Document Detail


Serum lipoprotein(a) concentrations and apolipoprotein(a) phenotypes in the families of NIDDM patients.
MedLine Citation:
PMID:  8786017     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We studied the quantitative and qualitative characteristics of lipoprotein(a) [Lp(a)] as a function of apolipoprotein(a) [apo(a)] phenotype in 87 members (42 males, 45 females) of 20 diabetic families, 26 of whom were diagnosed with non-insulin-dependent diabetes mellitus (NIDDM) with moderate glycaemic control (HbA1c 7.1 +/- 1.2%). Apo(a) phenotyping was performed by a sensitive, high-resolution technique using SDS-agarose/gradient PAGE (3-6%). To date, 26 different apo(a) phenotypes, including a null type, have been identified. Serum Lp(a) levels of NIDDM patients and non-diabetic members of the same family who had the same apo(a) phenotypes were compared, while case control subjects were chosen from high-Lp(a) non-diabetic and low-Lp(a) nondiabetic groups with the same apo(a) phenotypes in the same family. Serum Lp(a) levels were significantly higher in NIDDM patients than in non-diabetic subjects (39.8 +/- 33.3 vs 22.3 +/- 19.5 mg/dl, p < 0.05). The difference in the mean Lp(a) level between the diabetic and non-diabetic groups was significantly (p < 0.05) greater than that between the high-Lp(a) non-diabetic and low-Lp(a) non-diabetic groups. An analysis of covariance and a least square means comparison indicated that the regression line between serum Lp(a) levels [log Lp(a)] and apo(a) phenotypes in the diabetic patient group was significantly (p < 0.01) elevated for each apo(a) phenotype, compared to the regression line of the control group. These data together with our previous findings that serum Lp(a) levels are genetically controlled by apo(a) phenotypes, suggest that Lp(a) levels in diabetic patients are not regulated by smaller apo(a) isoforms, and that serum Lp(a) levels are greater in diabetic patients than in non-diabetic family members, even when they share the same apo(a) phenotypes.
Authors:
K Hirata; K Saku; S Jimi; S Kikuchi; H Hamaguchi; K Arakawa
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Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Diabetologia     Volume:  38     ISSN:  0012-186X     ISO Abbreviation:  Diabetologia     Publication Date:  1995 Dec 
Date Detail:
Created Date:  1996-09-24     Completed Date:  1996-09-24     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0006777     Medline TA:  Diabetologia     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  1434-42     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, Fukuoka University School of Medicine, Japan.
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MeSH Terms
Descriptor/Qualifier:
Apolipoproteins / blood*,  genetics
Apoprotein(a)
Biological Markers / blood
Blood Glucose / metabolism
Cholesterol / blood
Cholesterol, HDL / blood
Diabetes Mellitus, Type 2 / blood,  genetics*
Family Health
Female
Hemoglobin A, Glycosylated / analysis
Humans
Kidney Failure, Chronic / blood
Lipoprotein(a) / blood*,  genetics
Male
Pedigree
Phenotype
Reference Values
Regression Analysis
Triglycerides / blood
Chemical
Reg. No./Substance:
0/Apolipoproteins; 0/Biological Markers; 0/Blood Glucose; 0/Cholesterol, HDL; 0/Hemoglobin A, Glycosylated; 0/Lipoprotein(a); 0/Triglycerides; 57-88-5/Cholesterol; EC 3.4.21.-/Apoprotein(a)

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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