 +/- 0%, 101 +/- 25%; P less than 0.005). Unlabeled LDL from hypertriglyceridemic subjects with and without diabetes failed to suppress LDL receptor activity and sterol synthesis from 14C-acetate as efficiently as unlabeled LDL from healthy subjects. The ability of LDL from hypertriglyceridemic subjects, whether diabetic or not, to suppress LDL binding was inversely related to the ratio of triglyceride to protein in LDL (r = 0.71, P less than 0.01) and showed a positive correlation with the LDL cholesterol/protein ratio (0.69, P less than 0.01). Thus, LDL from patients with hypertriglyceridemia, with or without coexistent diabetes, shows impaired binding to LDL receptors and less ability to downregulate LDL receptor activity and sterol synthesis than does LDL from normolipidemic diabetic and nondiabetic subjects. These findings suggest that factors associated with hypertriglyceridemia rather than with diabetes result in altered metabolism of LDL in these disorders.

Adult↗
PubMed1988

Interrelationships among insulin's antilipolytic and glucoregulatory effects and plasma triglycerides in nondiabetic and diabetic patients with endogenous hypertriglyceridemia.

We tested the hypothesis that the previously observed association among hypertriglyceridemia, hyperinsulinemia, and insulin resistance could be explained by a defect in insulin's antilipolytic effect. Insulin action was measured in 10 nondiabetic and 8 diabetic patients with hypertriglyceridemia (fasting plasma triglyceride 800 +/- 154 and 1105 +/- 445 mg/dl, respectively, P NS; fasting plasma glucose 99 +/- 3 and 161 +/- 12 mg/dl, respectively, P less than .001) and in 8 weight-matched normolipemic nondiabetic individuals (fasting plasma triglyceride and glucose 110 +/- 21 and 91 +/- 3 mg/dl). The slope of the decay in plasma free fatty acid (FFA) during insulin infusion was used as an index of insulin's antilipolytic effect. Insulin stimulation of glucose uptake in vivo during intravenous hyperinsulinemic clamp and in vitro in adipocytes were measures of insulin's glucoregulatory action. Both glucoregulatory and antilipolytic effects were similarly reduced in both hypertriglyceridemic groups compared with normal subjects. The plasma triglyceride concentration correlated positively with the slope of FFA suppression by insulin (r = .81, P less than .0001) and the fasting FFA concentration (r = .65, P less than .0001). In multiple linear regression analysis, insulin's antilipolytic effect and the fasting FFA concentration explained 83% of the variation in the plasma triglyceride concentration. These associations were independent of insulin's glucoregulatory effect and the fasting plasma insulin concentration. The data indicate that patients with endogenous hypertriglyceridemia are resistant to both the antilipolytic and glucoregulatory actions of insulin and that increased flux of FFA as a result of the latter, rather than hyperinsulinemia, is responsible for elevation of very-low-density lipoprotein production.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1993

Does familial hypertriglyceridemia predispose to NIDDM?

OBJECTIVE: To determine the 10-yr incidence of impaired glucose tolerance and NIDDM in families with a clustering of endogenous hypertriglyceridemia. RESEARCH DESIGN AND METHODS: The prospective population study, where the oral glucose tolerance test and the measurement of serum lipids and lipoproteins were performed at the baseline examination and after the 10-yr follow-up, was conducted on 56 subjects (17-60 yr of age at the baseline). The subjects were from six pedigrees with a clustering of endogenous hypertriglyceridemia, and 47 of these subjects attended the follow-up 10 yr later. RESULTS: In the study families, the prevalence of glucose intolerance and NIDDM increased from 15 to 49% (P < 0.001) and from 2 to 21% (P < 0.001), respectively, over the 10-yr period. When grouped according to the baseline serum triglyceride tertiles, 76% (P < 0.01) of the family members with highest serum triglycerides were glucose intolerant (29% impaired glucose tolerance, 47% NIDDM) at follow-up compared with 20% of those with lowest serum triglycerides. In discriminant analysis, including age, body mass index, treatment with thiazides and beta-blocking agents, and 2-h serum insulin concentration, the baseline serum triglycerides still remained as an independent predictor of development of impaired glucose tolerance and NIDDM. CONCLUSIONS: Families with a clustering of hypertriglyceridemia are at increased risk of NIDDM, and in these families elevation of serum triglycerides serves as a risk marker of glucose intolerance and NIDDM.

Adult↗
PubMed1981

Excessive hypertriglyceridemia and pancreatitis in pregnancy. Association with deficiency of lipoprotein lipase.

Acute pancreatitis verified at laparotomy occurred in the 37th week in 1 of 4 women who developed excessive hypertriglyceridemia (type V hyperlipoproteinemia) during pregnancy. The hypertriglyceridemia was associated with and possibly caused by deficiency of lipoprotein lipase, measured as the NaCl sensitive component of post-heparin lipase activity. A severely fat-restricted diet controlled the hypertriglyceridemia in 1 of the patients, followed during a second pregnancy.

Adult↗
PubMed2002

High risk for hyperlipidemia and the metabolic syndrome after an episode of hypertriglyceridemia during 13-cis retinoic acid therapy for acne: a pharmacogenetic study.

BACKGROUND: Administration of 13-cis retinoic acid (isotretinoin) for acne is occasionally accompanied by hyperlipidemia. It is not known why some persons develop this side effect. OBJECTIVE: To determine whether isotretinoin triggers a familial susceptibility to hyperlipidemia and the metabolic syndrome. DESIGN: Cross-sectional comparison. SETTING: University hospital in Lausanne, Switzerland. PARTICIPANTS: 102 persons in whom triglyceride levels increased at least 1.0 mmol/L (> or =89 mg/dL) (hyperresponders) and 100 persons in whom triglyceride levels changed 0.1 mmol/L (< or =9 mg/dL) or less (nonresponders) during isotretinoin therapy for acne. Parents of 71 hyperresponders and 60 nonresponders were also evaluated. MEASUREMENTS: Waist-to-hip ratio; fasting glucose, insulin, and lipid levels; and apoE genotype. RESULTS: Hyperresponders and nonresponders had similar pretreatment body weight and plasma lipid levels. When reevaluated approximately 4 years after completion of isotretinoin therapy, hyperresponders were more likely to have hypertriglyceridemia (triglyceride level > 2.0 mmol/L [>177 mg/dL]; odds ratio [OR], 4.8 [95% CI, 1.6 to 13.8]), hypercholesterolemia (cholesterol level > 6.5 mmol/L [>252 mg/dL]; OR, 9.1 [CI, 1.9 to 43]), truncal obesity (waist-to-hip ratio > 0.90 [OR, 11.0 (CI, 2.0 to 59]), and hyperinsulinemia (insulin-glucose ratio > 7.2; OR, 3.0 [CI, 1.6 to 5.7]). In addition, more hyperresponders had at least one parent with hypertriglyceridemia (OR, 2.6 [CI, 1.2 to 5.7]) or a ratio of total to high-density lipoprotein cholesterol that exceeded 4.0 (OR, 3.5 [CI, 1.5 to 8.0]). Lipid response to isotretinoin was closely associated with the apoE gene. CONCLUSION: Persons who develop hypertriglyceridemia during isotretinoin therapy for acne, as well as their parents, are at increased risk for future hyperlipidemia and the metabolic syndrome.

Acne Vulgaris↗
PubMed1986

Pathogenesis of the hypertriglyceridemia at early stages of alcoholic liver injury in the baboon.

To study the mechanism of alcoholic hypertriglyceridemia, baboons were pair-fed liquid diets containing 50% of energy as ethanol or as additional carbohydrate for 5-16 months. Alcohol-fed animals developed hypertriglyceridemia and early stages of alcoholic injury, namely fatty liver with or without perivenular fibrosis. In the fasting state, the triglyceride content was sixfold higher in very low density (VLDL) and intermediate density (IDL) lipoproteins and twofold higher in low density (LDL) and high density (HDL) lipoproteins. The increase in VLDL was markedly exaggerated in the postprandial state. To investigate the source of these increases, we determined net output or removal of serum triglycerides during circulation through either splanchnic or extrasplanchnic (lower extremities) vascular beds. In the splanchnic territory, there was net output of triglycerides in VLDL and net removal from the other lipoproteins. In alcohol-fed baboons, the output of VLDL-triglycerides into the hepatic (but not into the portal) vein tripled. This increase was mainly due to production of VLDL particles that were larger and had a flotation (Sf greater than 400) different from the Sf 20-400 which predominated in controls. This was associated with increased splanchnic removal of labeled chylomicron- or VLDL-triglycerides. In the lower extremities, there was an arteriovenous difference in VLDL-triglyceride concentration and this was increased in the alcohol-fed animals. Thus, the primary mechanism of the hypertriglyceridemia in alcohol-fed baboons was increased production of large, chylomicron-like VLDL by the liver, whereas both the extrasplanchnic extraction of VLDL-triglycerides and the splanchnic extraction of triglycerides from chylomicron- and VLDL-remnants were secondarily enhanced.

Animals↗
PubMed1985

Hypertriglyceridemia in insulin dependent diabetes mellitus with peripheral vascular disease.

Hypertriglyceridemias are the most frequent lipid disorders in diabetes mellitus with peripheral vascular disease. In spite of increasing knowledges the arteriosclerotic risk of hypertriglyceridemias is still controversial. In 77 insulin dependent diabetes (IDDM) (23 m, 54 f, age: 52 +/- 18 y. body weight: 119 +/- 21% to Brocal) with hypertriglyceridemia (TG greater than or equal to 200 mg/dl) and 97 IDDM (39 m, 68 f, age: 47 +/- 18 y, body weight: 116 +/- 22% to Broca) without lipid disorders (TG less than 200 mg/dl, CH less than 260 mg/dl) we investigated whether measurement of lipoprotein-lipids is better indicator of arteriosclerotic risk than total triglycerides. Peripheral vascular diseases (PVD) were present in 45% of patients with HTG and in 32% of patients without lipid disorders. In both groups patients with PVD had lower HDL-cholesterol (p less than 0.05 resp. p less than 0.0005) and higher VLDL-cholesterol (p less than 0.025 resp. p less than 0.005). A negative relationship between VLDL-cholesterol and HDL-cholesterol was only significant in IDDM without lipid disorders (p less than 0.001). Considering a ratio of VLDL/HDL-cholesterol of greater than or equal to 1.0 resp. less than 1.0 to be discriminating for patients with or without PVD 65.1% of all PVD (specifity) and 60.7% of all Non-PVD (sensitivity) could be correctly characterized. It is concluded, that in IDDM the ratio of VLDL/HDL-cholesterol is a better indicator for the arteriosclerotic risk than total triglycerides or total cholesterol.

Adult↗
PubMed1977

Relation of lipoprotein lipase activity in adipose tissue to adipocyte volume and its influence in hypertriglyceridemia pathogenesis.

In the subcutaneous adipose tissue of 20 normal weight and overweight subjects with normo- or hypertriglyceridemia, the relation is examined between the lipoprotein lipase activity (LPLA) per gram adipose tissue and adipocyte volume. The following findings were obtained: 1. Significant positive correlations between the LPLA per gram adipose tissue and the adipocyte volume were ascertained in the groups of subjects having normal triglyceridemia or exhibiting hypertriglyceridemia. 2. The negative relation between the LPLA in the adipose tissue and the triglyceride level in serum described in literature could not be verified. Across a glyceride span of 76 to 600 mg% in serum we found a correlation coefficient of +0.34. 3. It can therefore be assumed that the LPLA per gram adipose tissue with increasing adipocyte volume does not represent an inhibiting factor to the triglyceride in serum breakdown in the development of hypertriglyceridemia.

Adipose Tissue↗
PubMed1983

Overproduction of a kinetic subclass of VLDL-apoB, and direct catabolism of VLDL-apoB in human endogenous hypertriglyceridemia: an analytical model solution of tracer data.

To investigate the participation of the major apoprotein involved in triglyceride transport in the pathogenesis of endogenous hypertriglyceridemia, five kinetic studies of apoprotein B were conducted in volunteer normolipidemic subjects and six studies in four patients with endogenous hypertriglyceridemia. The transport of apoprotein B within four kinetic subclasses of very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low density lipoprotein (LDL) was studied by injection of [75Se]selenomethionine. A 24-fold increase in the entry of newly synthesized apoprotein B at the initial kinetic subclass of the four-compartment VLDL delipidation sequence characterized the hypertriglyceridemic studies relative to normal subjects. Moreover, approximately 75 mg/kg per day of VLDL-B turnover reflected direct catabolism independent of conversion to IDL and/or to LDL, in contrast to the 8 mg/kg per day observed in controls. IDL-B was derived from VLDL-B in both normal and hypertriglyceridemic subjects, and was responsible for greater than 70% of all LDL-B synthesis. LDL-B pool size and turnover were indistinguishable in hypertriglyceridemic subjects from that observed in normal subjects. These studies suggest that two kinetic phenomena may characterize the pathophysiology of endogenous hypertriglyceridemia: a) over-production of apoB within a kinetic subclass of VLDL and b) preferential catabolism of hypertriglyceridemic VLDL without prior conversion to IDL/LDL.

Adult↗
PubMed1980

Effect of controlled alcohol feeding on triglycerides in patients with outpatient 'alcohol hypertriglyceridemia'.

Hypertriglyceridemia in alcohol-consuming out-patients that abates after the discontinuation of alcohol is assumed to be caused by alcohol. It is unclear, however, whether this hypertriglyceridemia is the consequence of the energy-content of alcohol or of a specific stimulation of triglycericde production. To evaluate this question triglyceride levels and removal rate were studied before and after isocaloric replacement of food with alcohol under metabolic ward conditions. In paired studies, triglyceride concentrations and removal rate were decreased with alcohol in four out of six patients on a mixed diet and three out of four on a fat-free diet. The plasma triglyceride levels and removal rates increased in the other three patients. Since the changes in level and removal rate were concordant, alcohol probably affects production more than removal. In conclusion, alcohol can be shown to have a specific hypertriglyceridemic effect in only three out of ten patients with 'alcohol hypertriglyceridemia'. Isocaloric substitution of alcohol for food does lead to a decrease in triglyceride level in seven out of ten patients, who respond with a drop in triglycerides to ethanol withdrawal as out-patients.

Adult↗
PubMed1976

[Oral vitamin A tolerance tests in hypertriglyceridemia (author's transl)].

HVA tolerance tests were performed to study the post-absorptive lipemia of 32 patients with hypertriglyceridemia. Among them 10 had a normal test and 22 a pathological test. This difference shows the existence of an exogenous factor in the second group of hypertriglyceridemias, which is poorly related to the typing of the WHO classification, but much more to the value of the cholesterol/triglycerides ratio of each patient. The separation of these two groups is of great interest for their therapeutical management, the hypertriglyceridemias with exogenous factor being more sensitive to diet than the others.

Administration, Oral↗
PubMed2003

Effects of simvastatin, an HMG-CoA reductase inhibitor, in patients with hypertriglyceridemia.

BACKGROUND: Patients with elevated levels of serum triglycerides (TG) often have other associated lipid abnormalities (e.g., low levels of high-density lipoprotein cholesterol [HDL-C]) and are at increased risk of developing coronary heart disease. Although the therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) in hypercholesterolemic patients have been well established, less is known about the effects of statins in patient populations with hypertriglyceridemia. HYPOTHESIS: The purpose of this study was to evaluate the lipoprotein-altering efficacy of simvastatin in hypertriglyceridemic patients. METHODS: This was a multicenter, randomized, double-blind, placebo-controlled study. In all, 195 patients with fasting serum triglyceride levels between 300 and 900 mg/dl received once daily doses of placebo or simvastatin 20, 40, or 80 mg for 6 weeks. RESULTS: Compared with placebo, simvastatin treatment across all doses resulted in significant reductions (p < 0.05 - < 0.001) in serum levels of triglycerides (-20 to -31% decrease) and TG-rich lipoprotein particles. Significant (p < 0.001) reductions were also seen in low-density lipoprotein cholesterol (-25 to -35%) and non-HDL-C (-26 to -40%). Levels of HDL-C were increased (7-11%) in the simvastatin groups compared with placebo (p < 0.05 - < 0.001). CONCLUSION: The results of this study demonstrate the beneficial effects of simvastatin in patients with hypertriglyceridemia.

Adult↗
PubMed2001

Plasmapheresis in the treatment of an acute pancreatitis due to protease inhibitor-induced hypertriglyceridemia.

The use of protease inhibitors such as ritonavir to treat HIV-infected individuals has been associated with lipodystrophy, combined hyperlipidemias, and hypertriglyceridemia-induced pancreatitis. We report here on the treatment by plasmapheresis of a HIV-patient who presented with a rapid onset of severe ritonavir-induced hypertriglyceridemia complicated with an acute pancreatitis. A 35-year-old HIV-1 positive male following 3 weeks of ritonavir treatment presented with nausea, abdominal pain, a distended abdomen, and the following laboratory values: amylase (238 U/L), lipase (864 U/L), total cholesterol (27.1 mmol/L), and triglycerides (62.9 mmol/L). Following two plasmaphereses, the levels of total cholesterol, triglycerides, lipase, and amylase declined drastically and the patient was discharged home after 4 days with lipid and pancreatic enzyme levels within the reference range. To our knowledge, this is the first case of pancreatitis due to a PI-induced hyperlipidemia in a HIV-patient treated with plasmapheresis in an acute setting.

Acute Disease↗
PubMed1991

Cyclosporin-induced hypertriglyceridemia with prompt response to plasma exchange therapy.

A case of severe cyclosporin-induced hypertriglyceridemia that prompted plasma exchange therapy is reported. Hyperlipemic retinitis, headache, stupor, and peripheral paresthesias became apparent when the level of triglycerides exceeded the 1,500 mg/dL level. Two plasma exchanges were required to halt disease progression. This is the second time that plasma exchange was used in a bone marrow transplanted patient on cyclosporin-A therapy. In both cases hypertriglyceridemia became apparent and symptomatic after approximately 7 months of therapy with cyclosporin.

Adolescent↗
PubMed2008

Severe acute hypertriglyceridemia during acute lymphoblastic leukemia induction successfully treated with plasmapheresis.

Children suffering from Acute Lymphoblastic Leukaemia (ALL) treated with asparaginase and corticosteroids are at risk of developing severe lipid abnormalities. The authors report the case of a 10-year-old male with extremely high plasma triglyceride concentrations (4,000 mg/dl) during the induction phase of ALL associated with mild pancreatitis. Hypertriglyceridemia was successfully managed with plasmapheresis with a decrease in triglyceride levels to 590 mg/dl. Apheresis appears to be safe and effective in reducing hypertriglyceridemia and preventing related complications.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1993

Altered hepatic production of apolipoproteins B and E in the fasted septic rat: factors in the development of hypertriglyceridemia.

The etiology of hypertriglyceridemia associated with sepsis remains unclear, but we will attempt to elucidate its character by studying the hepatic production of apolipoproteins B and E. Male Lewis rats (260-330 g) were assigned to two groups, control (n = 5) and septic (n = 5). The septic group was injected with 2 x 10(8) live Escherichia coli colonies/100 g body wt. Food was removed from all rats after injections. Twenty-four hours later a recirculating in situ liver perfusion was performed for 120 min with KRB buffer, containing L-[35S]methionine. The production of apolipoprotein B (apo B), apolipoprotein E (apo E), albumin, and transferrin was determined by immunoprecipitation. The septic rats showed a protein-specific response to sepsis. The total protein secreted increased throughout each perfusion, septic greater than control. Apo B production was increased 2.6-fold in the septic versus control groups (P = 0.037), while apo E production was decreased by 2.9 times control (P = 0.036). Albumin production was decreased 2-fold in the septic group (P = 0.002). The increased hepatic production of apo B represents an increased number of very low density lipoprotein (VLDL) particles and contributes to the elevated VLDL triglyceride levels seen in sepsis. In contrast, decreased apo E production may result in a diminished ability for peripheral and/or hepatic receptor recognition of VLDL and VLDL remnants, respectively. Each of these changes are factors in the development of hypertriglyceridemia in sepsis.

Albumins↗
PubMed1991

Pancreatitis related to severe acute hypertriglyceridemia during pregnancy: treatment with lipoprotein apheresis.

We report a clinical observation of acute pancreatitis due to severe hypertriglyceridemia in a pregnant woman. In order to decrease the serum triglyceride level rapidly, two lipaphereses were undertaken using the double-filtration technique. This lipoprotein apheresis technique is briefly described and the efficacy in reducing rapidly hypertriglyceridemia is outlined. Like in 3 previously published reports, the patient had a rapid recovery, confirming that lipoprotein apheresis should be an adequate and a well-tolerated treatment in such a condition.

Adult↗
PubMedDate not supplied

Comparison of effects of fibrates in patients with hypertriglyceridemia.

It has long been known that antihyperlipidemic agents categorized as fibrates are capable of reducing triglyceride concentrations, although the superiority of one over another remains questionable. In the present study, investigators compared treatment results from various fibrates. In all, 60 patients aged 54.1+/-12 y with hypertriglyceridemia were included in the study. Patients who had increased values on liver function tests, had been given a diagnosis of hypothyroidism or chronic renal failure, and who needed statin medication were excluded. Patients were divided into 4 groups according to the medication given; treatments consisted of Lipanthyl 1 x 1, Lipofentrade mark 1 x 1, Lopid 1 x 1, and Lopid 2 x 1. Biochemical and hematologic parameters of patients were recorded at the first visit and at the end of the 2-mo treatment period. A total of 18 patients (30%) were given Lipanthyl 1 x 1, 14 (23.3%) received Lipofen 1 x 1, 16 (26.7%) were treated with Lopid 1 x 1, and 12 (20%) were given Lopid 2 x 1. Effects on triglyceride values were assessed in all groups. Lopid 1 x 1 and Lopid 2 x 1 produced significant decreases in triglyceride values. Most adverse effects were reported in the group given Lopid 2 x 1. In the treatment of hypertriglyceridemia, fibrates have similar effects on tolerability and reliability. However, study findings indicated that Lopid 1 x 1 and 2 x 1 treatments have greater efficacy.

Adult↗