Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six fractions of serum apolipoproteins (apolipoprotein A-I, A-II, B, C-II, C-III and E) obtained from 100 patients with diabetes mellitus not administered any antihyperlipidemic drugs were measured to clarify the relationship between diabetes mellitus and the abnormal lipidosis. The serum concentrations of apolipoprotein B, C-II and C-III were significantly higher in these diabetics than in the controls (p < 0.05), and that of apolipoprotein E was significantly lower (p < 0.01). The serum concentrations of apolipoprotein C-II, C-III and E (p < 0.05) as well as HbA1C and FRA (p < 0.001) were significantly higher in the insufficient control group (FPG > or = 140 mg/dl) of diabetes mellitus. The serum concentrations of apolipoprotein C-II, C-III and E were significantly higher in the treated groups (p < 0.05). The serum concentrations of apolipoprotein B, C-II, C-III and E were significantly higher (p < 0.01) in the high cholesterol group (> 220mg/dl) and the high triglyceride group (> 150mg/dl) among the diabetic groups, but no significant differences were observed in the concentrations of apolipoprotein A-I and A-II.
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PMID:[Evaluation for serum apolipoproteins in patients with diabetes mellitus]. 813 26

The frequency of apolipoprotein E (apo E) phenotypes and genotypes due to allelic variation at amino acids 112 and 158 was analysed in 50 children with type I diabetes. Phenotypes were determined by isoelectric focusing and genotypes by the technique of polymerase chain reaction using allele-specific oligonucleotide probes (PCR/ASO) and the amplification refractory mutation system (ARMS). Discrepancies between phenotypes and genotypes as assigned by PCR/ASO were observed in 12 (24%) cases and by ARMS in eight (16%) cases. Results revealed the apo E3/3 genotype, as assigned by ARMS, to be the most frequent one (70%), followed by apo E3/4 in 16%, apo E2/2 in 2%, apo E2/3 in 8%, apo E2/4 in 2% and apo E4/4 in 2% of the cases. Apo E3/4 genotype and phenotype were more frequently present in the children with type I diabetes as compared with the diabetic adults previously reported on.
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PMID:Apolipoprotein E phenotypes and genotypes as determined by polymerase chain reaction using allele-specific oligonucleotide probes and the amplification refractory mutation system in children with insulin-dependent diabetes mellitus. 822 70

Phenotypes of apolipoprotein E (apo E) were determined by the iso-electric focusing method in 42 Japanese patients with nonfamilial late-onset Alzheimer's disease (AD) and 96 age-matched controls without hyperlipidemia and/or diabetes. There was a striking difference in the distribution of apo E phenotypes between patients with AD and controls (P < 0.0001). Such a difference was mostly attributable to different frequencies of phenotypes E4/3 and E3/3. The apo E4/3 phenotype was detected in 24 (57.1%) of 42 patients with AD, more than six times oftener than in nine (9.4%) of 96 controls. In contrast, apo E3/3, which is the most common apo E phenotype in various ethnic groups, was detected in only 15 (35.7%) patients with AD. These results indicate a strong association between apo E4 isoprotein and Japanese late-onset nonfamilial AD, and that apo E4 is a possible risk factor for the development of this type of AD.
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PMID:A high frequency of apolipoprotein E4 isoprotein in Japanese patients with late-onset nonfamilial Alzheimer's disease. 830 25

In the present study, we examined the levels of plasma lipids and apolipoproteins in patients with non-insulin dependent diabetes mellitus (NIDDM) with hypercholesterolemia in different apolipoprotein E (apo E) phenotypes. We also examined the influences of apo E polymorphism on the response to pravastatin. The patients were divided into three groups, E4/E3, E3/E3, and E3/E2. There were no differences in the baseline levels of plasma lipids and apolipoproteins, except that the level of triglycerides in E3/E2 heterozygotes was significantly higher than E3/E3 homozygotes. Three months of pravastatin administration significantly reduced plasma levels of total cholesterol and low-density lipoprotein cholesterol in each group to the same degree. We observed a significant reduction of apo B both in the E4/E3 and E3/E3 groups and apo E in the E3/E3 group. Such reduction was not observed in the E3/E2 group. We conclude that pravastatin is a potent drug to correct lipid abnormalities, particularly in NIDDM patients with apo E4/E3 and E3/E3. In the E3/E2 group, its effectiveness may be diminished.
Diabetes Res Clin Pract 1993 Apr
PMID:Apolipoprotein E polymorphism affects the response to pravastatin on plasma apolipoproteins in diabetic patients. 834 25

The effect of apolipoprotein E polymorphism on the established relationships between glucose tolerance, plasma insulin levels, and plasma lipoprotein concentrations were investigated in a sample of women defined on the basis of apolipoprotein E phenotypes. In women with the apolipoprotein E epsilon 2 allele (n = 22), fasting plasma insulin and glucose and insulin areas under the curve measured during an oral glucose tolerance test were positively correlated with plasma triglyceride levels (0.48 < or = r < or = 0.70; P < 0.05). In this group, very-low-density lipoprotein cholesterol and very-low-density lipoprotein triglyceride concentrations were positively correlated with fasting insulin levels, the insulin area, and with the ratio of insulin area to glucose area. In women (n = 24) homozygous for the apolipoprotein E epsilon 3 allele (the most common allele), essentially similar associations were found. In contrast, in women (n = 17) with the apolipoprotein E epsilon 4 allele, no association was found between glucose tolerance, fasting and postglucose plasma insulin levels, and plasma lipid and lipoprotein levels. These results suggest that apolipoprotein E polymorphism substantially modifies the associations between glucose tolerance, plasma insulin levels, and plasma lipoprotein concentrations. Additional analysis of the data revealed that apolipoprotein E polymorphism did not alter the relationships between body fat distribution and fasting insulin and postglucose insulin levels, but no correlation was observed between fatness indexes and glucose tolerance among apolipoprotein E epsilon 2 carriers.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1993 Oct
PMID:Apolipoprotein E polymorphism modifies relation of hyperinsulinemia to hypertriglyceridemia. 837 87

Probucol was given to rats made diabetic by streptozotocin. Compared with diabetic rats not receiving probucol or with nondiabetic rats, probucol lowered the plasma concentrations of triglycerides, phospholipids, cholesterol, and apolipoprotein B. The concentrations of serum chylomicrons and very low density lipoprotein (VLDL) were also reduced. In control and diabetic rats, probucol enhanced the clearance of endogenously radiolabeled VLDL from the plasma. Clearances from the plasma of rat lymph chylomicrons or chylomicron-like lipid emulsions were slow in diabetic rats. Probucol normalized chylomicron clearance in diabetic rats primarily by restoring hepatic uptake of remnants, which was decreased in diabetes. In diabetic rats, uptake of chylomicron remnants was increased in a number of extrahepatic tissues, including the heart and kidney. Probucol significantly decreased uptake in some extrahepatic tissues. Increased plasma clearance of VLDL and chylomicrons was associated with an increase in the apolipoprotein CII/CIII and apolipoprotein E/C ratios. Orally administered probucol was specifically incorporated into lymph chylomicrons, and clearance of probucol from the plasma exactly paralleled the clearance of chylomicron remnants, as traced with radiolabeled cholesteryl esters. Chylomicron-like emulsions incorporating probucol were exclusively cleared from the plasma by the liver in normal rats. We conclude that in streptozotocin diabetic rats, probucol is an effective hypolipidemic agent because it promotes the clearance of the triglyceride-rich lipoproteins.
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PMID:Effect of probucol on plasma clearance and organ uptake of chylomicrons and VLDLs in normal and diabetic rats. 838

The effect of the menopause on insulin metabolism has not received specific attention in populations prone to non-insulin-dependent (Type 2) diabetes mellitus (NIDDM). Insignificant or slight alterations in insulin levels have been reported in postmenopausal women of mainly European ancestry. We thus report on the results of a cross-sectional study on the correlates of fasting insulin levels in 177 healthy, Indian nurses aged between 25 and 55 years. Fasting insulin concentration was markedly higher in the 75 postmenopausal subjects (23.9 mU I-1) than in the 102 premenopausal women (11.7 mU I-1 (p < 0.0001). Forty-three (57%) of the postmenopausal subjects had insulin values more than 20 mU I-1 (the upper normal limit). Stepwise regression analysis on the entire group revealed menopause (p < 0.0001), waist:hip ratio (p = 0.0001), apolipoprotein E genotype (p = 0.002), and the testosterone: sex hormone binding globulin ratio (p = 0.0002) as statistically significant, independent predictors of log insulin levels. Age did not account for the difference between premenopausal and postmenopausal subjects. The apolipoprotein E genotype emerged as a significant correlate of insulin levels, only in postmenopausal women: epsilon 3/3, 26.3 mU I-1; epsilon 3/4, 51.8 mU I-1 (p = 0.0007). Hyperinsulinaemic postmenopausal subjects had higher fasting glucose levels than normoinsulinemic nurses (p = 0.03), but glycosylated haemoglobin and fructosamine values were all within the normal range. Thus fasting hyperinsulinaemia was marked and common among a group of healthy, postmenopausal Indian nurses below the age of 55 years, suggesting that the menopausal transition may permit or provoke insulin resistance in this susceptible population.
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PMID:Marked hyperinsulinaemia in postmenopausal, healthy Indian (Asian) women. 854 39

We examined the apolipoprotein E polymorphism of an obese patient presenting non-insulin-dependent diabetes, hypertension and moderate lipid disturbances. The apolipoprotein E genotyping carried out from leukocyte DNA using PCR amplification and restriction enzyme digestion demonstrated homozygosity for the rare apoE1[Gly127-->Asp; Arg158--> Cys] (Weisgraber allele). The nucleotide change results in a glycine to aspartic acid substitution at amino acid 127 in the apolipoprotein E2.
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PMID:Genotyping of a patient homozygous for a rare apolipoprotein E1 [Gly127-->Asp; Arg158-->Cys] (Weisgraber allele). 875 Jun 11

We have previously demonstrated alterations in apolipoprotein B-48 metabolism in the post-prandial state in patients with non-insulin-dependent diabetes mellitus. This study investigates the relationship between hypertriglyceridaemia and post-prandial lipoprotein metabolism. Four groups of patients were examined: non-insulin-dependent diabetic patients, with normal serum triglyceride levels (serum triglyceride < 2.1 mmol l-1; haemoglobin HbA1c 5.5% +/- 0.4%); poorly controlled, non-insulin-dependent diabetic patients with hypertriglyceridaemia (serum triglyceride > 2.1 mmol l-1; HbA1c 8.8% +/- 0.9%); non-diabetic subjects with serum triglycerides < 2.1 mmol l-1; and non-diabetic subjects with hypertriglyceridaemia (serum triglyceride > 2.1 mmol l-1). Subjects were studied fasting and following a high-fat meal (1300 kcal). The triglyceride-rich lipoprotein fraction was isolated by ultracentrifugation (d < 1.006 g ml-1). Apoprotein B-48, apoprotein B-100 and apoprotein E were separated on 4%-15% gradient gels and quantified as a percentage of the fasting concentration by densitometric scanning. Triglyceride-rich lipoprotein apolipoprotein B-48 and apolipoprotein B-100 post-prandial profiles demonstrated a maximum increase either at 2 h or rising still further to a peak at 6 h before falling in the diabetic groups and hypertriglyceridaemic non-diabetic subjects when compared with the normotriglyceridaemic control subjects whose levels decreased after 2 h (P < 0.05). A significantly different triglyceride-rich lipoprotein apolipoprotein E profile was also exhibited by the diabetic patients (P < 0.05). Levels of triglyceride-rich lipoprotein, cholesterol, triglyceride, total protein and apoprotein B were elevated in the hypertriglyceridaemic subjects, both diabetic and non-diabetic. These results indicate that hypertriglyceridaemia is associated with altered metabolism and composition of post-prandial triglyceride-rich lipoprotein particles in both poorly controlled diabetic and non-diabetic subjects.
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PMID:Intestinally derived lipoprotein particles in non-insulin-dependent diabetic patients with and without hypertriglyceridaemia. 875 Jul 63

Polymorphisms in the apolipoprotein E (apoE) phenotype (especially E4) are associated with increased cardiovascular risk and particularly with increased concentrations of LDL cholesterol. Little is known, however, about whether alterations in LDL size are associated with the apoE4 phenotype. LDL size was determined by gradient gel electrophoresis, and apoE phenotype was determined by isoelectric focus in 337 nondiabetic subjects from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular risk factors in Mexican Americans and non-Hispanic whites. ApoE4 was associated not only with increases in LDL cholesterol concentrations but also with decreased LDL size. After adjustment for age, sex, body mass index, waist-to-hip ratio, triglyceride, HDL cholesterol, fasting insulin, and diabetic status, the apoE phenotype remained significantly related to LDL size (A) in both men (apoE23, 260.0; apoE33; 256.3; and apoE34, 252.6; P = .01) and women (apoE23, 261.7; apoE33, 257.9; and apoE34, 256.7, P = .045). Variations in apoE phenotype are associated not only with changes in the absolute concentration of LDL cholesterol but also with changes in its composition. These changes are only partly explained by associations of apoE with insulin, triglyceride, and HDL cholesterol.
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PMID:Apolipoprotein E polymorphism and LDL size in a biethnic population. 879 73


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