The prevalence of the mitochondrial DNA 16189 variant in non-diabetic Korean adults and its association with higher fasting glucose and body mass index

被引:40
作者
Kim, JH
Park, KS
Cho, YM
Kang, BS
Kim, SK
Jeon, HJ
Kim, SY
Lee, HK
机构
[1] Seoul Natl Univ Hosp, Coll Med, Dept Internal Med, Seoul 110744, South Korea
[2] Seoul Natl Univ, Med Res Ctr, Inst Endocrinol Nutr & Metab, Seoul, South Korea
[3] Seoul Natl Univ Hosp, Clin Res Inst, Genome Res Ctr Diabet & Endocrine Dis, Seoul 110744, South Korea
关键词
mitochondrial DNA; 16189; variant; fasting glucose; body mass index; Korean;
D O I
10.1046/j.1464-5491.2002.00747.x
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
Aims To evaluate the prevalence of the 16189 variant of mitochondrial DNA in Korean adults and its association with insulin resistance. Methods We investigated 160 non-diabetic subjects from a community-based diabetes survey conducted in Yonchon County, Korea in 1993. We extracted the DNA from peripheral blood and examined the 16189 variant by polymerase chain reaction and restrictive enzyme digestion. We compared body mass index (BMI), blood pressure, fasting plasma glucose, 2-h plasma glucose after 75 g glucose load, fasting insulin, cholesterol, and homeostasis model assessment of insulin resistance and beta-cell function between the subjects with 16189 variant and wild type. Results The prevalence of the 16189 variant in Korean adults was 28.8% (46 of 160). Subjects with the 16189 variant had higher fasting glucose and BMI than those with wild type, but fasting insulin, homeostasis model assessment of insulin resistance and beta-cell function, cholesterol, and blood pressure were not different between two groups. Conclusion Our results provide evidence for an association of a frequent mitochondrial polymorphism with higher fasting glucose and the risk factors of diabetes mellitus.
引用
收藏
页码:681 / 684
页数:4
相关论文
共 18 条
[1]
MITOCHONDRIAL-DNA DIVERSITY IN THE KUNA AMERINDS OF PANAMA [J].
BATISTA, O ;
KOLMAN, CJ ;
BERMINGHAM, E .
HUMAN MOLECULAR GENETICS, 1995, 4 (05) :921-929
[2]
Mitochondrial 16189 variant, thinness at birth, and type-2 diabetes [J].
Casteels, K ;
Ong, K ;
Phillips, D ;
Bendall, H ;
Pembrey, M ;
Poulton, J ;
Dunger, D .
LANCET, 1999, 353 (9163) :1499-1500
[3]
MITOCHONDRIAL DIABETES-MELLITUS - A REVIEW [J].
GERBITZ, KD ;
VANDENOUWELAND, JMW ;
MAASSEN, JA ;
JAKSCH, M .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 1995, 1271 (01) :253-260
[4]
HORAI S, 1990, AM J HUM GENET, V46, P828
[5]
A SUBTYPE OF DIABETES-MELLITUS ASSOCIATED WITH A MUTATION OF MITOCHONDRIAL-DNA [J].
KADOWAKI, T ;
KADOWAKI, H ;
MORI, Y ;
TOBE, K ;
SAKUTA, R ;
SUZUKI, Y ;
TANABE, Y ;
SAKURA, H ;
AWATA, T ;
GOTO, Y ;
HAYAKAWA, T ;
MATSUOKA, K ;
KAWAMORI, R ;
KAMADA, T ;
HORAI, S ;
NONAKA, I ;
HAGURA, R ;
AKANUMA, Y ;
YAZAKI, Y .
NEW ENGLAND JOURNAL OF MEDICINE, 1994, 330 (14) :962-968
[6]
A RAPID NONENZYMATIC METHOD FOR THE PREPARATION OF HMW DNA FROM BLOOD FOR RFLP STUDIES [J].
LAHIRI, DK ;
NURNBERGER, JI .
NUCLEIC ACIDS RESEARCH, 1991, 19 (19) :5444-5444
[7]
Decreased mitochondrial DNA content in peripheral blood precedes the development of non-insulin-dependent diabetes mellitus [J].
Lee, HK ;
Song, JH ;
Shin, CS ;
Park, DJ ;
Park, KS ;
Lee, KU ;
Koh, CS .
DIABETES RESEARCH AND CLINICAL PRACTICE, 1998, 42 (03) :161-167
[8]
Maassen JA, 1996, DIABETOLOGIA, V39, P375
[9]
Do sequence variants in the major non-coding region of the mitochondrial genome influence mitochondrial mutations associated with disease? [J].
Marchington, DR ;
Poulton, J ;
Sellar, A ;
Holt, IJ .
HUMAN MOLECULAR GENETICS, 1996, 5 (04) :473-479
[10]
HOMEOSTASIS MODEL ASSESSMENT - INSULIN RESISTANCE AND BETA-CELL FUNCTION FROM FASTING PLASMA-GLUCOSE AND INSULIN CONCENTRATIONS IN MAN [J].
MATTHEWS, DR ;
HOSKER, JP ;
RUDENSKI, AS ;
NAYLOR, BA ;
TREACHER, DF ;
TURNER, RC .
DIABETOLOGIA, 1985, 28 (07) :412-419