Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apolipoprotein E (apoE) polymorphism is a genetic determinant of serum lipoprotein levels and coronary heart disease risk. ApoE appears in three major isoforms E2, E3 and E4, coded by corresponding alleles epsilon 2, epsilon 3 and epsilon 4. These give six different phenotypes. Patients with insulin dependent diabetes (IDDM) have been reported to have increased incidence of E2/2 homozygosity. We studied the frequencies of apoE phenotypes and their association with plasma lipids in 201 diabetic children, aged 2-17 years, and in 216 healthy controls with the same age range. Phenotyping was performed directly from plasma by iso-electric focusing and immunoblotting. Plasma total and high density lipoprotein (HDL) cholesterol (C) and triglycerides were determined by routine laboratory methods. Apolipoprotein A1 (apoA1) and B (apoB) were measured by turbidometry. There were no differences in apoE phenotype or allele distributions between the diabetic and control subjects. The frequencies of epsilon 2, epsilon 3, and epsilon 4 in the diabetic and control children were 0.08 versus 0.07, 0.73 versus 0.72 and 0.19 versus 0.21. The difference in apoE2/2 frequencies (2.0 in diabetic and 0.5% in normal children) was not statistically significant. In the diabetic children, there was a distinct relation between apoE phenotype and plasma lipids; presence of apoE2 was associated with the lowest and that of apoE4 with the highest concentrations of total and low density lipoprotein (LDL) C, and apoB. Ratios of HDL-C/LDL-C and apoA1/apoB showed on opposite trend. The influence of apoE polymorphism on plasma lipids was less clear in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Apolipoprotein E phenotypes and plasma lipids in diabetic children and adolescents. 835 14

Apolipoprotein A1 mimetic peptide (D-4F), synthesized from D-amino acid, enhances the ability of high-density lipoprotein to protect low-density lipoprotein (LDL) against oxidation in atherosclerotic disease. Using a rat model of type I diabetes, we investigated whether chronic use of D-4F would lead to up-regulation of heme oxygenase (HO)-1, endothelial cell marker (CD31(+)), and thrombomodulin (TM) expression and increase the number of endothelial progenitor cells (EPCs). Sprague-Dawley rats were rendered diabetic with streptozotocin (STZ) and either D-4F or vehicle was administered, by i.p. injection, daily for 6 weeks (100 microg/100 g b.wt.). HO activity was measured in liver, kidney, heart, and aorta. After 6 weeks of D-4F treatment, HO activity significantly increased in the heart and aorta by 29 and 31% (p < 0.05 and p < 0.49), respectively. Long-term D-4F treatment also caused a significant increase in TM and CD31(+) expression. D-4F administration increased antioxidant capacity, as reflected by the decrease in oxidized protein and oxidized LDL, and enhanced EPC function and/or repair, as evidenced by the increase in EPC endothelial nitric-oxide synthase (eNOS) and prevention of vascular TM and CD31(+) loss. In conclusion, HO-1 and eNOS are relevant targets for D-4F and may contribute to the D-4F-mediated increase in TM and CD31(+), the antioxidant and anti-inflammatory properties, and confers robust vascular protection in this animal model of type 1 diabetes.
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PMID:Long-term treatment with the apolipoprotein A1 mimetic peptide increases antioxidants and vascular repair in type I diabetic rats. 1748 82