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The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 5 1801-1804
Copyright © 2000 by The Endocrine Society

Original Studies

Significance of Pro12Ala Mutation in Peroxisome Proliferator-Activated Receptor-{gamma}2 in Korean Diabetic and Obese Subjects1

Eun Young Oh, Kyeong Min Min, Jae Hoon Chung, Yong-Ki Min, Myung-Shik Lee, Kwang-Won Kim and Moon-Kyu Lee

Division of Endocrinology and Metabolism, Department of Medicine, Samsung Medical Center, and Samsung Biomedical Research Institute (K.M.M.), Sungkyunkwan University School of Medicine, Seoul, Korea

Address all correspondence and requests for reprints to: Dr. Moon-Kyu Lee, Division of Endocrinology and Metabolism, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 135-710, Korea.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Peroxisome proliferator-activated receptors (PPARs) are a nuclear hormone receptor superfamily of ligand-activated transcription factors, and the PPAR{gamma} subtype regulates adipocyte differentiation, lipid metabolism, and insulin sensitivity. There have been several reports on the relationship between the PPAR{gamma}2 Pro12Ala genotype and obesity or diabetes in Caucasians. The objective of this study was to examine the relationship between this mutation and obesity or diabetes in Korean subjects. Two hundred and twenty-nine Korean subjects, including 111 obese subjects (body mass index, >25 kg/m2) were included in this study. One hundred and eleven subjects had normal glucose tolerance, 60 had impaired glucose tolerance, and 58 had diabetes mellitus. We evaluated these subjects for the Pro12Ala mutation in the PPAR{gamma} gene using PCR-restriction fragment length polymorphism. Allele frequencies of the Pro12Ala missense mutation of PPAR{gamma}2 were not different among Korean subjects with normal glucose tolerance (qAla = 0.045), those with impaired glucose tolerance (qAla = 0.033), and those with diabetes mellitus (qAla = 0.043; P > 0.05). Allele frequencies of PPAR{gamma}2 Ala in obese subjects (qAla = 0.036) were not significantly different from those in nonobese subjects (qAla = 0.047). These results suggest that the Pro12Ala mutation in PPAR{gamma} is not associated with either diabetes or obesity and may not be an important determinant of obesity or diabetes in Korean subjects.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
OBESITY IS A complex metabolic disorder with strong genetic influence (1). The search for candidate genes for obesity has been active, and candidate genes may be involved in forming both structural and regulatory proteins from various tissues (2, 3). However, the exact genes have not been identified. Peroxisome proliferator-activated receptors (PPARs) are a nuclear hormone receptor superfamily of ligand-activated transcription factors and consist of three subtypes: PPAR{alpha}, PPAR{delta}, and PPAR{gamma} (4). PPAR{gamma} has a higher affinity for fat-specific peroxisome proliferator response elements (PPREs) than PPAR{alpha} or PPAR{delta} (4). It has been shown to play an important role in adipocyte differentiation and to regulate lipid metabolism and insulin sensitivity (4, 5). Two isoforms, PPAR{gamma}1 and PPAR{gamma}2, are constituted by use of alternative promoters and differential splicing of the same gene (6, 7). Human PPAR{gamma}2 has 28 additional amino acids at its amino-terminus compared to PPAR{gamma}1 and is expressed almost exclusively in adipose tissue, whereas PPAR{gamma}1 is expressed in various tissues (6, 7). There is an evidence to suggest that the endogenous ligands for PPAR{gamma} are fatty acids and PG derivatives (5, 6, 8). It is also the target molecule for thiazolidinediones, the agents that stimulate adipocyte differentiation and enhance sensitivity to insulin in vitro (9). Thiazolidinediones result in significant reductions in both blood glucose and lipid levels in noninsulin-dependent diabetes mellitus (NIDDM) animal models, and their antidiabetic effects are proportional to their binding affinity for PPAR{gamma} (10). They also reduced the insulin resistance in nondiabetic animals and humans (11, 12). Thiazolidinediones improve insulin sensitivity and decrease hypertriglyceridemia in human NIDDM subjects (13). Therefore, it is suggested that PPAR{gamma} play an important role in lipid and energy metabolism. Recently, there have been several reports on the relationship between the PPAR{gamma}2 Pro12Ala genotype and obesity or diabetes in Caucasian subjects; however, debates on the relationship have also been reported (14, 15, 16, 17). To our knowledge, however, this relationship has not been addressed in Asians, especially Oriental subjects. The paucity of data on the Pro12Ala mutation in the Asian population led us to study the relationship between the Pro12Ala missense mutation of PPAR{gamma}2 and obesity or type 2 diabetes in Korean subjects. Compared to Caucasians, most of the Korean NIDDM subjects are nonobese (18). In this study we examined whether the Pro12Ala mutation of the PPAR{gamma}2 is associated with diabetes mellitus or obesity in Korean subjects.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Subjects

We studied 229 Korean subjects, including 111 obese subjects (defined as those with body mass index of >25 kg/m2). The obese group consisted of 50 women and 61 men, with a mean (±SD) body mass index of 29.4 ± 4.6 kg/m2 and a mean age of 46.3 ± 13.9 yr. The nonobese group were 33 women and 85 men, with a mean (±SD) body mass index of 22.8 ± 1.8 kg/m2 and a mean age of 49.5 ± 11.3 yr. On the basis of WHO criteria for oral glucose tolerance testing, 111 subjects had normal glucose tolerance, 60 had impaired glucose tolerance, and 58 had diabetes mellitus. The normal glucose tolerance group consisted of 42 women and 69 men, with a mean (±SD) body mass index of 26.8 ± 5.1 kg/m2 and a mean age of 45.2 ± 12.9 yr. The impaired glucose tolerance group comprised 17 women and 43 men with a mean (±SD) body mass index of 25.5 ± 4.3 kg/m2 and a mean age of 50.5 ± 13.4 yr. The diabetes group comprised 24 women and 34 men with a mean (±SD) body mass index of 24.9 ± 4.4 kg/m2 and a mean age of 50.5 ± 10.5 yr.

Blood pressure, waist to hip ratio, percent body fat, body weight, height, and body mass index were measured, and serum total, high density lipoprotein, and low density lipoprotein cholesterol and tri-glycerides were measured with an autoanalyzer (Hitachi, Tokyo, Japan). Fasting serum insulin and C peptide concentrations were measured by immunoradiometric assay.

Methods

The genomic DNAs of 229 subjects were isolated from peripheral blood leukocytes and amplified by PCR using a sense primer (5'-GCCAATTCAAGCCCAGTC-3') and an antisense primer (5'-GATATGTTTGCAGACAGTGTATCAGTGAAGGAATCGCTTTCCG-3') that flank the region containing the 12-amino acid site of PPAR{gamma}2 (14). Use of these primers gave a PCR product of 270 bp. The PCR conditions were an initial denaturation step at 95 C for 5 min, followed by 30 cycles of denaturation at 95 C for 1 min, annealing at 56 C for 1 min, and extension at 72 C for 1 min, with a final extension of 10 min at 72 C. BstU-I digests CG-CG only when the C->G substitution at nucleotide 34 is present. The PCR products were digested with BstU-I at 60 C for 60 min, electrophoresed on a 2.5% agarose gel, and stained with ethidium bromide. The expected products after digestion with BstU-I were 270 bp for normal homozygotes, 227 and 43 bp for Pro12Ala homozygotes, and 270, 227, and 43 bp for heterozygotes (Fig. 1Go).



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  		Figure 1. PCR-restriction fragment length polymorphism detection of the Pro12Ala PPAR{gamma}2 missense mutation. PCR followed by digestion with BstU-1–2.5% agarose gel electrophoresis followed by ethidium bromide staining and UV transillumination was performed. The expected product sizes are: normal homozygote, 270 bp; Pro12Ala homozygote, 227 and 43 bp; and Pro12Ala heterozygote, 270, 227, and 43 bp, respectively. Lane 1, Molecular marker; lane 2, normal homozygote; lane 3, Pro12Ala homozygote; lane 4, Pro12Ala heterozygote. The 43-bp fragments are not visualized.

 
Statistical analyses

Statistical analyses were performed using the SPSS/PC+ software program (SPSS, Inc., Evanston, IL). The frequency of mutations in the obese subjects was compared with that in nonobese subjects by two-tailed Fisher’s exact test, and the laboratory data were compared by Mann-Whitney U test.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
The overall allele frequency of PPAR{gamma}2 Ala was 0.041. The frequency included 1 homozygous mutant and 17 heterozygous mutants among 229 Korean subjects (Table 1Go). There was no significant difference in body mass index, percent body fat, waist to hip ratio, blood pressure, total cholesterol, triglycerides, high or low denisty lipoprotein cholesterol, fasting serum insulin, or C peptide concentrations between the two different PPAR{gamma} genotypes (Table 1Go).


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  		Table 1. Characteristics of patients according to PPAR{gamma}2 genotype

 
The allele frequencies of the Pro12Ala missense mutation of PPAR{gamma}2 were not different among Korean subjects with normal glucose tolerance (qAla = 0.045), those with impaired glucose tolerance (qAla = 0.033), and those with diabetes mellitus (qAla = 0.043; P > 0.05; Table 2Go). The allele frequencies of PPAR{gamma}2 Ala in obese subjects (qAla = 0.036) were not significantly different from those in nonobese subjects (qAla = 0.047; Table 3Go). The allele frequencies of PPAR{gamma}2 Ala in men tended to be higher than those in women, but there was no statistical significance.


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  		Table 2. PPAR{gamma}2 genotype frequencies according to glucose tolerance

 

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  		Table 3. PPAR{gamma}2 genotype frequencies in obese and nonobese subjects

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
Obesity is a well established risk factor for a number of chronic diseases, including type 2 diabetes mellitus, hypertension, cardiovascular disease, and hyperlipidemia. Both type 2 diabetes mellitus and obesity are probably caused by complex interactions between a variety of genetic and environmental factors (1). Several recent advances have been made on the molecular control of adipogenesis and adipocyte-specific gene expression (3). In 1990, the first PPAR was described by Isselmann and Green, who have shown that it was activated by peroxisome proliferators, hence the term PPAR (19). Since then, the search for the functions of these receptors has been performed eagerly. In 1994, Tontonoz et al. demonstrated that PPAR{gamma}, when expressed and activated in fibroblasts, efficiently stimulates the expression of adipocyte-specific genes and induces adipocyte differentiation (7, 20). Yen et al. reported a study on a molecular scanning of the PPAR{gamma} gene in diabetic Caucasians and identified a missense mutation in the PPAR{gamma}2 isoform involving a C->G substitution at nucleotide 34 that resulted in the exchange of a proline for an alanine in position 12 of the PPAR{gamma}2 protein (14). They also reported a significant association between this mutation and type 2 diabetes in a small group of Caucasian patients (14). Beamer et al. demonstrated that the Pro12Ala missense mutation in the PPAR{gamma}2 gene is associated with higher body mass index and body weight and suggested that the genetic variation at the PPAR{gamma} locus may influence susceptibility to obesity in humans (15). Ringel et al., however, reported that there is no significant relationship between this mutation and diabetes in a large group of Caucasian patients (16). We found no significant association between the PPAR{gamma} Pro12Ala genotype and diabetes mellitus, and the PPAR{gamma} genotype was not related to obesity, hypertension, dyslipidemia, or serum insulin levels. Beamer et al. (15) showed no significant association between the Pro12Ala mutation of the PPAR{gamma}2 gene and fasting serum insulin or glucose levels, although there has been a report that PPAR{gamma} messenger ribonucleic acid is elevated in direct relation to body mass index and fasting insulinemia in skeletal muscle and adipose tissue of obese subjects (21, 22). Despite the statistically insignificant associations, there still is a possibility that the PPAR{gamma} mutation has only a small effect on obesity and/or diabetes. The small effect might become a significant influence if other gene mutations or environmental factors occurred at the same time. This possibility should be explored further in future studies. Our study also showed that the allele frequency of Ala PPAR{gamma}2 is 0.041 in Korean subjects. The frequency is quite different from that in Caucasian subjects [P < 0.05 vs. 0.14 in the study by Ringel et al. (16)]. This might be an ethnic difference and needs to be further clarified in other races (14). In summary, the Pro12Ala mutation of the PPAR{gamma} gene may not be associated with diabetes mellitus, obesity, or related disorders in Korean subjects.


   Footnotes
 
1 This work was supported by a grant from Samsung Biomedical Research Institute (SBRI C-98–008) Back

Received October 7, 1999.

Revised December 1, 1999.

Accepted December 15, 1999.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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  3. Spiegelman BM, Flier JS. 1996 Adipogenesis and obesity: rounding out the big picture. Cell. 87:377–389.[CrossRef][Medline]
  4. Brun RP, Tontonoz P, Forman BM, Ellis R, Chen J, Evans RM, Spiegelman BM. 1996 Differential activation of adipogenesis by multiple PPAR isoforms. Genes Dev. 10:974–984.[Abstract/Free Full Text]
  5. Latruffe N, Vamecq J. 1997 Peroxisome proliferators and peroxisome proliferator activated receptors (PPARs) as regulators for lipid metabolism. Biochimie. 79:81–94.[Medline]
  6. Elbrecht A, Chen Y, Cullinan CA, Hayes N, Leibowitz MD, Moller DE, Berger J. 1996 Molecular cloning, expression and characterization of human peroxisome proliferator activated receptor {gamma}1 and {gamma}2. Biochem Biophys Res Commun. 224:431–437.[CrossRef][Medline]
  7. Tontonoz P, Hu E, Graves RA, Budavari AI, Spiegelman BM. 1994 mPPAR{gamma}2: tissue-specific regulator of an adipocyte enhancer. Genes Dev. 8:1224–1234.[Abstract/Free Full Text]
  8. Kliewer SA, Lenhard JM, Willson TM, Patel I, Morris DC, Lehmann JM. 1995 A prostaglandin J2 metabolite binds peroxisome proliferator-activated receptor {gamma} and promotes adipocyte differentiation. Cell. 83:813–819.[CrossRef][Medline]
  9. Lehmann JM, Moore LB, Smith-Oliver TA, Wilkison WO, Willson TM, Kliewer SA. 1995 An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-activated receptor{gamma} (PPAR{gamma}). J Biol Chem. 270:12953–12956.[Abstract/Free Full Text]
  10. Berger J, Bailey P, Biswas C, et al. 1996 Thiazolidinediones produce a conformational change in peroxisomal proliferator-activated receptor-{gamma}: binding and activation correlate with antidiabetic actions in db/db mice. Endocrinology. 137:4189–4195.[Abstract]
  11. Lee M-K, Miles PD, Khoursheed M, Gao K-M, Moossa AR, Olefsky JM. 1994 Metabolic effects of troglitazone on fructose-induced insulin resistance in the rat. Diabetes. 43:1435–1439.[Abstract]
  12. Nolan JJ, Ludvik B, Beerdsen P, Joyce M, Olefsky J. 1994 Improvement in glucose tolerance and insulin resistance in obese subjects treated with troglitazone. N Engl J Med. 331:1188–1193.[Abstract/Free Full Text]
  13. Iwamoto Y, Kosaka K, Kuzuya T, Akanuma Y, Shigeta Y, Kaneko T. 1996 Effects of troglitazone: a new hypoglycemic agent in patients with NIDDM poorly controlled by diet therapy. Diabetes Care. 19:151–156.[Abstract]
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