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PubMed1985

Apolipoprotein AI and AII metabolism in patients with primary high-density lipoprotein deficiency associated with familial hypertriglyceridemia.

Plasma high-density lipoproteins (HDL) and their major proteins--apolipoprotein (apo) AI and apo AII--are subnormal in most patients with familial hypertriglyceridemia. However, the pathophysiology of low-plasma apo AI and apo AII is unclear. The kinetic parameters (turnover) of HDL apo AI and apo AII were studied in six lean patients with primary HDL deficiency associated with familial hypertriglyceridemia and five normolipidemic controls. Autologous 125I labeled HDL were injected intravenously (IV; 25 microCi) and blood samples drawn ten minutes after the injection and periodically thereafter for 12 days. Urine samples were collected daily and their radioactivity measured. Kinetic parameters were calculated from the area under the decay curve using three exponentials. Mean plasma apo AI and apo AII were significantly lower (P less than 0.001) in patients than normals (70.4 +/- 2.7 v 106.9 +/- 7.0; 24.2 +/- 1.6 v 39.2 +/- 0.9 mg/dL, respectively). The mean fractional catabolic rates (FCR) obtained from plasma 125I-HDL, apo AI, apo AII radioactivity decay curves and by Berson and Yalow's method (urine/plasma radioactivity ratios) were significantly greater (P less than 0.05) in patients than in controls (0.387 v 0.299; 0.391 v 0.309; 0.361 v 0.275; 0.272 v 0.207/d; respectively). The mean synthetic rates (SR) of apo AI and apo AII were significantly lower in patients than in controls (11.12 v 14.17 mg/kg body weight/d, P less than 0.05; 3.53 v 4.68 mg/kg body weight/d, P less than 0.05, respectively). In vitro lipolysis of triglyceride (TG) rich lipoproteins by bovine lipoprotein lipase, and measurement of hepatic TG lipase and lipoprotein lipase in postheparin plasma were similar in patients and controls, indicating no abnormality in these factors that are linked to HDL and TG catabolism. However, a significant positive correlation between hepatic TG lipase and the FCR of apo AI and apo AII was found. The data suggest that in this series of patients with HDL deficiency the low plasma HDL-cholesterol, apo AI, and apo AII levels resulted from decreased synthesis and an increased fractional catabolic rate of apo AI and apo AII, the major proteins of HDL.

Adult↗
PubMed1985

Altered HDL subclasses in endogenous hypertriglyceridemia are not affected by weight reduction.

Reduction of body weight is commonly used to decrease the plasma lipids of patients with primary endogenous hypertriglyceridemia, but the effects of stabilized weight reduction on lipoprotein compositions and distribution are not well known. Since lipoprotein structures are perhaps as important in normal and abnormal metabolism and atherogenesis as are the levels of lipoproteins, we examined the effects of weight loss on the plasma concentrations, compositions, and ultracentrifugal flotation properties of plasma lipoproteins. Nine patients (eight males, one female) with endogenous hypertriglyceridemia and low high-density lipoprotein (HDL)-cholesterol levels who were approximately 130% of ideal body weight were studied during two dietary periods (basal and low weight). Subjects consumed an isocaloric diet for 5 weeks consisting of approximately 15% protein, approximately 45% carbohydrate, approximately 40% fat, approximately 500 mg/d cholesterol, P/S ratio 0.43 (basal), followed by a hypocaloric diet of the same composition, which was eaten for 16 to 52 weeks, until the desired weight was lost (9.6 +/- 3.6 kg). Then patients continued to eat a diet of the same composition lower in calories but sufficient in quantity to maintain their new lower body weights for the final 5 weeks (low-weight period). The last weeks of the basal and the low-weight periods were spent in a metabolic ward. Thus, high and low body weights were known to be stable for at least 5 weeks. Fasting (12 to 14 hours) plasma total triglycerides decreased in all patients (from 328 +/- 204 mg/dL at basal to 185 +/- 77 mg/dL at low weight, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Plasma apolipoprotein CII levels in hypertriglyceridemia.

It is known that hypertriglyceridemia is associated with the elevation of plasma apolipoprotein CII (apoCII). In an attempt to look at the relationship between the two, the present study was conducted. We examined 30 patients with hypertriglyceridemia (TG, 210 to 9,127 mg/dL) and ten normolipidemic controls. Hypertriglyceridemic patients included 7 of type I hyperlipoproteinemia (HL), 17 of type IV, and 6 of type V. Plasma apoCII was measured by the single radial immunodiffusion method. Major cause for any difference in plasma apoCII could be attributed to differences in the TG-rich lipoproteins. Since a model for the lipoprotein structure indicates that TG-rich lipoproteins are spherical, with apoCII as a surface component and TG as a core substance, we calculated the square roots and the cubic roots of the values of apoCII and TG to make comparison possible. When the two variables were plotted on the X and Y axes respectively, we obtained the regression line of square root of apoCII = 0.37 X 3 the square root of TG - 0.03 with a correlation coefficient of r = .95 (P less than 0.001). The result indicates that a lipoprotein structural model accounts well for the relationship between apoCII and TG. Although a previous report suggested a compensatory increase of apoCII in lipoprotein lipase deficiency, our patients with type I HL had apoCII levels similar to those who had comparable levels of plasma TG.

Adult↗
PubMed1980

Hypertriglyceridemia associated with Trypanosoma brucei brucei infection in rabbits: role of defective triglyceride removal.

Rabbits infected with Trypanosoma brucei brucei develop a hypertriglyceridemia characterized by an increase in very low density lipoprotein and, to a lesser extent, low density lipoprotein, with a decrease in high density lipoprotein. Triglyceride production studies showed that the triglyceride production rate was not significantly different in trypanosome-infected rabbits from controls. Studies of triglyceride degradation using very low density lipoprotein triglyceride endogenously labelled with [3H]palmitate demonstrated a marked slowing of triglyceride removal in the infected rabbits when compared to controls. Lipase activity in post-heparin plasma was found to be deficient in trypanosome-infected animals. Furthermore, the greater the decrease in lipolytic activity, the greater the increase in serum triglyceride level. We conclude that the hypertriglyceridemia associated with T. b. brucei infection in rabbits results predominantly from a defect in triglyceride degradation.

Animals↗
PubMed1978

Ethanol-induced hypertriglyceridemia. Prevalence and contributing factors.

Seventy-seven chronic alcoholic subjects admitted to two alcoholic detoxification centers were evaluated for lipid abnormalities. Nineteen (26%) of these male patients had serum triglyceride levels greater than 150 mg/100 ml and six (9%) had serum cholesterol levels greater than 250 mg/100 ml. Compared to 33 age-matched, nonalcoholic control subjects, there was a significantly greater incidence of hypertriglyceridemia in the alcoholic subjects. All patients with triglyceride abnormalities had type IV electrophoretic patterns. The triglyceride elevations were not related to serum amylase, lipase, liver function, obesity, and abnormal fasting glucose. We conclude that there is a significant increase in hypertriglyceridemia in chronic alcoholic patients.

Alcoholism↗
PubMed1983

Favorable effects of L-carnitine treatment on hypertriglyceridemia in hemodialysis patients: decisive role of low levels of high-density lipoprotein-cholesterol.

Twenty-nine hemodialyzed patients with hypertriglyceridemia were given L-carnitine (20 mg/kg iv at the end of each dialysis) for 120 days and then placebo for the same duration in order to evaluate the lipid-lowering effects of the metabolite. A dramatic reduction in triglyceride levels was observed only in the group of patients (n = 12) with high basal triglyceride values, low levels of high-density lipoprotein-cholesterol, and with apoprotein A at the lower limit of normal range. During L-carnitine treatment these patients exhibited significantly increased high-density lipoprotein-cholesterol and apoprotein A. No rebound effects were observed. L-Carnitine did not provoke changes in the lipid parameters in the group (n = 17) with high basal triglyceride values, and normal high-density lipoprotein-cholesterol and apoprotein A. Hematocrit values increased in all the 29 patients during L-carnitine treatment. At the end of the experimental protocol, L-carnitine dosage was increased to 60 mg/kg iv (at the end of each dialysis) in four patients of the group of nonresponders and prolonged for 60 days. This produced a considerable reduction in triglyceride levels. The above results suggest that L-carnitine can be effective in the management of hypertriglyceridemia in the hemodialyzed patient especially when low high-density lipoprotein-cholesterol levels are present.

Adult↗
PubMed1988

Long-term effect of a low-fat, high-carbohydrate diet on plasma lipids of patients affected by familial endogenous hypertriglyceridemia.

We evaluated the effect of a low-fat, high carbohydrate (LFHC) diet on plasma lipids in 10 patients affected by familial endogenous hypertriglyceridemia. All the patients studied underwent a base-line period of 4 wk, a 12-wk intervention period, and an 8-wk switch-back period. During the control periods patients consumed approximately 45% of energy as fat and approximately 40% as carbohydrate. During the intervention period they consumed an isocaloric diet containing approximately 25% of energy as fat and approximately 60% as carbohydrate. Total plasma triglyceride and cholesterol levels decreased significantly after 45 and 90 d of treatment (p less than 0.01). The reduction of plasma cholesterol was associated mostly with the decrease in VLDL cholesterol (p less than 0.01) while LDL cholesterol increased at days 45 and 90 of the LFHC diet (p less than 0.01). Finally, we observed a significant increase in HDL cholesterol both at days 45 and 90 of the LFHC diet (p less than 0.01). The LFHC diet we used may be an useful tool in the management of hypertriglyceridemia.

Cholesterol↗
PubMed1976

Increased prevalence of coronary heart disease in analgesic nephropathy: relation to hypertension, hypertriglyceridemia and combined hyperlipidemia.

The prevalence of coronary heart disease (58%) in 43 patients with analgesic nephropathy with moderate to severe chronic renal failure was significantly higher than in the general population of the same age and sex. Mean serum triglyceride concentration and mean diastolic blood pressure were significantly higher in the group with coronary heart disease (214 mg/dl and 102 mm Hg, respectively) than in the group without it (162 and 94). Serum triglyceride values correlated inversely with GFR, indicating that hypertriglyceridemia was largely due to associated chronic renal failure; a specific effect of analgesic abuse on prevalence of heart disease, noted by others, could not be assessed in the absence of GFR-matched controls. The prevalence of coronary heart disease was significantly higher (81%) in the group with combined hyperlipidemia (hypertriglyceridemia and hypercholesteremia) compared to the groups without it or with normal serum triglyceride concentrations (44 and 41%, respectively). Hypotryptophanemia (a possible cause of hyperlipidemia in the nephrotic syndrome) was present in 77% of patients.

Adult↗
PubMedDate not supplied

Triglyceride-lowering effect of marine polyunsaturates in patients with hypertriglyceridemia.

Twenty male patients with primary hypertriglyceridemia were treated for 4 weeks with daily supplements (15 g) of oil, which provided approximately 6 g of polyunsaturated fatty acid (PUFA) either of fish or of vegetable origin. Total plasma cholesterol concentrations were unaffected, but both types of supplement increased high density lipoprotein-3 (HDL3) cholesterol concentrations. The fish, but not the vegetable, oil supplement led to a decrease in plasma triglyceride concentrations. Very low density lipoprotein (VLDL), fatty acid composition, and VLDL triglyceride kinetics were subsequently studied in five patients (four male, one female) before and after 4 weeks of therapy with 15 g of the same fish oil. The fish oil led to increases in the proportion of eicosapentaenoic acid in both the VLDL triglyceride and phospholipid fractions, but the increase was greater in the latter. In contrast, the proportion of docosahexanoic acid was increased only in the VLDL triglycerides. The decrease in plasma triglyceride concentrations that occurred with fish-oil therapy was accompanied by a reduction in the absolute catabolic rate of VLDL triglyceride, implying a concomitant change in synthetic rate; the fractional catabolic rate of VLDL triglyceride was unaltered. It is suggested that polyunsaturated fatty acids of marine origin may be therapeutically useful for hypertriglyceridemia.

Adult↗
PubMedDate not supplied

Apo E allele frequency in primary endogenous hypertriglyceridemia (type IV) with and without hyperapobetalipoproteinemia.

Apolipoprotein E polymorphism is responsible for the existence in the population of six apo E phenotypes determined by three alleles acting at a single gene locus. We have previously reported an enrichment in the epsilon 2 allele and the E2-bearing phenotypes in an unselected sample of subjects with primary hyperlipidemia consisting mainly of endogenous hypertriglyceridemia (Type IV). A study was carried out on 214 Type IV hypertriglyceridemic subjects to determine whether there was the same distribution in subjects with hyperapobetalipoproteinemia as in those without. The study showed that the relative enrichment in the epsilon 2 allele was associated only with Type IV subjects without hyperapobetalipoproteinemia. Since hyperapobetalipoproteinemia is a presumed marker for familial combined hyperlipidemia (FCHL), this finding may provide further evidence that FCHL and familial hypertriglyceridemia, both associated with a Type IV lipoprotein pattern, are truly separate disease entities.

Adult↗
PubMed1967

Tissue lipoprotein lipase in normal individuals and in individuals with exogenous hypertriglyceridemia and the relationship of this enzyme to assimilation of fat.

Lipoprotein lipase activity (LLA) was measured in the adipose tissue of six healthy subjects and five members of a family in whom the trait for familial exogenous hypertriglyceridemia was segregating. The lipase activity measured was characteristic of lipoprotein lipase: increased by feeding, dependent on the presence of serum, and inhibited by sodium chloride and protamine sulfate. When compared with lipase activity in healthy individuals, LLA was grossly deficient in two siblings with postabsorptive chylomicronemia and was intermediate in both parents and one sibling, who had normal postabsorptive triglycerides. These findings are compatible with autosomal recessive inheritance. The hormone-sensitive lipolytic enzyme responsible for mobilization of free fatty acids from adipose storage was normal in the hyperlipemic subjects. After a 104-g fat meal, the serum triglyceride increased more in subjects heterozygotic for LLA deficiency than in the healthy subjects, and there was a relatively greater increase in chylomicrons and very low density lipoproteins in the affected individuals. These observations demonstrate the physiologic importance of lipoprotein lipase in removal of these lipoprotein groups and further clarify the differences between endogenous and exogenous hypertriglyceridemia.

Adipose Tissue↗
PubMed1978

Control of 3-hydroxy-3-methylglutaryl-CoA reductase activity in cultured human fibroblasts by very low density lipoproteins of subjects with hypertriglyceridemia.

Very low density lipoproteins (VLDL) and low density lipoproteins (LDL) from human normolipemic plasma, and the VLDL, the intermediate density lipoprotein (IDL), and LDL from patients with Type III hyperlipoproteinemic plasma were tested for their abilities to suppress the activity of 3-hydroxy-3-methylglutaryl-Coenzyme A (HMG-CoA) reductase in cultured human fibroblasts from normal subjects and a Type III patient. Regulation of cholesterol synthesis in the fibroblasts of a patient with Type III hyperlipoproteinemia appears to be normal. VLDL from normal subjects, isolated by angle head ultracentrifugation (d < 1.006) or by gel filtration on BioGel A-5m, were about 5 times less effective than LDL in suppressing HMG-CoA reductase activity, based on protein content, in agreement with previous reports with normal fibroblasts. Zonal centrifugation of normal VLDL isolated by both methods showed that the VLDL contained IDL. Normal VLDL from the angle head rotor, refractionated by the zonal method, had little, if any, ability to suppress the HMG-CoA reductase activity in either normal or Type III fibroblasts. VLDL, IDL, and LDL fractionated by zonal ultracentrifugation from Type III plasma gave half-maximum inhibition at 0.2-0.5 mug of protein/ml, indistinguishable from the suppression caused by normal LDL. Type III VLDL did not suppress HMG-CoA reductase in mutant LDL receptor-negative fibroblasts. Zonally isolated VLDL obtained from one Type IV and one Type V patient gave half-maximal suppression at 5 and 0.5 mug of protein/ml, respectively. Molecular diameters and apoprotein compositions of the zonally isolated normal and Type III VLDL were similar; the major difference in composition was that Type III VLDL contained more cholesteryl esters and less triglyceride than did normal VLDL. The compositions and diameters of the Type IV and Type V VLDL were similar to normal VLDL. These findings show that the basic defect in Type III hyperlipoproteinemia is qualitatively different from the cellular defect found in familial hypercholesterolemia, since the regulation of HMG-CoA reductase activity is normal in Type III fibroblasts. The metabolic defect in hypertriglyceridemia is related to the triglyceriderich lipoproteins which, free of other lipoproteins, have an enhanced ability to interact with cultured fibroblasts to regulate HMG-CoA reductase activity. These studies suggest that, in hypertriglyceridemia, there is a mechanism for direct cellular catabolism of VLDL which is not functional for normal VLDL.

Adult↗
PubMed1986

Apolipoprotein C-II deficiency syndrome. Clinical features, lipoprotein characterization, lipase activity, and correction of hypertriglyceridemia after apolipoprotein C-II administration in two affected patients.

Two patients (brother and sister, 41 and 39 yr of age, respectively) have been shown to have marked elevation of plasma triglycerides and chylomicrons, decreased low density lipoproteins (LDL) and high density lipoproteins (HDL), a type I lipoprotein phenotype, and a deficiency of plasma apolipoprotein C-II (apo C-II). The male patient had a history of recurrent bouts of abdominal pain often accompanied by eruptive xanthomas. The female subject, identified by family screening, was asymptomatic. Hepatosplenomegaly was present in both subjects. Analytical and zonal ultracentrifugation revealed a marked increase in triglyceride-rich lipoproteins including chylomicrons and very low density lipoproteins, a reduction in LDL, and the presence of virtually only the HDL3 subfraction. LDL were heterogeneous with the major subfraction of a higher hydrated density than that observed in plasma lipoproteins of normal subjects. Apo C-II levels, quantitated by radioimmunoassay, were 0.13 mg/dl and 0.12 mg/dl, in the male and female proband, respectively. A variant of apo C-II (apo C-IIPadova) with lower apparent molecular weight and more acidic isoelectric point was identified in both probands by two-dimensional gel electrophoresis. The marked hypertriglyceridemia and elevation of triglyceride-rich lipoproteins were corrected by the infusion of normal plasma or the injection of a biologically active synthesized 44-79 amino acid residue peptide fragment of apo C-II. The reduction in plasma triglycerides after the injection of the synthetic apo C-II peptide persisted for 13-20 d. These results definitively established that the dyslipoproteinemia in this syndrome is due to a deficiency of normal apo C-II. A possible therapeutic role for replacement therapy of apo C-II by synthetic or recombinant apo C-II in those patients with severe hypertriglyceridemia and recurrent pancreatitis may be possible in the future.

Adult↗
PubMed1983

Parenteral nutrition in a patient with familial Type IV hypertriglyceridemia: a dilemma.

Patients with a Type IV familial hypertriglyceridemia should never receive intravenous fat emulsions. In addition, the amount of carbohydrate that can be given is limited. A 33-year-old white female, with Type IV hypertriglyceridemia, began receiving a parenteral nutrition regimen that included fat. A series of lipid studies was planned, coordinated with fat emulsion and glucose administration. The patient had persistently elevated basal triglyceride levels (greater than 250 mg/dL), which rose in response to both fat and carbohydrate administration. Serum cholesterol levels remained within the normal range. The disease was once known as "carbohydrate-induced lipemia" because of the dramatic rise in serum triglyceride following high carbohydrate diets. We suggest that serum triglyceride levels be monitored in all patients receiving parenteral nutrition; when such a patient is identified, fat emulsion should not be given and dextrose should be used in the smallest possible amounts to achieve a positive nitrogen balance.

Adult↗
PubMed2004

Ciprofibrate therapy in patients with hypertriglyceridemia and low high density lipoprotein (HDL)-cholesterol: greater reduction of non-HDL cholesterol in subjects with excess body weight (The CIPROAMLAT study).

BACKGROUND: Hypertriglyceridemia in combination with low HDL cholesterol levels is a risk factor for cardiovascular disease. Our objective was to evaluate the efficacy of ciprofibrate for the treatment of this form of dyslipidemia and to identify factors associated with better treatment response. METHODS: Multicenter, international, open-label study. Four hundred and thirty seven patients were included. The plasma lipid levels at inclusion were fasting triglyceride concentrations between 1.6-3.9 mM/l and HDL cholesterol < or = 1.05 mM/l for women and < or = 0.9 mM/l for men. The LDL cholesterol was below 4.2 mM/l. All patients received ciprofibrate 100 mg/d. Efficacy and safety parameters were assessed at baseline and at the end of the treatment. The primary efficacy parameter of the study was percentage change in triglycerides from baseline. RESULTS: After 4 months, plasma triglyceride concentrations were decreased by 44% (p < 0.001). HDL cholesterol concentrations were increased by 10% (p < 0.001). Non-HDL cholesterol was decreased by 19%. A greater HDL cholesterol response was observed in lean patients (body mass index < 25 kg/m2) compared to the rest of the population (8.2 vs 19.7%, p < 0.001). In contrast, cases with excess body weight had a larger decrease in non-HDL cholesterol levels (-20.8 vs -10.8%, p < 0.001). There were no significant complications resulting from treatment with ciprofibrate. CONCLUSIONS: Ciprofibrate is efficacious for the correction of hypertriglyceridemia / low HDL cholesterol. A greater decrease in non-HDL cholesterol was found among cases with excess body weight. The mechanism of action of ciprofibrate may be influenced by the pathophysiology of the disorder being treated.

Journal Article↗
PubMed2003

Genome-wide scan for quantitative trait loci influencing LDL size and plasma triglyceride in familial hypertriglyceridemia.

Small, dense LDLs and hypertriglyceridemia, two highly correlated and genetically influenced risk factors, are known to predict for risk of coronary heart disease. The objective of this study was to perform a whole-genome scan for linkage to LDL size and triglyceride (TG) levels in 26 kindreds with familial hypertriglyceridemia (FHTG). LDL size was estimated using gradient gel electrophoresis, and genotyping was performed for 355 autosomal markers with an average heterozygosity of 76% and an average spacing of 10.2 centimorgans (cMs). Using variance components linkage analysis, one possible linkage was found for LDL size [logarithm of odds (LOD) = 2.1] on chromosome 6, peak at 140 cM distal to marker F13A1 (closest marker D6S2436). With adjustment for TG and/or HDL cholesterol, the LOD scores were reduced, but remained in exactly the same location. For TG, LOD scores of 2.56 and 2.44 were observed at two locations on chromosome 15, with peaks at 29 and 61 cM distal to marker D15S822 (closest markers D15S643 and D15S211, respectively). These peaks were retained with adjustment for LDL size and/or HDL cholesterol. These findings, if confirmed, suggest that LDL particle size and plasma TG levels could be caused by two different genetic loci in FHTG.

Apolipoproteins↗
PubMed1976

Relationship between insulin secretory function and endogenous hypertriglyceridemia in obese humans with insulin resistance.

Eighteen obese inpatients with insulin resistance revealed by i.v. insulin test and expressed in various grades of hyperinsulinemia and hyperglycemia were examined for plasma lipid levels. A significant positive correlation was found to be present between the plasma triglyceride (TG) level and the insulin response to glucose load. A stepwise multiple regression analysis revealed that the insulin secretory response, the plasma cholesterol level and the relative body weight contributed to the level of plasma TG. No difference was found in the grades of insulin resistance between patients with and without elevated TG. The ratio of sum of plasma insulin values to that of blood glucose values during glucose tolerance test was markedly increased in patients with elevated TG. The patients with relatively blunted insulin response and impaired glucose tolerance curves showed only slight slight hypertriglyceridemia. Endogenous hypertriglyceridemia in obesity seems to be more closely correlated with plasma insulin level, and therefore, with insulin action rather than insulin resistance.

Adult↗
PubMed1976

Insulin response to oral glucose in patients with a previous myocardial infarction and in patients with peripheral vascular disease. Hyperinsulinism and its relationships to hypertriglyceridemia and overweight.

The insulin response to an oral glucose load (100 gm.) in 127 patients with a previous myocardial infarction (MI) (six months to one year) and in 65 patients with surgically treated or arteriographically identified peripheral vascular disease (PVD) was compared with that of 89 controls after matching the three collectives for age, glucose tolerance, and per cent ideal body weight (% IBW). The insulin response was of greater magnitude in MI and PVD groups than in respective control groups also in the absence of hyperglycemia, hypertriglyceridemia, and obesity. This finding suggests that hyperinsulinism may represent an early metabolic alteration associated with the development of MI and PVD. The insulin secretion pattern was prevalently of the delayed type in association with impaired glucose tolerance and with hypertriglyceridemia but not with overweight. Correlations between serum insulin, triglyceride (TG) levels, and % IBW were also investigated. We found a strong correlation (p less than 0.001) between stimulated insulin levels and % IBW in MI patients and none in PVD patients; conversely, the correlation between serum insulin and TG levels was very high (p less than 0.001) in PVD patients and only weak (p less than 0.05) in MI patients. No correlation was found between cholesterol (CH) levels and any of the other parameters studied. According to these results, it seems likely that hyperinsulinism plays a major role as a closely associated factor to obesity in those subjects who develop an MI, whereas in PVD patients the raised insulin levels may favor lipid accumulation in the arterial intima and accelerate the progress of atherosclerosis.

Adult↗