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PubMed1988

Increased superoxide production by mononuclear cells of patients with hypertriglyceridemia and diabetes.

Diabetic patients with hypertriglyceridemia frequently develop atherosclerosis. Because superoxide (O2-) is suspected to play an important role in the initiation of atherosclerosis, we investigated whether an abnormal amount of O2- was produced by circulating mononuclear cells of patients with both diabetes mellitus and hypertriglyceridemia. The rate of production of superoxide dismutase-inhibitable O2- was measured when cells were stimulated by either 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA) or by opsonized zymosan (OZ). In addition, the rates of O2- production by mononuclear cells drawn from three other groups (normal, solely diabetic, and solely hypertriglyceridemic) were determined. We found that the rate of O2- production by mononuclear cells from the diabetic hypertriglyceridemic group was significantly higher than that from normal, diabetic, and hypertriglyceridemic groups. When the rates of O2- production by mononuclear cells were plotted against the levels of plasma triglyceride for all individuals tested, they correlated positively (r = .73 in PMA stimulation and r = .79 in OZ stimulation, P less than .01). However, the rate of O2- production did not relate to other parameters, i.e., plasma cholesterol level, hemoglobin A1 level in erythrocytes, and the molar ratio of free cholesterol to phospholipid in mononuclear cells. Thus, we concluded that the observed elevated rate of O2- production in the diabetic hypertriglyceridemic mononuclear cells was a reflection of a hypertriglyceridemic condition and was not unique to the diabetic hypertriglyceridemic condition. Also, O2- may be involved in the pathogenesis of atherosclerosis in diabetic hypertriglyceridemic patients when atherogenic factors specific to diabetes are concomitantly present.

Adult↗
PubMed1997

Sequencing of Lipoprotein Lipase Gene in 11 Cases of Chinese Patients with Severe Endogenous Hypertriglyceridemia.

Sequencing analysis of lipoprotein lipase (LPL) gene exons l-9 was made in 11 cases of Chinese patients with severe endogenous hypertriglyceridemia (serum TG > 7.68 mmol/L) by the dideoxy chain termination method using Sequenase PCR Product Sequencing Kit. Four of the patients were found to possess 3 variants at the LPL gene locus. One novel mutation was observed at exon 8 Thr(361)-Thr (C(1338)-A). This was a conservative mutation with an allele frequency of 1l.4% in the 74 of the Chinese controls. Two others Ala(261)-Thr (G(1037)-A) in exon 6 and Ser(447)-Ter (C(1595)-G) in exon 9, which were also found in Caucasians and have been reported to have disease associations with dyslipidaemia, showed at frequencies of 0% and 10.7% in the Chinese controls respectively. However, it is the first time that these three genetic variants have been reported in Chinese subjects. The results show that the gene variation of LPL may not be associated with endogenous hypertriglyceridemia in Chinese population.

Journal Article↗
PubMed1976

[Effect of clofibrate on glucose tolerance and insulin secretion in patients with endogenous hypertriglyceridemia (author's transl)].

In 22 patients with endogenous hypertriglyceridemia, oral and intravenous glucose tolerance showed significant improvement under clofibrate treatment which was in no way correlated to the fall in triglycerides. Basal and stimulated insulin, cholesterol and fasting blood sugar did not change, body weight remained constant and was not correlated to the degree of hypertriglyceridemia. On the other hand a positive correlation between body weight and insulin concentrations was found. Improvement of glucose tolerance independently of body weight and insulin may be due to a direct effect of clofibrate on glucose metabolism without any correlation to its triglyceride-lowering.

Administration, Oral↗
PubMed1976

Regulation of plasma lecithin:cholesterol acyltransferase in man. I. Increased activity in primary hypertriglyceridemia.

Patients with primary hypertriglyceridemia have been reported to manifest increased in vivo turnover of plasma cholesteryl esters. To ascertain if this is due to plasma lecithin:cholesterol acyltransferase (LCAT) and to explore a possible link between triglyceride and cholesteryl ester turnover, we have measured LCAT in 15 patients with Type IV, 2 with Type V, 1 with Type III, and 9 with Type II B hyperlipoproteinemia. LCAT was significantly elevated (p less than 0.001) in hypertriglyceridemic subjects, regardless of lipoprotein pattern. In the Type IV group, but not in normal subjects, LCAT correlated significantly with measures of very low-density lipoprotein (VLDL) elevation, including plasma triglycerides and particularly VLDL-unesterified cholesterol, but not with body weight or substrate high-density lipoprotein (HDL) lipid levels. On repeated determinations in individual subjects, a relationship between triglyceride fluctuations and LCAT could be demonstrated in only one subject over an extreme range of triglyceride levels. Analysis of lipoprotein lipids revealed that the ester:free cholesterol ratio in VLDL was increased in hypertriglyceridemia, but was not correlated with enzyme level. In vitro removal of endogenous VLDL or addition of VLDL from lipemic plasmas to normal plasmas was without effect on enzyme activity. Regulation of enzyme activity does not appear to be a direct function of VLDL level.

Acyltransferases↗
PubMed1975

Metabolism of glucose and fatty acid by leukocytes from patients with endogenous hypertriglyceridemia.

The metabolic abnormalities responsible for endogenous hypertriglyceridemia have not been defined. Some in vivo studies have suggested that excessive triglyceride production is the cause of this defect. In an attempt to obtain direct evidence concerning this mechanism, we have compared in vitro the metabolism of radioactive glucose and palmitate by leukocytes from patients with endogenous hypertriglyceridemia and normal subjects. Leukocytes from the patients incorporated 9.82 plus or minus 1.7 (S.E.M.) nanomoles of glucose into cellular lipid per 10-8 cells per hour. When the cell lipid extract was sugjected to mild alkaline hydrolysis, 92 per cent of the glucose radioactivity was recovered in the glycerol backbone of the lipid esters. Comparison of specific yields of CO2 from glucose labeled in the 1- or 6- position revealed that 0.53 plus or minus 0.02 per cent was metabolized via the pentose cycle. The leukocytes from hypertriglyceridemic persons incorproated 140 plus or minus 6.9 nanomoles of [1-14C]-palmitate per 10-8 cells per hour. Eighty-four per cent of the radioactivity was in triglycerides and 14 per cent in phospholipids. The major phospholipid into which palmitate was incorporated was phosphatidyl choline. The leukocytes oxidized palmitate at a rate of 2.88 plus or minus 0.23 nanomoles per 10-8 cells per hour. There were no differences in any of the above values between leukocytes from hypertriglyceridemic patients and normal subjects. Likewise, there was no correlation between the plasma triglyceride concentration and glucose or palmitate incorporation into triglycerides. To the extent that leukocytes reflect systemic metabolic processes, these data provide no support for the interpretation that the mechanism of the plasma triglyceride elevation is excessive biosynthesis.

Adult↗
PubMedDate not supplied

Effects of slow-release bezafibrate on serum lipids, lipoproteins, apolipoproteins, and postheparin lipolytic activities in patients with type IV and type V hypertriglyceridemia.

The effects of bezafibrate on serum lipids, lipoproteins, apolipoproteins, and post-heparin lipolytic activities were studied in 17 patients with hypertriglyceridemia. All patients received 400 mg of slow-release (SR) bezafibrate daily for four months. In the nine patients with type IV hypertriglyceridemia, mean serum triglyceride (TG) levels decreased significantly, by 53% (P less than 0.01) at two months and 50% (P less than 0.001) after four months of bezafibrate, while in the eight patients with type V, the levels decreased by 61% (P less than 0.001) and 51% (P less than 0.001), respectively. Total cholesterol levels decreased significantly (P less than 0.05) in type V patients at two and four months, by 19% and 18%, respectively, while low-density lipoprotein cholesterol levels increased significantly (P less than 0.05) in type IV patients at two and four months, by 63% and 62%, respectively. High-density lipoprotein (HDL) levels increased significantly (P less than 0.05) at two months in both patient groups. HDL subfraction analysis showed a significant (P less than 0.05) rise in HDL3-cholesterol levels in type V but not in type IV patients. Apolipoprotein (apo) A-I, A-II, and B levels increased, while apo C-II, C-III, and E levels decreased in both groups. The apo A-I/apo A-II ratio decreased significantly (P less than 0.05) at two and four months in type V patients, which also supports increased HDL3 fractions in that group. Lipoprotein lipase and hepatic TG lipase levels tended to rise, and the particle size of TG-rich lipoprotein (TGRL) and the TGRL-apo C-III/TGRL-apo C-II ratio decreased in both patient groups. These data indicate that bezafibrate-induced changes in lipoprotein profiles differed slightly in type IV and type V patients. The results confirm the usefulness of bezafibrate as a lipid-lowering agent.

Adult↗
PubMed1988

Plasma exchange for the management of cyclosporin A-induced hypertriglyceridemia.

The authors report a case of hypertriglyceridemia complicating the course of a patient receiving cyclosporin A after bone marrow transplantation. When the patient was seen at the hemapheresis unit the clinical picture was characterized by headache, increasing visual and neurological disturbances. Plasma triglyceride level was 3215 mg/dl. Two plasma exchange sessions reduced triglycerides to 486 mg/dl and halted the disease progression. This may represent the first plasma exchange treatment of cyclosporin A-induced hypertriglyceridemia.

Adult↗
PubMed1985

Gemfibrozil therapy in primary hypertriglyceridemia associated with coronary heart disease. Effects on metabolism of low-density lipoproteins.

Certain primary hypertriglyceridemias cause abnormalities in lipoproteins that seemingly predispose patients to coronary heart disease. We examined metabolism of low-density lipoproteins (LDL) in 11 men with both hypertriglyceridemia and coronary heart disease and compared them with that of controls. The LDL turnover was measured during placebo and gemfibrozil therapy. With placebo, LDL-cholesterol level usually was normal, but production and fractional clearance of LDL were high. The LDL composition also was abnormal. Gemfibrozil reduced triglycerides, lowered production and fractional clearance of LDL, and normalized LDL composition. The LDL-cholesterol level usually rose, but generally not to abnormally high levels. Therefore, normalization of LDL metabolism and marked reduction of triglycerides by gemfibrozil suggest benefit to hypertriglyceridemic patients who are at high risk for coronary heart disease. However, when LDL-cholesterol level rises excessively, gemfibrozil may not be sufficient therapy.

Adult↗
PubMed1973

Some factors indicative of hypertriglyceridemia in patients investigated for diabetes mellitus.

A study was done of 160 patients with abnormal blood glucose levels, 91 (57%) of whom fulfilled standard criteria for the diagnosis of diabetes mellitus. The overall prevalence (36%) and the age-related characteristics of fasting hypertriglyceridemia were similar to distributions reported in groups of patients with coronary artery disease. Fasting hypercholesterolemia occurred in four patients (2.5%), in three of whom there was evidence of associated hyperchylomicronemia on lipoprotein electrophoresis. For effective application of the OGTT response to the detection of hypertriglyceridemic patients, somewhat lower blood glucose levels than those generally accepted for the diagnosis of diabetes mellitus are necessary. Fasting hyperglycemia and the retention of body weight gained after age 25 were features of hypertriglyceridemic patients. Insufficient basal insulin action could explain the development of fasting hypertriglyceridemia in patients in whom the diagnosis of diabetes mellitus is being considered.

Adolescent↗
PubMed1977

Hypertriglyceridemia in homozygous beta-thalassemia.

A case of hypertriglyceridemia in association with homozygous beta-thalassemia in an 11-month-old female infant is reported. The hypertriglyceridemia proved to be secondary, as it was indicated by clinical features as well as laboratory findings. Attention is called to a possible alteration of lipid metabolism in association with thalassemia major.

Cholesterol↗
PubMed1982

Hyperinsulinemia and hypertriglyceridemia, a vicious cycle with atherogenic potential.

This paper reviews and integrates a number of experiments which suggest the existence of a vicious cycle. In this cycle hypertriglyceridemia can lead to insulin resistance even without concomitant obesity or non-insulin dependent diabetes. This insulin resistance may be the basis for the hyperinsulinemia response to a glucose challenge. The hyperinsulinemia can stimulate VLDL-triglyceride production. This increase in production, if it is not accompanied by an equivalent increase in removal, will result in hypertriglyceridemia. The whole cycle would accelerate VLDL-triglyceride turnover and may increase the supply of potentially atherogenic VLDL-remnants.

Animals↗
PubMed1980

[Dietary treatment of hypertriglyceridemia (author's transl)].

The wide spread of hypertriglyceridemias throughout the population can be most convincingly referred to defective or over-nourishment. Consequently the possibilities of correcting this symptom by a change of diet are considerable. In discussing the relevant diets, the 200 calorie protein diet, the SO3D diet and the null diet (for hospital patients) and guiding principles for outpatients are refered to. The assumption that increased blood lipids can be corrected exclusively through a low fat diet is only true for the rare type 1 hypertriglyceridemia.

Diet, Reducing↗
PubMed1980

Granulocyte-function in pancreatitis. Nitroblue tetrazolium-test related to clinical signs of bacterial infection and to hypertriglyceridemia.

Out of 26 patients with acute pancreatitis, 8 had several signs of bacterial infection such as high nitroblue tetrazolium (NBT) reduction of granulocytes, fever, elevated ESR and leukocytosis with granulocytosis. 2 patients had a high NBT-value without all other clinical signs of infection and 6 had such signs without a high NBT-value. --An NBT-value lower than normal was found in 6 patients, 3 of whom also had other signs of infection. The level of serum lipids, determined in only 3 of the 6, demonstrated concomitant hypertriglyceridemia. Hyperlipidemia is known to decrease granulocyte activity and might have prevented a stimulation to increased NBT-reduction otherwise brought about by bacterial infection. Further, 3 of the 6 patients with low NBT-reductions suffered from a very severe type of pancreatitis and two of them developed pneumonia. --Bacterial infection may thus contribute to a severe clinical course of pancreatitis, especially in patients with hypertriglyceridemia in whom the granulocyte function is depressed.

Acute Disease↗
PubMed1978

Studies on the hypertriglyceridemia in the pregnant rat.

The in vivo tracer method and in vitro incorporation experiments were used to obtain information on the mechanism responsible for the hypertriglyceridemia found in 21 days pregnant rats. The results indicate that the uptake of plasma free fatty acids (FFA) by liver triglycerides of pregnant rats (2.0 mumoles FFA/min/300 g) did not differ from that of non-pregnant rats (2,1 mumoles FFA/min/300 g). The rate of liver fatty acid synthesis in pregnant rats (0,4 mumoles fatty acids/min/liver) is higher than that of non-pregnant rats (0,05 mumoles fatty acids/min/liver). In non-pregnant female and pregnant rats the turnover rates of plasma chylomicron and VLDL triglycerides were almost identical (about 2.8 mumoles triglyceride fatty acids/min/300 g, and about 2.3 mumoles triglyceride fatty acids/min/300 g, respectively). These various observations, when taken together, strongly suggest that increased hepatic triglyceride production cannot be the mechanism responsible for the hypertriglyceridemia in pregnant rats.

Animals↗
PubMed1982

Cord blood hypertriglyceridemia in Chinese newborns: an index of fetal distress.

Cord serum triglyceride concentrations in 214 Chinese newborns were measured at birth with the Hitachi Model 716 autoanalyzer using the G-3-PDH UV end point method. The mean and the 95th percentile value in a normal population of 100 newborns were found to be 28 mg/100 ml and 48 mg/100 ml, respectively. Using 48 mg/100 (P95) as a cut-off point, maternal-fetal factors were evaluated in 35 hypertriglyceridemic and 35 normotriglyceridemic newborns. A significant association was demonstrated between high cord serum triglyceride levels and toxemia, overterm, meconium-stained amniotic fluid, deceleration of fetal heart rate, intrauterine growth retardation, low one-minute Apgar score (less than or equal to 7), and low umbilical arterial pH (less than 7.20). These findings pointed out that cord serum hypertriglyceridemia was an index of fetal distress and associated with many unfavorable intrauterine conditions. They also suggested that hypertriglyceridemia might be related to the activated sympathetic nervous system and the enhanced release of catecholamines.

Adipose Tissue↗
PubMed1982

Spurious elevations in glycosylated hemoglobin (HbA1) secondary to hypertriglyceridemia.

Measurement of glycosylated hemoglobin (HbA1) is frequently helpful to clinicians in treating patients with diabetes, since a number of studies show that this reflects a reliable index of diabetic control over time. There are several methods of measuring HbA. The chromatographic method is the most frequently used and is the standard method for large demand. We recently encountered a patient with diabetes mellitus who had substantial lactescent plasma secondary to hypertriglyceridemia that falsely raised the HbA1 level. We examined the patient in detail and determined that triglyceride concentrations greater than 1,750 mg/dL would falsely raise the HbA1 levels. In vitro studies performed by adding lipemic plasma to a control sample confirmed this. Thus, spurious elevations in HbA1 can occur in patients with lactescent plasma. This would further complicate the already existing interrelationship between glucose intolerance and hypertriglyceridemia.

Chromatography↗
PubMed1978

[Adipocyte size in primary hypertriglyceridemia with and without obesity (author's transl)].

Adipose tissue cellularity of patients with endogenous hypertriglyceridemia whether associated with obesity or not has been studied by means of a semiautomatic method of counting and sizing osmium tetroxide fixed adipocytes. Cell population distributions were analyzed by mathematical computation. The Coulter Counter system was able to determine mean diameter (or volume) and cell size dispersion which defined adipocyte population. An overall shift of cell population size has been found to characterize adipose tissue cellularity of the different groups examined. Adipocyte population in the obese was defined by increased fat cell size with overlapping distributions between both groups of same weight. Nevertheless normolipemic obese patients were characterized by larger cell size than hypertriglyceridemic subjects matched for adiposity index. The results are discussed in relation to the removal defect found in endogenous hypertriglyceridemia.

Adipose Tissue↗
PubMed1981

Quantitation of human apolipoprotein C-III and its subspecie by radioimmunoassay and analytical isoelectric focusing: abnormal plasma triglyceride-rich lipoprotein apolipoprotein C-III subspecie concentrations in hypertriglyceridemia.

A specific, accurate, and sensitive double antibody radioimmunoassay for measuring human apolipoprotein (apo) C-III has been developed. Anti-apoC-III(1) developed in rabbits cross-reacted completely with apoC-III subspecies. Analytical isoelectric focusing of delipidated triglyceride-rich lipoproteins (TRL) was done to assess the percentage of total apoC-III mass comprised by apoC-III(0), C-III(1), and C-III(2), and the data were used to compute the absolute plasma TRL apoC-III subspecie concentration. Total plasma apoC-III was 11.1 +/- 0.9 mg/dl (mean +/- SEM) in 29 normolipidemic healthy subjects; 21.3 +/- 4.9, 27.5 +/- 2.2, and 53.6 +/- 7 mg/dl in 3, 16, and 13 patients with primary types III, IV, and V hyperlipoproteinemia, respectively, and significantly (P < 0.01) higher than normal. Total plasma triglycerides (TG) correlated positively with total plasma apoC-III (r = 0.88; P = 0.0001) and TRL apoc-III (r = 0.88; P = 0.0001). Progressive hypertriglyceridemia was associated with a rise in the percent of total apoC-III in TRL isolated at d < 1.006 g/ml (r = 0.78; P < 0.0001; n = 43) and a reciprocal decline in the TRL-free plasma fraction (d > 1.006 g/ml). ApoC-III comprised significantly more of HDL(2) than HDL(3) protein (7.3 +/- 0.2 versus 1.6 +/- 0.2%, respectively, P < 0.01). HDL(2) and HDL(3) isolated from patients with type IV hyperlipoproteinemia had subnormal apoC-III as percent of total protein (2.4 +/- 0.5 and 0.6 +/- 0.1, respectively). Total plasma TG correlated negatively with i) apoC-III as percent of total HDL protein (r = -0.67; P = 0.002, n = 20); ii) apoC-III as percent of total HDL(2) protein (r = -0.52; P = 0.019); and iii) apoC-III as percent of total HDL(3) protein (r = -0.72; P = 0.0004). Plasma TRL apoC-III subspecie concentrations were significantly higher in the three hypertriglyceridemic groups (primary types III, IV, and V) compared to normals. TRL apoC-III(0) levels in patients with type IV and V were comparable (2.4 +/- 0.3 and 2.2 +/- 0.6 mg/dl, respectively). However, TRL apoC-III(1) and C-III(2) in patients with type V hyperlipoproteinemia were significantly higher (P < 0.01) than in patients with types IV or III hyperlipoproteinemia. Total plasma TG correlated positively with TRL apoC-III(0) (r = 0.56; P = 0.0004), TRL apoC-III(1) (r = 0.82; P = 0.0001) and TRL apoC-III(2) (r = 0.76; P = 0.0001). The slope of regression line relating total plasma TG with TRL apoC-III(1) was significantly steeper (P < 0.0001) than that for apoC-III(0). Thus, for a given interval of plasma TG, the change in concentration of TRL apoC-III(1) was much greater than that in TRL apoC-III(0). The development of the RIA and its combined use with analytical isoelectric focusing thus allows quantitation of this important glycopeptide and its subspecies in human plasma and its subfractions. Because apoC-III inhibits not only tissue lipoprotein lipase but also the hepatic uptake of triglyceride-rich lipoproteins and remnants, the data support the possibility that an abnormal metabolism of apoC-III subspecies may be linked pathogenetically to elevated plasma TG levels.-Kashyap, M. L., L. S. Srivastava, B. A. Hynd, P. S. Gartside, and G. Perisutti. Quantitation of human apolipoprotein C-III and its subspecies by radioimmunoassay and analytical isoelectric focusing: abnormal plasma triglyceride-rich lipoprotein apolipoprotein C-III subspecie concentrations in hypertriglyceridemia.

Apolipoprotein C-III↗