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PubMed1987

Severe hypertriglyceridemia, large lipoproteins and protection against atherosclerosis.

Alloxan-diabetic cholesterol-fed rabbits exhibiting severe hypertriglyceridemia are protected against atherosclerosis. In such rabbits most of the plasma cholesterol is found in lipoproteins with a diameter of 75 nm or larger. In the present report it is hypothesized, that due to their large sizes, the lipoproteins of the severely hypertriglyceridemic diabetic rabbits are not able to penetrate the endothelial layer of the arteries. Therefore, the macrophages and smooth muscle cells of the intima will only come in contact with relatively small amounts of cholesterol-carrying lipoproteins. Consequently, cellular accumulation of cholesterol, which is a necessary step in the formation of an atherosclerotic lesion, will be retarded. There are certain parallels between hypertriglyceridemic cholesterol-fed alloxan-diabetic rabbits and humans with familial lipoprotein lipase deficiency, familial apolipoprotein C-II deficiency and insulin-dependent diabetes mellitus in the ketoacidotic state. Based on reports about patients with these metabolic disorders, we suggest that cholesterol in very large lipoproteins also in humans is less atherogenic than cholesterol in smaller lipoproteins.

Animals↗
PubMed1987

Effects of gemfibrozil on plasma lipoprotein-apolipoprotein distribution and platelet reactivity in patients with hypertriglyceridemia.

The effects of gemfibrozil on plasma lipoprotein distribution and composition and on platelet function were investigated in 11 patients with stable hypertriglyceridemia, six belonging to Fredrickson type IIb and five to type IV. Gemfibrozil (600 mg twice a day) significantly reduced total and very low density lipoprotein (VLDL)--associated triglyceridemia (respectively-32.4% and -40.4%, after 6 weeks of treatment). No significant variations were noted in the lipid components of low-density lipoproteins; by contrast, a marked increase (18%) was detected in high-density lipoprotein (HDL)--associated cholesterol. Comparison of the two patient groups (type IIb and type IV) showed that those with type IIb had both a more significant reduction of triglyceridemia and a more marked increase of HDL-cholesterol. Apolipoprotein B levels were reduced in both groups (-12%) with no change in apolipoprotein AI. The cholesterol content in the HDL subfractions, separated by rate zonal ultracentrifugation, was raised in HDL3 (18%) and in HDL2 (14%). Both particles also showed significant increases of the cholesterol/protein and the cholesterol/phospholipid ratios. A non-statistically significant decrease in collagen-induced aggregation and in the release of thromboxane B2 was noted after treatment. These findings suggest that, similar to what was recently reported in normal individuals and in laboratory animals, the probable mode of action of gemfibrozil is in reducing the secretion of atherogenic lipoproteins, particularly VLDL, while stimulating the production of small HDL particles.

Adult↗
PubMed1987

Hypertriglyceridemia--acute pancreatitis--ischemic heart disease. A case study in a pair of monozygotic twins.

Hyperlipoproteinemia type V, with serum triglyceride concentrations of about 20 mmol/l, was detected in a pair of monozygotic, 40-year-old twin brothers. One of them had had recurrent attacks of pancreatitis, the other not. The endocrine and exocrine pancreatic functions were apparently normal, supporting that the pancreatitis was secondary to the hypertriglyceridemia. After successful lipid-lowering therapy the attacks of abdominal pain disappeared and remained absent during a 13-year follow-up period. The other twin died of ischemic heart disease nine years after the discovery of his lipid abnormality. The reduction of his lipid levels had been much less successful. His average "atherogenic index" (the ratio of cholesterol in low density to that in high density lipoproteins) was normal but increased to a very high value if cholesterol in very low density lipoproteins was also included together with the low density ones in the numerator. Lipoprotein particles modified in composition may have contributed to an increased uptake through a scavenger pathway and promoted atherosclerosis.

Acute Disease↗
PubMed1978

Influence of chenodeoxycholic acid on serum triglycerides in patients with primary hypertriglyceridemia.

Administration of chenodeoxycholic acid (CDCA) to patients with primary hypertriglyceridemia caused the diminution of serum triglyceride concentrations of 54.31% and 46.04% at dosages of 500 mg/day and of 250 mg/day, respectively. Results after 1 month of treatment with 250 mg/day are not statistically different from those obtained with 500 mg/day. Administration of CDCA did not change the serum cholesterol, SGOT, SGPT, total bilirubin, gammaGT or alkaline phosphatase levels.

Adult↗
PubMed1987

[Metabolism kinetic characterization of hypertriglyceridemias in drug therapy variations].

In 26 male patients with primary hypertriglyceridemia (HTG) the radioglycerol labelling technique was used to assess triglyceride production rates and fractional catabolic rates pertaining to the rapidly turning-over compartment of endogenously produced triglycerides (TG). On the basis of these data the patients were allotted to 3 groups: group I with predominating TG overproduction, group II with predominating disturbances of TG removal from the bloodstream, and group III with a combination of both dysfunctions. All patients were examined prior to and after 4 weeks of drug intake at the metabolic ward. Each group got a medical treatment aiming at removing the pathogenetic cause of the HTG. Biguanides used in group I decreased TG production rates without affecting fractional catabolic rates. In group II an anabolic steroid (chlormethyltestosterone) proved to be able to improve TG removal, but this improvement was accompanied by a significant lowering of HDL cholesterol and an increase in LDL cholesterol. In contrast, clofibric acid influenced both overproduction and removal impairment in group III. Our results give an insight into mechanisms of action of certain lipid-lowering drugs providing a basis for future improvements in the elimination of the risk factor HTG.

Adult↗
PubMed1977

[Regression of xanthomas in endogenous hypertriglyceridemia under low carbohydrate diet].

Report on two patients with endogenous hypertriglyceridemia. In both patients normal serum lipid values were reached in a comparatively short time under a diet with reduced carbohydrates and calories. In one diabetic patient who needed insulin at the beginning of the treatment the disease could be controlled by dietary measures alone after a few days. Different biological half-life periods of the various serum lipid fractions explain why, under a reducing diet, the rate of decrease of lipids is variable according to the respective component. Thus, the ratio of triglycerides and cholesterol can vary in the same patient within a few days and may change his classification under different types of hyperlipidemia according to Fredrickson. It would appear that in these cases a classification based on etiological considerations is more recommendable.

Adult↗
PubMed1982

Lipoatrophic diabetes: endocrine dysfunction and the response to control hypertriglyceridemia.

Endocrine function was studied in a 24 year old female with lipoatrophic diabetes (LD). Baseline endocrine studies (serum triglycerides: 2600 mg/dl) demonstrated hyperprolactinemia (serum prolactin 51 ng/ml), increased ACTH levels, absence of suppression of ACTH to a high dose of dexamethasone which suppressed serum cortisol normally and, hyperresponsiveness of TSH to stimulation with TRH. Thyroid hormone levels (total and free fraction) were essentially normal. Major metabolites of thyroid hormone (T3, rT3, 3, 3'-T2, and 3', 5'-T2) were also normal and exhibited a normal response to the administration of L-thyroxine and propylthiouracil. Exchange of 84% of the patient's plasma resulted in a decrease in serum triglycerides (700 mg/dl) which was followed by a rebound to the original level in seven days. After the sixth plasmapheresis serum triglycerides stabilized at less than 1000 mg/dl. Plasmapheresis was associated with the appearance of amenorrhea and galactorrhea; also hypertension and proliferative retinopathy developed during this therapy. Repeat endocrine function studies (serum triglycerides: 700 mg/dl) showed a further rise in serum prolactin (greater than 160 ng/ml), persistence of abnormal ACTH secretion and normalization of TSH responsiveness. Lipoatrophic diabetes is associated with abnormal central endocrine function but appropriate peripheral target gland secretion. A course of plasmapheresis improves the hypertriglyceridemia but not the endocrine dysfunction. In this patient with LD the most important side effect of plasmapheresis was the development of cardiovascular complications.

Adrenocorticotropic Hormone↗
PubMed1980

[Drug therapy of hypertriglyceridemias (author's transl)].

As a rule, the causal therapy of hypertriglyceridemia is possible only for its secondary forms. Indications for therapy are: a critical rise in triglyceride levels leading to symptoms of acute abdomen, disturbances of the lesser circulation, insulin-resistance or a reduction in the patient's working capacity. Triglyceride levels of 200 mg/dl are considered the threshold value for long-term therapy. In most cases, the desired can be obtained with dietary measures. Drug therapy mainly consists of nicotinic acid and its derivates, clofibrinic acid and its derivates as well as clofibrate successors.

Clofibrate↗
PubMed1980

[Diabetic ketoacidosis with severe hypertriglyceridemia and eruptive xanthomata (author's transl)].

A boy of 6 with diabetic ketoacidosis presented with a disturbance of lipid metabolism characterised by eruptive xanthomata, hepatomegaly, lipaemia retinalis, milky serum and hypertriglyceridemia with type V electrophoretic pattern. All the findings are typical diabetic hyperlipidaemia. The severity of the abnormalities are not solely due to delay in treatment because they are also caused by the unusual sensitivity of lipoprotein lipase to insulin deficiency. A histological and ultrastructural study of the xanthomata was performed.

Child↗
PubMed1981

[Hypertriglyceridemia and tumors. Production of stable cultures of Green's lymphoma].

In Golden Hamster the Greene malignant lymphoma is a subcutaneous and homotransplantable tumor whose development is associated with a constant hypertriglyceridemia and a large-decreased plasma post-heparin lipase activity. The tumoral cell line is well maintained on a human fibroblast monolayer culture and is demonstrated to secrete two IgG immunoglobulins.

Animals↗
PubMed1981

[Disorders of glucose metabolism and manifestation of diabetes during treatment of endogenous hypertriglyceridemias (author's transl)].

Disturbances of glucose metabolism are frequent concomitant findings with hypertriglyceridemias (HTG). Whether the manifestation of diabetes mellitus is favored by it is, however, unknown. In an observation study disturbed glucose metabolism was present in 47 of 91 cases of HTG, without drug therapy of diabetes being carried out. The study shows that glucose metabolism disorders in HTG annually regress in about 3% of cases and about 0.6 to 0.7% of the cases require drug treatment. Since retrospective and prospective analyses show that development of glucose tolerance disorders is closely related to changes in triglyceride concentrations, HTG must be considered as factors favoring diabetes mellitus.

Adult↗
PubMed1982

Studies on the hypertriglyceridemia in pregnant rats.

The study has been performed in order to obtain information on the mechanism responsible for the hypertriglyceridemia found in pregnant rats. The results show that the whole plasma triglyceride flux is increased by 65% in late gestation. It has been found that labeled VLDL triglyceride originating from pregnant rats shows no delay in plasma disappearance when injected into the circulation of non pregnant female rats. Contrariwise, labeled VLDL triglyceride originating from non pregnant rats when injected into pregnant rats shows a delay in disappearance from the circulation. From these results the conclusion can be drawn that the delay in labeled plasma triglyceride disappearance in late gestation is not caused by a possibly abnormal VLDL showing a decrease in affinity of lipoprotein substrate for lipoprotein lipase. Therefore, we interpret the delay in labeled plasma triglyceride disappearance in late gestation in terms of a lowered removal capacity of plasma triglyceride by extrahepatic tissue.

Animals↗
PubMed1980

A uremic peptide containing polyamine: formation and possible role in uremic hypertriglyceridemia.

Concentrations of peptidic compounds in blood plasma of uremics are increased. Evidence for participation of intestinal bacteria in the production of such peptides (presumably toxic) was obtained by isolation of a strongly basic peptide containing covalently bound spermidine from peritoneal dialysate of patients with chronic uremia. The same peptide was found in blood plasma of patients with end-stage chronic renal failure. The absence of glutamic acid in the spermidinepeptide molecule suggests that an enzyme different from the transglutaminase of mammalian cells must take part in the synthesis of spermidinepeptide. This conjugate forms a relatively stable complex with insulin, thus altering the action of the hormone on adipose cell metabolism. Also, interaction of spermidinepeptide with insulin and lipoproteins may contribute to hypertriglyceridemia and accelerated atherosclerosis in patients with chronic uremia.

Humans↗
PubMed1981

Accelerated hypertriglyceridemia in patients on continuous ambulatory peritoneal dialysis - a preventable abnormality.

Increasing hypertriglyceridemia is a recognised complication of CAPD. To investigate the etiology lipid clearance studies using the intravenous fat tolerance test were performed in control subjects and in uremic patients before and after six months CAPD treatment. Oral carbohydrate intake was restricted and the use of hypertonic dialysate kept to a minimum. Although serum triglycerides were elevated in the uremic patients before CAPD (3.1 +/- 0.3 mMol/L) no further increase occurred during therapy. Oral carbohydrate intake was restricted to 240-250 Gms/24 hrs and hypertonic dialysate to 5.7 +/- 4.1% of the total. There were no significant changes in fractional removal rate of lipid. Therefore further increases in serum triglycerides in CAPD may be prevented by simple dietary manoeuvres.

Adult↗
PubMed1982

[The influence of clofibrate on glucose metabolism in diabetes mellitus without endogenous hypertriglyceridemia (author's transl)].

The antidiabetic effect of clofibrate is well documented in the treatment of endogenous hypertriglyceridemia (HTG). Whether it is also effective in diabetic patients without HTG remains to be seen. 19 Type II diabetics without HTG (4 males, 15 females, age 61 +/- 21 years, duration of diabetes 9 +/- 6 years, body weight 118 +/- 20% according to Broca, triglycerides 140 +/- 156 mg/dl) were included in a randomised cross-over study and given a daily dose of 1.5 g clofibrate verum and clofibrate placebo, respectively, over 10 days while staying in hospital. The results showed that only in 8 patients under additional clofibrate therapy no changeover to insulin was required. Although blood glucose levels did not significantly improve, statistical evidence (as determined by the Grizzle analysis of variance) was given of an increased effect of sulfonylurea therapy. There was a negative correlation between the therapeutic effect and the individual blood glucose/insulin ratio following tolbutamide which was injected prior to the study. However, the incidence of insulin-demand was higher in patients with a high ratio than in those with a low ratio. Therefore, the specific antidiabetic effect of clofibrate seems to be only of minor clinical significance.

Adult↗
PubMed1994

Targeted disruption of the apolipoprotein C-III gene in mice results in hypotriglyceridemia and protection from postprandial hypertriglyceridemia.

Using gene targeting in embryonic stem cells, we have generated mice lacking apolipoprotein C-III (ApoC-III). Homozygous mutant animals show absence of ApoC-III protein and no expression of ApoC-III mRNA in the liver or in the intestine. Expression of the neighboring genes, coding for apolipoprotein A-I and apolipoprotein A-IV, are not altered in the liver but are reduced in the intestine. This suggests that these three genes share a tissue-specific element for intestinal expression and that insertion of an additional promoter for the neomycin-resistant gene into the locus affects interaction between the tissue-specific element and the promoter of the individual gene. Fasted plasma triglyceride levels in the homozygous mutants are reduced to about 70% of normal, while heterozygotes have values intermediate between those of the homozygous mutants and wild types. Plasma levels of total cholesterol and of high density lipoprotein cholesterol in homozygotes are consistently lower than those in normal mices but the reduction does not reach statistical significance. A fat meal test showed that postprandial hypertriglyceridemia is abolished in homozygotes lacking ApoC-III. The homozygous mutants also clear chylomicrons faster than wild type controls. These data indicate that ApoC-III modulates the catabolism of triglyceride-rich lipoproteins and plays a role in the postprandial management of triglycerides.

Animals↗