To determine whether rigorous insulin therapy, which normalized the routinely measured plasma lipids, also reversed qualitative abnormalities in the composition of lipoproteins in noninsulin-dependent diabetes mellitus (NIDDM), we studied 18 NIDDM patients (eight men and 10 women) before and 2 months after intensive insulin therapy. Glycosylated hemoglobin levels (11.7% vs. 8.7%), plasma triglyceride (TG) (250 +/- 91 vs. 164 +/- 56 mg/dl, p less than 0.001), and cholesterol (214 +/- 43 vs. 198 +/- 31 mg/dl, p less than 0.025) all fell, and both HDL2 cholesterol and HDL3 cholesterol increased (59.1% and 10.9%, respectively, p less than 0.001). However, abnormalities in two indices of lipoprotein surface constituents, which were present before insulin therapy, remained so thereafter. The first of these, the new cardiovascular risk factor, the plasma free cholesterol/lecithin ratio, which was increased before treatment, fell only slightly after therapy (pre-therapy 1.02 +/- 0.29 vs. post-therapy 0.90 +/- 0.17, p less than 0.4; reference group, 0.83 +/- 0.14), and remained elevated in very low density lipoprotein (VLDL) and low density lipoprotein (LDL). Secondly, the sphingomyelin/lecithin ratio, an index of the surface rigidity of lipoproteins, was abnormal before treatment in VLDL, HDL2, and HDL3, and this alteration persisted after insulin therapy in HDL3 (p less than 0.001). Lipoprotein core lipid abnormalities were also present before treatment: the TG/cholesteryl ester ratio was reduced in VLDL and increased in LDL, HDL2, and HDL3. Rigorous insulin therapy improved, but failed to fully correct, this disturbance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

The 13th annual meeting of the European Lipoprotein Club.

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Animals↗

PubMedDate not supplied

Changes of high density lipoprotein subfraction concentration and composition by intralipid in vivo and by lipolysis of intralipid in vitro.

Serum lipoproteins were measured during a single infusion of intralipid and during parenteral nutrition with intralipid and glucose. Postheparin plasma lipolytic enzymes and plasma LCAT activity were assayed before and after the parenteral nutrition. Both single and repeated infusions of intralipid were followed by a significant rise of HDL2 concentration (p less than 0.01), whereas the HDL3 decreased. The composition of HDL subclasses altered. The HDL2 triglyceride and phospholipids increased, while the HDL3 esterified cholesterol and protein decreased. In vitro incubation of serum with intralipid alone caused no changes in the zonal profile of HDL subclasses, but hydrolysis of intralipid by lipoprotein lipase was followed by conversion of HDL3 into lighter particles floating in the density range of HDL2. The present results provide additional evidence for a precursor-product relationship between the HDL2 and HDL3. During 4 days of parenteral nutrition with intralipid, the basal (morning) values of serum total and VLDL triglyceride did not change. The LDL phospholipids increased progressively (from 67 to 98 mg/dl, p less than 0.05). The total HDL cholesterol decreased and this change was due to the fall of HDL3 cholesterol esters (from 19 to 12 mg/dl, p less than 0.05). Also the basal values of apo A-I and A-II in HDL3 decreased. The basal level of the HDL2 remained constant. Postheparin plasma LPL activity increased by 52% (p less than 0.01) but hepatic lipase activity fell by 49% (p less than 0.05). These changes may account for the maintenance of plasma HDL2, whereas the progressive fall of the basal HDL3 is probably due to the lack of intestinal apoprotein synthesis during absent intestinal absorption.

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PubMedDate not supplied

Lack of sex differences in high density lipoproteins in Pima Indians. Studies of obesity, lipase activities, and steroid hormones.

To investigate the reasons for the lack of sex differences in high density lipoproteins (HDL) observed in population studies of the Pima Indians, we selected 18 lean (9 men, 9 women, body mass index (BMI) less than 27) and 22 obese (12 men, 10 women, BMI greater than 27) Pima Indians for an inpatient study of HDL composition. We measured lipase activities and steroid hormone concentrations, both of which have previously been implicated in the control of HDL. The lean women had higher concentrations of HDL and HDL2 than did either the obese women or the lean or obese men. Lean women had significantly lower hepatic lipase activities and significantly higher concentrations of estradiol compared to obese women. Lean women also had different HDL2 composition, as indicated by the molar ratio of HDL2 cholesterol/A-I. Significant negative correlations between HDL and obesity measured by either BMI or percent body fat were observed in both sexes, but the slope of the relationship was steeper in women. Significant negative associations were observed between HDL or HDL2 concentrations and hepatic lipase in both sexes, and there were significant positive associations between HDL2 and plasma estradiol in women. The data suggest that obesity in this population has a stronger negative influence on HDL concentrations in women, possibly through changes in estradiol and hepatic lipase activities. Since there are so few lean women in the Pima population, the net result is that HDL levels in women in the population as a whole do not differ from those of men.

Adult↗

PubMedDate not supplied

Insulin therapy induces antiatherogenic changes of serum lipoproteins in noninsulin-dependent diabetes.

To study the effects of rigorous insulin therapy on serum lipoproteins in patients with noninsulin-dependent diabetes not controlled with oral agents only, we measured serum lipoproteins, apoproteins, lipolytic enzymes, and glucose disposal using an insulin clamp technique before and after 4 weeks of insulin therapy. Lipoproteins were isolated by ultracentrifugation and high density lipoprotein (HDL) subfractions, by rate-zonal density gradient ultracentrifugation. The group included 11 women and eight men (age 58 +/- 1 years and RBW 125 +/- 4%). Body weight, glycosylated hemoglobin, mean diurnal glucose, plasma free insulin, and glucose uptake (M-value) were 75 vs. 76 kg; 11.9 vs. 8.9%; 234 vs. 124 mg/dl; 12 vs. 27 microU/ml; and 5.0 +/- 0.4 vs. 7.1 +/- 0.6 mg/kg/min before and after insulin therapy, respectively. After insulin therapy there was a decrease of very low density lipoprotein (VLDL) triglyceride (-60%, p less than 0.001) but an increase of HDL2 cholesterol (+21%, p less than 0.001); HDL2 phospholipids (+38%, p less than 0.001); HDL2 proteins (+23%, p less than 0.01); and HDL2 mass (127 +/- 11 vs. 158 +/- 12 mg/dl, p less than 0.001). There was a decrease of HDL3 cholesterol (-13%, p less than 0.05); HDL3 phospholipids (-16%, p less than 0.05); HDL3 proteins (-18%, p less than 0.001); and HDL3 mass (179 +/- 6 vs. 146 +/- 6, p less than 0.01). Zonal profiles showed a redistribution of particles from HDL3 to HDL2. Serum apo A-I increased (p less than 0.05), apo A-II remained constant, but apo B decreased (-29%, p less than 0.001). The most marked change during insulin therapy was a 2.3-fold increase in adipose tissue lipoprotein lipase (LPL) activity (p less than 0.001). The changes of VLDL and HDL subfractions were not explained by respective changes of the blood glucose, free insulin, or M-value. The data indicate that intensive insulin therapy induces antiatherogenic changes in serum lipids and lipoproteins and suggest that the induction of LPL by insulin is the major factor responsible for redistribution of HDL particles from HDL3 to HDL2.

Adult↗

PubMedDate not supplied

Apoprotein E polymorphism and coronary artery disease. Increased prevalence of apolipoprotein E-4 in angiographically verified coronary patients.

Several studies have indicated that genetic polymorphism of apolipoprotein (apo) E is related to coronary artery disease (CAD). We therefore determined the apo E phenotype in 91 consecutive Finnish men with angiographically confirmed CAD. The apo E phenotype distribution differed significantly from that observed in the Finnish population (p less than 0.05). In the patient group, the frequency of the epsilon 4 allele was 0.324, which is 1.4-fold higher than in the normal Finnish population and twice as high as in other Caucasian populations. Serum lipoproteins and postheparin plasma lipase activities did not display any significant variation according to apo E phenotype. These studies confirm and extend, in a population with high epsilon 4 allele frequency, the previous data on the impact of the epsilon 4 allele on the risk of CAD and suggest that the high epsilon 4 allele frequency in the Finnish population may be one factor contributing to Finns' increased susceptibility to CAD.

Adult↗

PubMedDate not supplied

Serum lipids and lipoproteins in insulin-dependent diabetic subjects during high-carbohydrate, high-fiber diet.

The response of blood glucose and serum lipids and lipoproteins to a high-carbohydrate, high-fiber, low-fat diet was assessed in 10 insulin-dependent diabetic subjects. The diet contained approximately 60% of calories as carbohydrate (CHO) and 20% as fat. The patients were followed for 2 wk in a metabolic ward and subsequently for 4 wk at home without changing insulin dosage. During this 6-wk period, the fasting blood glucose fell from 10.6 +/- 1.1 to 8.9 +/- 1.3 mmol/L (NS); HbA1 fell from 11.7 +/- 0.5 to 11.0 +/- 0.7% (P less than 0.05). Serum total triglyceride and very-low-density lipoprotein levels remained unchanged. After 2 wk in the ward on a high-CHO diet, total cholesterol fell by 15% (P less than 0.01), LDL cholesterol by 16% (P less than 0.001), and HDL cholesterol by 10% (P less than 0.05). The fall of HDL cholesterol was due to a decrease of HDL3 cholesterol only. After the 4-wk home period on a high-CHO diet, the observed lipoprotein changes were reversed. Heparin-releasable adipose tissue LPL activity was not influenced by a high-CHO diet. In conclusion, a high-carbohydrate, high-fiber, low-fat diet did not deteriorate the diabetic control, and it had no unfavorable effects on serum lipids or lipoproteins.

Adolescent↗

PubMedDate not supplied

The effect of insulin delivery route on lipoproteins in type I diabetic patients on CAPD.

OBJECTIVE: To evaluate the influence of subcutaneous and intraperitoneal (i.p.) insulin on plasma lipoproteins in type I diabetic (IDDM) patients with end-stage renal failure (ESRD) treated with continuous ambulatory peritoneal dialysis (CAPD). DESIGN: A before-after trial. SETTING: University hospital outpatient care. PARTICIPANTS: Eleven IDDM patients with stabilized peritoneal dialysis, age 42.9 +/- 2.9 (SEM) years and duration of diabetes 31.4 +/- 3.4 years. INTERVENTION: Two treatment periods during stabilized CAPD. All patients were first treated with subcutaneous and then with i.p. insulin. The studies were performed after a median time of 3 months on each treatment. MAIN OUTCOME MEASURES: Plasma lipids; apoproteins (Apo) A-I, A-II, and B; high-density lipoprotein (HDL) subfractions; glycemic status; and uremic status. RESULTS: After changing from subcutaneous insulin to i.p. insulin, plasma HDL cholesterol decreased (from 1.29 +/- 0.13 mmol/L to 0.96 +/- 0.06 mmol/L, p < 0.05), and the low density to high density lipoprotein (LDL/HDL) cholesterol ratio increased (p < 0.05). The HDL cholesterol decreased in both HDL2 and HDL3 fractions, but significantly so only in HDL3 (p < 0.01). ApoA-I (p < 0.05) decreased while the ApoB/ApoA-I ratio (p < 0.01) and the ApoA-I/HDL-cholesterol ratio (p < 0.01) increased during i.p. insulin therapy. Intraperitoneal insulin resulted in significantly better glycemic control than subcutaneous insulin (p < 0.01). CONCLUSIONS: In diabetic patients on CAPD therapy, i.p. insulin, although inducing better glycemic control than subcutaneous insulin, was associated with lowered plasma HDL cholesterol and ApoA-I levels. The atherogenic potential is probably less than expected as the relative particle size of HDL remained unchanged.

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