PubMed Health⌕ Search

Biomedical subjects

M R Taskinen

Publications and source records attributed to M R Taskinen.

At least 19 recordsLinked to original sources
PubMed1995

HDLs containing apolipoproteins A-I and A-II (LpA-I:A-II) as markers of coronary artery disease in men with non-insulin-dependent diabetes mellitus.

BACKGROUND: Abnormalities in HDL and an increased risk of coronary artery disease (CAD) coexist in non-insulin-dependent diabetes mellitus (NIDDM). HDLs can be separated by their apolipoprotein (apo) content into particles containing apoA-I but not apoA-II (LpA-I) and those containing both apoA-I and apoA-II (LpA-I:A-II). The LpA-I particles have been suggested to be more effective in conferring protection against CAD than the LpA-I:A-II particles. However, data are sparse, and no studies have defined the role of these two classes of particles in NIDDM. METHODS AND RESULTS: LpA-I and LpA-I:A-II particles were quantified by a differential electroimmunoassay in four groups of men with similar age and body mass index (BMI) distributions. Group 1 consisted of 50 patients with NIDDM and angiographically verified CAD; group 2, 50 men with CAD but no diabetes; group 3, 50 men with NIDDM but no CAD; and group 4, 31 healthy men. Serum apoA-I and apoA-II concentrations were measured by immunoturbidimetry, and HDL2 and HDL3 were separated by ultracentrifugation. Concentrations of LpA-I:A-II particles in group 1 were 13.8%, 18.3%, and 26.9% lower than in groups 2 through 4, respectively. In a two-by-two factorial ANOVA, adjusted for age and BMI, the differences were significant for both CAD (P < .001) and NIDDM (P < .001), with no interaction between the factors. These results were confirmed by comparable differences in the serum concentrations of apoA-I and apoA-II. LpA-I particles were related to the presence or absence of CAD (P = .013), but the difference was lost in a multivariate analysis. A low HDL3 cholesterol concentration characterized both CAD (P = .002) and NIDDM (P = .024). HDL2 cholesterol differed significantly with regard to the presence of NIDDM (P = .033) but only borderline with respect to CAD (P = .073). CONCLUSIONS: ApoA-II-containing lipoproteins and HDL3 cholesterol are powerful markers of CAD in men with NIDDM.

Apolipoprotein A-I↗
PubMed1995

Changes of lipolytic enzymes cluster with insulin resistance syndrome. Botnia Study Group.

The activities of hepatic and lipoprotein lipase and the levels of lipo- and apoproteins were compared in two groups of normoglycaemic men representing the highest (n = 18) and lowest (n = 15) fasting insulin quintiles of first degree male relatives of non-insulin-dependent diabetic patients. The high insulin group representing insulin-resistant individuals had significantly lower post-heparin plasma lipoprotein lipase activity than the low insulin group (14.2 +/- 4.0 vs 20 +/- 5.8 mumol NEFA.ml-1.h-1, p < 0.001); hepatic lipase activity did not differ between the two groups (24.2 +/- 11 vs 18.0 +/- 5.3 mumol NEFA.ml-1.h-1, NS). The lipoprotein lipase/hepatic lipase ratio in the high insulin group was decreased by 66% as compared to the low insulin group (0.75 +/- 0.57 vs 1.25 +/- 0.65, p < 0.01). In the high insulin group both total and VLDL triglycerides were higher than in the low insulin group (1.61 +/- 0.57 vs 0.86 +/- 0.26 mmol/l, p < 0.001 and 1.00 +/- 0.47 vs 0.36 +/- 0.16 mmol/l, p < 0.001, respectively) whereas HDL cholesterol and HDL2 cholesterol were lower (1.20 +/- 0.30 vs 1.43 +/- 0.22 mmol/l, p < 0.05 and 0.49 +/- 0.21 vs 0.71 +/- 0.17 mmol/l, p < 0.05, respectively). Total cholesterol, LDL cholesterol or HDL3 cholesterol did not differ between the two groups. The mean particle size of LDL was smaller in the high insulin group than in the low insulin group (258 +/- 7 vs 265 +/- 6 A, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Insulin resistance and abnormal albumin excretion in non-diabetic first-degree relatives of patients with NIDDM.

Microalbuminuria has recently been associated with insulin resistance in both insulin-dependent and non-insulin-dependent (NIDDM) diabetes mellitus. To establish whether microalbuminuria in non-diabetic subjects as well is associated with insulin resistance and associated abnormalities in glucose and lipid metabolism, oral glucose tolerance tests were performed with measurement of urinary albumin excretion rate, lipids and lipoproteins in 582 male non-diabetic first-degree relatives of patients with NIDDM. In addition, insulin sensitivity was assessed in 20 of these subjects with the euglycaemic hyperinsulinaemic clamp technique. Abnormal albumin excretion rate (AER), defined as AER 15-200 micrograms/min, was associated with higher systolic blood pressure (p < 0.05), higher fasting glucose values (p < 0.05), lower HDL-cholesterol (p < 0.05) and lower apolipoprotein A-I (p < 0.05) concentrations than observed in subjects with normal AER. The rate of glucose metabolism was lower in subjects with abnormal compared to subjects with normal albumin excretion rate (38.0 +/- 2.8 vs 47.3 +/- 2.4 mumol.kg lean body mass-1.min-1; p = 0.028). This difference was almost completely accounted for by a reduction in non-oxidative glucose metabolism (17.7 +/- 1.9 vs 27.4 +/- 2.7 mumol.kg lean body mass-1.min-1; p = 0.010), which correlated inversely with the AER (r = -0.543; p = 0.013). These results suggest that in non-diabetic individuals genetically predisposed to NIDDM, abnormal AER is associated with insulin resistance and abnormalities in glucose and lipid metabolism.

Albuminuria↗
PubMed1995

LDL particle size in mildly hypertriglyceridemic subjects: no relation to insulin resistance or diabetes.

We examined 18 Type 2 diabetic and 19 non-diabetic subjects in order to determine the association between insulin resistance and LDL particle size distribution in mildly hypertriglyceridemic and hyperinsulinemic subjects with and without Type 2 diabetes. Insulin sensitivity of the patients was characterized by their insulin-stimulated glucose uptake rate determined by euglycemic clamp technique. LDL particle size distribution was determined by nondenaturing polyacrylamide gradient gel electrophoresis. Type 2 diabetic and non-diabetic subjects had closely similar serum lipid and lipoprotein concentrations as well as the mean particle diameters of the major LDL peak (246 +/- 6 A and 244 +/- 6 A, respectively). To evaluate the effect of insulin resistance on LDL particle size the participants were categorized into two subgroups using the median of their insulin-stimulated glucose uptake rate (14.67 mumol/kg/min) as a cut-off point. Neither lipid and lipoprotein concentrations nor the LDL particle size distributions differed between the more insulin resistant group (nine diabetic and nine non-diabetic subjects) and less insulin resistant group (nine diabetic and ten non-diabetic subjects). LDL particle size was not associated with the insulin-stimulated glucose uptake rate or with the mean 24-h concentration of serum insulin. Mean 24-h concentration of serum triglycerides was the strongest discriminator for LDL particle size (r = -0.44, P < 0.01). In conclusion, neither Type 2 diabetes nor insulin resistance seem to have any direct effect on LDL particle size in mildly hypertriglyceridemic subjects. The fact that LDL particle size was associated with serum triglycerides indicates that the effect of diabetes and insulin resistance on LDL particle size could be explained by the effects of insulin resistance and/or hyperinsulinism on VLDL metabolism.

Blood Glucose↗
PubMed1995

Decreasing triglyceride by gemfibrozil therapy does not affect the glucoregulatory or antilipolytic effect of insulin in nondiabetic subjects with mild hypertriglyceridemia.

We studied the effects of gemfibrozil on glucose and fatty acid metabolism in subjects with mild endogenous hypertriglyceridemia. Twenty subjects (serum triglycerides, 3.2 +/- 1.4 mmol/L; age, 52 +/- 7 years; body mass index, 27.8 +/- 1.8 kg/m2) were randomly allocated to receive either placebo or gemfibrozil 1,200 mg daily for 12 weeks in a double-blind study. Gemfibrozil decreased serum total and very-low-density lipoprotein (VLDL) triglycerides by 53% and 57%, respectively, and serum apolipoprotein (apo) B concentration by 21%. Gemfibrozil had no effect on the diurnal concentration of free fatty acids (FFA). Neither did gemfibrozil change diurnal blood glucose or serum insulin concentrations. The endogenous glucose production rate remained unchanged in both groups during the treatment period, and was similarly suppressed by hyperinsulinemia. The rate of insulin-induced whole-body glucose disposal increased similarly both before (basal 10.8 +/- 1.8, low-dose insulin 10.5 +/- 2.1, and high-dose insulin 20.9 +/- 11.9 mumol.kg-1.min-1) and after (11.1 +/- 1.7, 10.7 +/- 1.2, and 18.6 +/- 7.9, respectively) gemfibrozil treatment. Rates of oxidative and nonoxidative glucose metabolism remained unchanged during gemfibrozil treatment. Basal pretreatment and posttreatment FFA turnover rates were similar in both study groups, as were the rates of substrate oxidation. In summary, gemfibrozil proved to be an effective serum triglyceride-lowering agent in patients with mild hypertriglyceridemia, but had no effect on the insulin sensitivity of glucose metabolism or of antilipolysis. These data support the idea that triglycerides per se do not cause insulin resistance, and that the triglyceride-lowering effect of gemfibrozil is not mediated via antilipolytic action.

Analysis of Variance↗
PubMed1995

Insulin resistance and lipoprotein metabolism.

Dyslipidaemia in insulin resistance comprises elevated plasma triglycerides, decreased HDL, a preponderance of small, dense LDL and increased postprandial lipaemia. In terms of cause and effect, small, dense LDL, alimentary hyperlipidaemia and changes in HDL are consequences of elevated triglycerides. These abnormalities can become frequent if triglycerides exceed a threshold value of approximately 1.5 mmol/l. Therefore, it is mandatory to maintain plasma triglycerides as low as possible in noninsulin-dependent diabetic and insulin-resistant individuals to prevent the potentially atherogenic and metabolic consequences of hypertriglyceridaemia.

Aging↗
PubMed1995

Lipid intolerance in smokers.

OBJECTIVES: Smokers have recently been shown to be insulin resistant and to exhibit several characteristics of the insulin resistance syndrome (IRS). In this study, we assessed fasting and postprandial lipid levels in healthy, normolipidaemic, chronic smokers and a matched group of non-smoking individuals. DESIGN: A standardized mixed meal (containing 3.78 MJ and 51 g of fat) was given in the morning after an overnight fast. The smokers were either abstinent from tobacco for 48 h or were allowed to smoke freely, including being allowed to smoke six cigarettes during the study. SUBJECTS: Twenty-two middle-aged, healthy male subjects, nine habitual smokers and 13 non-smoking control subjects, were recruited to the study. The smokers had all been smoking at least 10 cigarettes per day for at least 10 years. RESULTS: The smokers exhibited a lipid intolerance in that their postprandial increase in triglyceride levels was more than 50% higher than in the non-smokers' group. This lipid intolerance could not be discerned in the postabsorptive state because the fasting triglyceride levels were the same in both groups, while the smokers had significantly lower high-density lipoprotein (HDL) cholesterol. The peak postprandial triglyceride level correlated closely and negatively with fasting HDL cholesterol, indicating an impaired lipolytic removal capacity in smokers. CONCLUSIONS: Healthy, normotriglyceridaemic smokers exhibit an abnormal postprandial lipid metabolism consistent with lipid intolerance. It is suggested that postprandial hyperlipidaemia is a characteristic trait of the insulin resistance syndrome and that the defect in lipid removal is related to the low HDL cholesterol in this syndrome. The insulin resistance syndrome is likely to be an important reason for the increased propensity for cardiovascular disease in smokers.

Eating↗
PubMed1995

Effect of gemfibrozil on the regulation of HDL subfractions in hypertriglyceridaemic patients.

OBJECTIVES: To study changes of HDL subfractions and their regulation during gemfibrozil treatment in hypertriglyceridaemia. DESIGN: Twenty patients with hypertriglyceridaemia were randomized to receive either 1200 mg day-1 gemfibrozil or placebo for 3 months. After a 6-week, single-blind placebo period, the patients were randomized to receive either gemfibrozil or placebo for 3 months in a double-blind study. SETTING: The patients were studied as outpatients in the Third Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland. MAIN OUTCOME MEASURES: Ultracentrifugally isolated HDL subclasses; concentrations of apoA-I, apoA-II, LpA-I and LpA-I:A-II particles; post-heparin plasma lipoprotein lipase (LPL), hepatic lipase (HL) and plasma cholesteryl ester transfer protein (CETP) activities; phospholipid transfer protein (PLTP) and lecithine cholesteryl acyltransferase (LCAT) activities were measured in plasma from six patients from both groups. RESULTS: Gemfibrozil increased the concentration of HDL cholesterol (+11.1%) because of the rise of HDL3 cholesterol (34.5%, P < 0.01). The concentration of LpA-I particles was reduced during gemfibrozil treatment (-12.4%, P < 0.05), while that of apoA-II increased (+12.3%, P < 0.01). The LpA-I to LpA-I:A-II ratio decreased significantly in the gemfibrozil group (-18.9%, P < 0.01). Gemfibrozil increased LPL and HL activities by 18.2% (P < 0.05) and by 19.6%, respectively. Plasma CETP activity was also increased during gemfibrozil treatment (+15.8%, P < 0.05). CONCLUSION: The gemfibrozil-induced elevation of HDL3 and apoA-II may reflect the combined action of LPL, HL and CETP on plasma HDL metabolism.

Adult↗
PubMed1995

ApoA-IHelsinki (Lys107-->0) associated with reduced HDL cholesterol and LpA-I:A-II deficiency.

A Finnish kindred with premature coronary heart disease and decreased HDL cholesterol levels was identified as having an apoA-I variant, apoA-I (Lys107-->0), caused by a 3-bp deletion of nucleotides 1396 through 1398 in exon 4 of the apoA-I gene. These subjects (n = 10) were heterozygous for this mutation. The mean serum HDL cholesterol concentration (26.7 +/- 9.7 mg/dL) of affected family members was 36%, lower than that of unaffected family members (P < .05). Mean serum apoA-I and apoA-II concentrations in heterozygotes were reduced by 18% and 22%, respectively, compared with normal family members (P < .05). In heterozygotes the mean concentration of lipoprotein containing both apoA-I and apoA-II (LpA-I:A-II) was 31% lower than in those with normal apoA-I (P < .001), while the mean level of lipoproteins containing apoA-I without apoA-II was similar in the two groups. HDL density-gradient ultracentrifugation showed a lack of HDL2 and small dense HDL3 in heterozygotes compared with unaffected family members. The HDL particle size distribution, as analyzed by nondenaturing gradient gel electrophoresis of heterozygotes, revealed one major peak at 8.0 to 9.7 nm, a minor peak at 7.8 to 8.5 nm, and an absence of HDL2b and HDL2a peaks. These latter peaks were observed in unaffected family members. Serum levels of LDL cholesterol, triglycerides, VLDL, IDL, and LDL subclasses were similar in the two groups. However, in heterozygotes the cholesterol-to-triglyceride ratios in VLDL2, LDL1, LDL3, HDL2b, HDL2a, and HDL3a were 8% to 54% lower than in unaffected family members (P < .05). Cholesteryl ester transfer protein activity in heterozygotes was reduced by 25% compared with unaffected family members (P < .05), while the plasma lecithin:cholesterol acyltransferase (LCAT) activity did not differ between heterozygotes and unaffected family members. The ability of isolated variant apoA-I to serve as a cofactor for LCAT in vitro did not differ from that of normal apoA-I. Our data are consistent with the concept that a low HDL cholesterol level in subjects heterozygous for the apoA-IHelsinki mutation (Lys107-->0) having normal LCAT activity is a consequence of decreased concentration of LpA-I:A-II particles and of a smaller size and reduced cholesterol content of HDL particles.

Apolipoprotein A-I↗
PubMed1992

A novel polymorphism of apolipoprotein A-IV is the result of an asparagine to serine substitution at residue 127.

We have identified a hitherto unknown genetic polymorphism of apolipoprotein A-IV (apoA-IV). The molecular basis for this polymorphism is an A to G substitution at nucleotide 1687 resulting in an Asn to Ser change of amino acid 127. The frequencies of the two apoA-IV alleles (designated apoA-IV127Asn and apoA-IV127Ser), determined by Hin c II restriction analysis of PCR amplified exon three of the apoA-IV gene, were 0.788 and 0.212, respectively, in a Finnish population sample. Allele frequencies of another polymorphism due to a Thr to Ser substitution at amino acid 347 were determined using Hinf I restriction analysis. The allele frequencies were 0.823 for apoA-IV347Thr and 0.177 for apoA-IV347Ser. None of the apoA-IV polymorphisms (apoA-IV127:Asn----Ser, apoA-IV347:Thr----Ser and apoA-IV360:Gln----His) had any effect on plasma lipid and lipoprotein concentrations in cohorts of dyslipidemic men and in a population sample of normolipidemic controls. There was also no association between the history of previous myocardial infarction and any of the apoA-IV alleles.

Alleles↗
PubMed1992

Metabolism of HDL apolipoprotein A-I and A-II in type 1 (insulin-dependent) diabetes mellitus.

Concentrations of HDL cholesterol and apolipoprotein A-I are commonly increased in Type 1 (insulin-dependent) diabetes mellitus but the mechanisms whereby diabetes influences HDL metabolism have not been studied. We investigated the metabolism of HDL apoproteins A-I and II in normolipidaemic Type 1 diabetic men (n = 17, HbA1 6.4-11.9%) without microalbuminuria but with a wide range of HDL cholesterol (0.85-2.10 mmol/l) and in nondiabetic men (n = 18) matched for body mass index and the range of HDL cholesterol. Input rates and fractional catabolic rates for apolipoproteins A-I and II were determined following injection of 125I-apolipoprotein A-I and 131I-apolipoprotein A-II tracers. Additional multicompartmental analysis was performed using a model to describe the kinetics of HDL particles containing only apolipoprotein A-I (Lp A-I) and apolipoprotein A-I and apolipoprotein A-II (Lp A-I/A-II). No gross differences from normal subjects were observed in the mean levels of lipids, lipoproteins, apoproteins and the lipolytic enzymes in the diabetic men as a result of the selection process. Furthermore, the relationship between apolipoprotein A kinetics and plasma HDL cholesterol levels appeared to be preserved in the diabetic group. However, some normal interrelationships were disrupted in the diabetic men. Firstly, the rate of apolipoprotein A-II synthesis was 22% lower than in control subjects (p less than 0.05). Modelling indicated that this was due to decreased input of Lp A-I/A-II particles whereas the input of Lp A-I particles was similar in the two groups. Secondly, there was no correlation between VLDL triglyceride and HDL cholesterol or VLDL triglyceride and the fractional catabolic rate of apolipoproteins A-I and A-II in diabetic men in contrast to that seen in control subjects. We conclude that there is a disruption in the normal association between VLDL and HDL metabolism in Type 1 diabetic men and postulate that the observed differences may be due to the therapeutic use of exogenous insulin.

Adult↗
PubMed1992

Effects of interferon alpha on insulin binding and glucose transport in human adipocytes.

We have previously demonstrated that interferon administration impairs glucose tolerance and causes insulin resistance in healthy man. Whether this is a direct effect of interferon is not known. The present study was undertaken to examine directly the effect of interferon alpha on insulin binding and action on glucose transport in isolated human adipocytes. Different concentrations of interferon alpha (range 10(-3)-10(5) IU ml-1) and different incubation times (0-5-24 h) with interferon were employed. Acute and 5-h and 24-h exposure of human adipocytes to 10(-2)-10 IU ml-1 of interferon increased the high affinity binding of 125I-insulin (P less than 0.05). In contrast, human interferon alpha had no effect on insulin binding in rat adipocytes. In short-term studies interferon had no effect on 14C-glucose transport clearance. 24-h preincubation of human adipocytes with 10(-2), 10, 10(4) IU ml-1 interferon increased maximally-insulin stimulated 14C-glucose transport clearance (P less than 0.05) and glucose transport responsiveness to insulin was enhanced by 24% (P less than 0.05) in cells exposed to 10(-2) IU ml-1 interferon. After 5 and 24-h preincubations with interferon we observed modest changes in glucose transport sensitivity to moderate concentrations of insulin (50-100 pM) with upregulation in the presence of 10(-2)-10 IU ml-1 interferon and downregulation in the presence of 10(4)-10(5) IUm ml-1 interferon (P less than 0.05). The insulin sensitivity index (ED50) did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1992

One-year response to evening insulin therapy in non-insulin-dependent diabetes.

We studied the 1-year response and predictors of the response to combination therapy with evening insulin and oral agents in NIDDM patients with a secondary failure. Injection of intermediate-acting (Monotard HM) or long-acting (Ultratard HM) insulin was added to previous oral therapy in 17 diabetics (of mean age (+/- SD) 54 +/- 2 years, BMI 27.6 +/- 0.5 kg m-2). The initial insulin dose was in the range 10-16 U, and the mean dose was 23 +/- 2 U d-1 at 12 months. During the year, combination therapy reduced the mean fasting blood glucose concentration (12.7 +/- 0.6 vs. 8.4 +/- 0.7 mmol l-1, P less than 0.001) and HbA1 (10.7 +/- 0.3 vs. 9.8 +/- 0.4%, P less than 0.01). Body weight increased by 4.4 +/- 0.7 kg (P less than 0.001). The serum cholesterol concentration decreased by 14% (P less than 0.01), but serum triglyceride and HDL-cholesterol levels remained unchanged. Elevation of serum triglycerides and plasma free fatty acids (FFAs) at baseline predicted a poor long-term outcome to this mode of therapy. In conclusion, the addition of evening injections of insulin to oral therapy improves glycaemic control in poorly controlled NIDDM patients. However, initial hypertriglyceridaemia predicts a poor long-term outcome to evening insulin supplementation.

Adult↗
PubMed1992

Increased volume of gastric contents in diabetic patients undergoing renal transplantation: lack of effect with cisapride.

Gastroparesis is a frequently unrecognized complication of insulin-dependent diabetes mellitus, which subjects these patients to the risk of aspiration at induction of anaesthesia. The effect of oral cisapride on volume and pH of gastric contents was studied in 24 diabetic and 24 non-diabetic uraemic patients undergoing renal transplantation. All patients were allocated randomly in a double-blind fashion to receive either 10 mg of cisapride or placebo orally approximately 100 min before anaesthesia and three times daily for the first 2 postoperative days. After the induction of anaesthesia, gastric contents were aspirated through a nasogastric tube, and the pH and volume were measured. The emptiness of the stomach was verified by gastroscopy. Gastric volumes exceeding 0.4 ml.kg-1 were observed in 12/24 of the diabetic and 4/24 of the non-diabetic uraemic patients (P < 0.01). The pH of the gastric contents did not differ between the groups, ranging from 1-8 in diabetics and 1-7 in non-diabetics. Cisapride lacked effect on gastric contents and postoperative gastrointestinal motility. Diabetic uraemic patients had larger gastric volumes than their non-diabetic controls at induction of anaesthesia. Cisapride had no effect on gastric emptying preoperatively nor on postoperative bowel function.

Administration, Oral↗
PubMed1992

Lipoproteins and their genetic variation in subjects with and without angiographically verified coronary artery disease.

To examine the concentration of serum lipoproteins and the association of their genetic variation with the occurrence of coronary artery disease (CAD), composite serum lipoprotein profiles including lipoprotein(a) (Lp[a]), apolipoprotein (apo) E phenotypes, and apo B Xba I genotypes were determined in patients with angiographically verified CAD (CAD+ group, n = 111) and in subjects with no angiographic evidence of CAD (CAD- group, n = 46). In addition, we determined the concentrations of serum lipids, lipoproteins, and apolipoproteins in 96 healthy controls. Both CAD- and CAD+ groups had lower concentrations of apos A-I and A-II but higher concentrations of serum total and very low density lipoprotein triglyceride and very low density lipoprotein cholesterol than did healthy controls. The mean concentrations of serum total and low density lipoprotein cholesterol and the median values of Lp(a) were similar in the CAD+ and CAD- groups, both having higher concentrations of low density lipoprotein cholesterol and apo B than the healthy controls. Irrespective of gender, patients with CAD had significantly lower serum high density lipoprotein cholesterol than did those without CAD (1.48 +/- 0.40 versus 1.16 +/- 0.29 mmol/l, p less than 0.001). In women, the mean serum total and very low density lipoprotein triglyceride concentration was also higher in the CAD+ than in the CAD- group. The frequency of the apo E4 allele (epsilon 4) was significantly higher in the CAD+ group (0.293) than in the CAD- group (0.174; p less than 0.001). The frequencies of the two apo B alleles, X1 (Xba I restriction site absent) and X2 (Xba I restriction site present), were similar in the two groups. Stepwise discriminant analysis revealed that in men, serum high density lipoprotein cholesterol had the highest power to discriminate for CAD. In addition, the concentration of plasma apo B levels and the occurrence of apo E phenotypes were independently associated with CAD in men. In women, the only independent factor associated with CAD after adjustment for beta-blocker and diuretics usage was the concentration of serum triglycerides.

Adult↗
PubMed1992

Quantitative and qualitative lipoprotein abnormalities in diabetes mellitus.

In people with diabetes, the concentration of an individual lipoprotein or apolipoprotein can be highly variable and is totally different in the two major forms of the disease. Alterations in the concentrations of major lipids and lipoproteins are well characterized in both IDDM and NIDDM. In general, the lipoprotein pattern is antiatherogenic in individuals with IDDM who are treated and have optimal glycemic control. In contrast, NIDDM is associated with atherogenic changes of serum lipids and lipoproteins regardless of the mode of treatment. In people with both types of diabetes, the distribution of apoE phenotype seems to be similar to that in nondiabetic populations. IDDM patients with microalbuminuria show atherogenic changes of lipoproteins and have elevated levels of Lp(a), which is a risk factor of coronary artery disease. Whether glycemic control influences the concentration of Lp(a) is still an open question. An important issue is that the concentration of a lipoprotein can be normal without excluding compositional abnormalities that are potentially atherogenic. Such alterations are present in people with both IDDM and NIDDM. Consequently, it has been questioned whether the target values to start treatment should be lower in diabetic than in nondiabetic populations.

Diabetes Complications↗