Indian Journal of Human Genetics
Home Current Issue Archives Guidelines Subscriptions e-Alerts Login 
Users online: 127
Print this page  Email this page Small font sizeDefault font sizeIncrease font size

Year : 2008  |  Volume : 14  |  Issue : 3  |  Page : 87-91

Apolipoprotein E gene polymorphism and dyslipidaemia in adult Asian Indians: A population based study from calcutta, India

1 Post Graduate Department of Anthropology, Sree Chaitanya College, Habra, West Bengal, India
2 Human Genetic Engineering Research Centre, Calcutta, India
3 Department of Anthropology, Biomedical Research Laboratory, Visva Bharati University, Santiniketan, West Bengal, India

Correspondence Address:
Arnab Ghosh
Department of Anthropology, Biomedical Research Laboratory, Palli Charcha Kendra, Visva Bharati University, Sriniketan-731 236, West Bengal
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-6866.45000

Rights and Permissions



Aim : The study was aimed to determine the association of Apolipoprotein E (apo E) gene polymorphisms on lipid levels in Asian Indian population.
Methods : A total of 350 (184 males and 166 females) adult (30 years and above) Asian Indians of Calcutta and suburb participated in the study. Anthropometric measures, lipids profiles, and blood glucose measures were collected. Out of 350 subjects, a sample of 70 individuals was selected randomly for genotyping after adjusting for age and sex. The apo E gene polymorphisms were determined by agarose gel electrophoresis.
Results : The apo E polymorphism showed significant association with dyslipidaemia (P=0.0135) with e3/4 combination has had the highest occurrence of dyslipidaemia and metabolic syndrome (MS) followed by ε4/4 <ε3/3 <ε2/4 <ε2/3 in decreasing order.
Conclusions : The ε4 allele of apo E gene independent of other risk factors is associated with dyslipidaemia in particular with low HDLc and high TC: HDLc ratio.

Keywords: Apo E polymorphism, Asian Indians, dyslipidaemia, metabolic, syndrome, obesity

How to cite this article:
Das M, Pal S, Ghosh A. Apolipoprotein E gene polymorphism and dyslipidaemia in adult Asian Indians: A population based study from calcutta, India. Indian J Hum Genet 2008;14:87-91

How to cite this URL:
Das M, Pal S, Ghosh A. Apolipoprotein E gene polymorphism and dyslipidaemia in adult Asian Indians: A population based study from calcutta, India. Indian J Hum Genet [serial online] 2008 [cited 2017 Feb 28];14:87-91. Available from:

   Introduction Top

Apolipoprotein E (apoE) plays a key role in the metabolism of cholesterol and triglyceride by serving as a receptor binding ligand mediating the clearance of chylomicron and remnants of very low-density lipoprotein cholesterol from plasma. [1],[2],[3],[4] Three different apoE alleles (ε2, ε3, and ε4) on chromosome number 19 are responsible to encoding three different apo E isoform (apo E2, apo E3, and apo E4 respectively), resulting in six different genotypes (ε2/2, ε3/3, ε4/4, ε2/3, ε2/4, and ε3/4). [5],[6] It has been estimated that apo E polymorphisms may account for 2-16% of the variability of LDL cholesterol levels, a contribution incomparable with any other gene in the general population. [2],[3] Compared with ε3 homozygotes, carriers of the ε2 allele, which has defective receptor-binding ability, have lower circulating cholesterol levels and higher triglyceride levels, whereas carriers of the ε4 allele appear to have higher plasma levels of total and low-density lipoprotein cholesterol. [1] Since the first demonstration of apoE gene polymorphism on dysbetalipoproteinemia, [7] numerous studies have investigated the relation between apoE genotypes and coronary heart disease (CHD). [7],[8],[9] Recent evidence also indicates that apoE may play additional role in the development of CHD. [2],[10],[11],[12],[13]

Globally, the apoE locus shows substantial allelic variation with ranges 0-20% for ε2, 60-90% for ε3 and 10-20% for ε4 alleles [14],[15],[16],[17],[18] with some exception. In Asian Indians, studies have investigated the allele frequencies with ranges 0.031-0.094 for ε2; 0.803-0.968 for ε3 and 0.000-0.133 for ε4. [19] Frequency of apoE ε3 allele was found to be high (0.913) in people of north India. [17] In another study on Asian Indians, individuals with at least a e4 allele were considered at risk to develop premature Myocardial Infarction (MI), independent of other risk conventional risk factors. [20] Most of these studies are either from the north, west, central, and southern part of India. [15],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32] Studies from eastern part of India are lacking. The present study is an attempt to investigate the apo E gene polymorphism and its association with dyslipidemmia in people belongs to the eastern part of India.

   Materials and Methods Top

Study population

The data were collected from adult men and women aged 30 years and above from Calcutta and suburb. A total of 350 individuals (184 males and 166 females) participated in the study. Prior to participation, public advertisement was given about the study with the help of the council officials. An arbitrary list was made to conduct the study. Individuals were selected randomly after their response through local advertisement. The response rate was quite high (~85%). The institute ethical committee has had approved the study. Written consent was obtained from participants prior to actual commencement of the study.

Anthropometric measurements

Anthropometric variables namely height, weight, circumference of waist (WC) and hip were taken using standard techniques. [33] Height was measured to nearest 0.1 cm with a standard anthropometer and weight to the nearest 0.5 kg with a portable weighing machine in light clothing. Waist and hip circumferences were measured to the nearest 0.1 cm using non-elastic tape. The body mass index (BMI in kg/m 2 ) and waist-hip ratio (WHR) was calculated accordingly.

Biochemical estimations

A 7 ml of venous blood was drawn from each individual after an overnight fast of ≥12 h for estimation of metabolic variables. Lipids profile namely the total cholesterol (TC), triglycerides (TG), high density lipoprotein cholesterol (HDLc), low density lipoprotein cholesterol (LDLc), and very low density lipoprotein cholesterol (VLDLc) were taken into consideration. Values of LDLc were estimated using standard formula (LDLc= TC - (HDLc + TG/5)) and VLDLc as TG/5 provided TG was <400 mg/dl. Otherwise, TG was estimated directly. Fasting (FBG), post prandial blood glucose (PPBG) (2 h after meal) and TC: HDLc ratio was also considered. All biochemical analyses were done at the 'Human Genetic Engineering Research Center (HGERC), Calcutta and were measured in mg/dl (mg %) unit. Subjects with one or more of the followings were considered as dyslipidaemic (post entry): TC ≥ 240 mg/dl; [34] TG ≥ 200 mg/dl; [35] and TC: HDLc ratio ≥ 4.4. [36]


DNA was extracted from blood using QI Aamp Kit (QIAGEN, Germany). Apo E isoforms were amplified by polymerase chain reaction with a thermal cycler (Bio Rad, USA) and specific oligonucleotides as described. [37] The amplified fragments were digested with the enzyme HhaI overnight at 37C and separated on a 4% agarose (Promega, USA) gel electrophoresis with ethidium bromide staining and visualized under UV spectrophotometer.

Statistical analyses

Descriptive statistics such mean and standard deviation (SD) of anthropometric and biochemical measures was calculated by sex and the sex differences for these variables were calculated using unpaired t test. Differences in genotype frequency were examined by χ2 analyses. Analysis of variance (ANOVA) was undertaken to see the differences of obesity and metabolic variables across the apo E genotypes.

All statistical analyses were computed using the SPSS (PC + version10.0). [38] A P value of <0.05 (two tailed) was considered as significant.

   Results Top

The mean and SD (unadjusted for age) of anthropometric, lipids profile and blood glucose variables by sexes are presented in [Table 1]. There existed no significant sex differences for variables except for age, TC and FBG. Since, age differed significantly, age and sex matched 70 subjects were selected randomly to study the association of apo E polymorphism and dyslipidaemia.

The distribution of risk variables by apo E genotypes are presented in [Table 2]. It was observed that ε3/4 individuals have relatively higher mean value for BMI, WC, TC, LDLc, low HDLc, and TC: HDLc ratio as compared to rest of the genotypes. Homozygous for ε4 allele on contrary have had relatively higher TG value whereas, individual homozygous for ε3 allele have had relatively higher FBG and PPBG compared to other groups. One way ANOVA revealed significant difference across the groups for HDLc (P=0.039) and TC: HDLc ratios (P=0.013) only. Individuals heterozygous for ε3/4 alleles have had lowest average HDLc and highest TC: HDLc ratio followed by ε4/4 individuals and ε3/3 individuals. The allele frequencies are as follows: ε2 = 0.100; ε3 = 0.771, and ε4 = 0.129 and the genotype frequencies are: γ2/3 = 0.171; ε2/4 = 0.029; ε3/4 = 0.114; ε3/3 = 0.629, and ε4/4 = 0.057 (not shown in Tables).

The incidence of dyslipidaemia by apo E genotypes is presented in [Table 3]. The Chi-square revealed significant (P=0.0135) group differences in incidence of dyslipidaemia by genotypes. Incidence percentage of dyslipidaemia is shown in [Figure 1]. The incidence is 25% for ε2/3, 75% for ε3/4, 63.64% for ε3/3 and 100% for ε4/4 genotypes.

   Discussion Top

The present investigation was aimed to examine whether significant association does exist between apo E gene polymorphism and dyslipidaemia in adult Asian Indians living in the eastern part of India. Previous studies from other parts of India have had reported the allele frequencies ranges from 0.031 to 0.094 for ε2; 0.803-0.968 for ε3, and 0.000-0.133 for ε4. The present study from Eastern India have had shown an almost similar frequency of ε4 allele. It has been found that individuals with ε3/4 combination as well as homozygous for e4 allele (e4/4) have significantly higher occurrence of dyslipidaemia compare to other genotypes combinations. The occurrence of dyslipidaemia as found in the study could be summarized in the following way (decreasing order): ε3/4 < ε4/4 < ε3/3< ε2/4< ε2/3. In a similar study on Omani dyslipidaemic patients, it was observed that thirty-one percent of patients with CHD had the APOE*4 allele compared to 26% with the APOE*3 allele, but this difference was not significant. [39] In another study, it was observed that the prevalence of the e4-containing phenotypes were significantly higher in ischemic patients and that apo ε4 is an independent risk factor associated with an altered lipid profiles. [40] In the Ouro Preto admixed population in Brazil, it demonstrated that the presence of APOE*2 can confer a protective effect, whereas the presence of APOE*4 implies an enhanced risk for dyslipidemia. [41]

The major limitation of the study was that it was performed on a small sample size and therefore is not representative of Asian Indian population. Owing to ethnic and cultural heterogeneity in Asian Indian population, it is imperative to study the ethnic groups collectively, possibly through collaborative research. This will give more insight into proper understanding of the association lying between apo E gene polymorphisms and dyslipidaemia among Asian Indians.

   Conclusion Top

It seems that the allele frequency of e4 is quite high in the present studied population as compare to most of the other parts of India. Prevalence of dyslipidaemia is significantly high among individuals with ε3/4 and ε4/4 genotypes compare to other combinations. It seems reasonable to argue that ε4 allele has an independent effect on lipids metabolism particularly increased TC: HDLc ratio causing dyslipidaemia in the study population.

   Acknowledgments Top

Authors are thankful to Bodhisattva Pal of Human Genetic Engineering Research Centre (HGERC), Calcutta for providing logistic support to conduct this work. Authors are also indebted to all the subjects participated in the study.

   References Top

1.Dallongeville J, Lussier-Cacan S, Davignon J. Modulation of plasma triglyceride levels by apoE phenotype: A meta-analysis. J Lipid Res 1992;33:447-54.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Davignon J, Cohn JS, Mabile L, Bernier L. Apolipoprotein E and atherosclerosis: Insight from animal and human studies. Clin Chim Acta 1999;286:115-43.  Back to cited text no. 2    
3.Eichner JE, Dunn ST, Perveen G, Thompson DM, Stewart KE, Stroehla BC. Apolipoprotein E polymorphism and cardiovascular disease: A HuGE review. Am J Epidemiol 2002;155:487-95.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Ordovas JM, Schaefer EJ. Genetic determinants of plasma lipid response to dietary intervention: The role of the APOA1/C3/A4 gene cluster and the APOE gene. Br J Nutr 2000;83:S127-36.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Paik YK, Chang CA, Reardon GE, Davies GE, Mahley RW, Taylor JM. Nucleotide sequence and structure of the human apolipoprotein E gene. Proc Natl Acad Sci USA 1985;82:3445-9.  Back to cited text no. 5    
6.Das HK, McPherson J, Bruns GA, Karathanasis SK, Breslow JL. Isolation, characterization and mapping to chromosome 19 of the human apolipoprotein E gene. J Biol Chem 1985;260:6240-7.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Utermann G, Hees M, Steinmetz A. Polymorphism of apolipoprotein E and occurrence of dysbetalipoproteinaemia in man. Nature 1977;269:604-7.  Back to cited text no. 7  [PUBMED]  
8.Eichner JE, Kuller LH, Orchard TJ, Grandits GA, McCallum LM, Ferrell RE, et al. Relation of apolipoprotein E phenotype to myocardial infarction and mortality from coronary artery disease. Am J Cardiol 1993;71:160-5.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Moghadasian MH, McManus BM, Nguyen LB, Shefer S, Nadji M, Godin DV, et al. Pathophysiology of apolipoprotein E deficiency in mice: Relevance to apo E-related disorders in humans. FASEB J 2001;15:2623-30.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Stannard AK, Riddell DR, Sacre SM, Tagalakis AD, Langer C, von Eckardstein A, et al. Cell-derived apolipoprotein (ApoE) particles inhibit vascular cell adhesion molecule-I (VCAM-I) expression in human endothelial cells. J Biol Chem 2001;276:46011-6.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.van Bockxmeer FM, Mamotte CD. Apolipoprotein epsilon 4 homozygosity in young men with coronary heart disease. Lancet 1992;340:879-80.  Back to cited text no. 11  [PUBMED]  
12.Stengard J, Pekkanen HJ, Ehnholm A, Nissinen A, Sing CF. Genotypes with the apolipoprotein epsilon-4 allele are predictors of coronary heart disease mortality in a longitudinal study of elderly Finnish men. Hum Genet 1996;97:677-84.  Back to cited text no. 12    
13.Song Y, Stampfer MJ, Liu S. Meta-analysis: Apolipoprotein E genotypes and risk for coronary heart disease. Ann Intern Med 2004;141:137-47.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Gerdes LU, Gerdes C, Hansen PS, Klausen IC, Faergeman O, Dyerberg J. The apolipoprotein E polymorphism in Greenland Inuit in its global perspective. Hum Genet 1996;98:546-50.  Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Mastana SS, Calderon R, Pena J, Reddy PH, Papiha SS. Anthropology of apolipoprotein E (apoE) gene: Low frequency of apoE4 allele in Basques and in tribal (Baiga) populations of India. Ann Hum Biol 1998;25:137-43.  Back to cited text no. 15  [PUBMED]  
16.Corbo RM, Scacchi R. Apolipoprotein (ApoE) allele distribution in the world: Is APOE*4 a thrifty allele? Ann Hum Genet 1999;63:301-10.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Singh PP, Singh M, Gerdes U, Mastana SS. Apolipoprotein E polymorphism in India: High APOE*E3 allele frequency in Ramgarhia of Punjab. Anthrop Anz 2001;59:27-34.  Back to cited text no. 17    
18.Singh PP, Singh M, Mastana SS. Genetic variation of apolipoprotein in North India. Hum Biol 2002;74:673-82.  Back to cited text no. 18  [PUBMED]  
19.Singh PP, Singh M, Mastana SS. APOE distribution in world populations with new data from Indian and the UK. Ann Hum Biol 2006;33:279-308.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]
20.Kumar P, Luthra K, Dwivedi M, Behl VK, Pandey RM, Misra A. Apolipoprotein E gene polymorphisms in patients with premature myocardial infarction: A case-controlled study in Asian Indians in North India. Ann Clin Biochem 2003;40:382-7.  Back to cited text no. 20  [PUBMED]  [FULLTEXT]
21.Mastana SS, Reddy PH, Das MK, Reddy P, Das K. Molecular genetic diversity in 5 populations of Madhya Pradesh, India. Hum Biol 2000;72:499-510.  Back to cited text no. 21  [PUBMED]  
22.Thelma BK, Juyal RC, Dodge HH, Pandav R, Chandra V, Ganguli M. APOE polymorphism in a rural older population-based sample in India. Hum Biol 2001;73:134-44.  Back to cited text no. 22    
23.Inamdar PA, Kelkar SM, Devasagayam TP, Bapat MM. Apolipoprotein E polymorphism in non-insulin-dependent diabetics of Mumbai, India and its effect on plasma and lipoproteins. Diabetes Res Clin Pract 2000;47:217-23.  Back to cited text no. 23  [PUBMED]  [FULLTEXT]
24.Das K, Das MK, Mastana SS. Genetic diversity of serum proteins in three subpopulations of the Maria Gond tribe of Madhya Pradesh, India. Anthropol Anz 2006;61:261-8.  Back to cited text no. 24    
25.Luthra K, Bhargav B, Chhabra S, Das N, Misra A, Agarwal DP, et al. Apolipoprotein E polymorphism in Northern Indian patients with coronary heart disease: Phenotype distribution and relation to serum lipids and lipoproteins. Mol Cell Biochem 2002;232:97-102.  Back to cited text no. 25    
26.Chhabra S, Agarwal DP, Vasisht S, Luthra K, Narang R, Manchanda SC, et al. Study of apolipoprotein E polymorphism in normal healthy controls from northern India. Dis Markers 2000;16:159-61.  Back to cited text no. 26  [PUBMED]  [FULLTEXT]
27.Srivastava N, Achyut BR, Prakash J, Agarwal CG, Pant DC, Mittal B. Association of cholesteryl ester transfer protein (TaqIB) and apolipoprotein E (HhaI) gene variants with obesity. Mol Cell Biochem 2008;314:171-7.  Back to cited text no. 27  [PUBMED]  [FULLTEXT]
28.Rai TS, Khullar M, Sehrawat BS, Ahuja M, Sharma PK, Vijayvergiya R, et al. Synergistic effect between apolipoprotein E and apolipoprotein A1 gene polymorphisms in the risk for coronary artery disease. Mol Cell Biochem 2008;313:139-46.  Back to cited text no. 28  [PUBMED]  [FULLTEXT]
29.Singh PP, Singh M, Bhatnagar DP, Kaur TP, Gaur SK. Apolipoprotein E polymorphism and its relation to plasma lipids in coronary heart disease. Indian J Med Sci 2008;62:105-12.  Back to cited text no. 29  [PUBMED]  Medknow Journal
30.Singh PP, Naz I, Gilmour A, Singh M, Mastana S. Association of APOE (HhaI) and ACE (I/D) gene polymorphisms with type 2 diabetes mellitus in North West India. Diabetes Res Clin Pract 2006;74:95-102.  Back to cited text no. 30  [PUBMED]  [FULLTEXT]
31.Ashavaid TF, Kondkar AA, Todur SP, Dherai AJ, Morey J, Raghavan R. Lipid, lipoprotein, apolipoprotein and lipoprotein(a) levels: Reference intervals in a healthy Indian population. J Atheroscler Thromb 2005;12:251-9.  Back to cited text no. 31  [PUBMED]  [FULLTEXT]
32.Dixit M, Bhattacharya S, Mittal B. Association of CETP TaqI and APOE polymorphisms with type II diabetes in North Indians: A case control study. BMC Endocr Disord 2005;1:5-7.  Back to cited text no. 32    
33.Lohman TG, Roche AF, Martorell R. Anthropometric standardization reference manual. Champaign, IL: Human Kinetics; 1988.  Back to cited text no. 33    
34.Deurenberg-Yap M, Chew SK, Lin VF, Tan BY, van Staveren WA, Deurenberg P. Relationships between indices of obesity and its comorbidities in multi-ethnic Singapore. Int J Obes Relat Disord 2001;25:1554-62.  Back to cited text no. 34    
35.Ho SC, Chen YM, Woo JL, Leung SS, Lam TH, Janus ED. Association between simple anthropometric indices and cardiovascular risk factors. Int J Obes Relat Metab Disord 2001;25:1689-97.  Back to cited text no. 35  [PUBMED]  [FULLTEXT]
36.Ghosh A. Comparison of anthropometric, metabolic and dietary fatty acids profiles in lean and obese dyslipidaemic Asian Indian subjects. Eu J Clin Nutr 2007;61:412-9.  Back to cited text no. 36    
37.Mailly F, Moll P, Kottke BA, Kamboh MI, Humphries SE, Ferrell RE. Estimation of the frequency of isoform-genotype discrepancies at the apolipoprotein E locus in heterozygotes for the isoforms. Genet Epidemiol 1992;9:239-48.  Back to cited text no. 37  [PUBMED]  
38.Das M, Pal S, Ghosh A. Rural urban differences of cardiovascular disease risk factors in adult Asian Indians. Am J Hum Biol 2008;20:440-5.   Back to cited text no. 38  [PUBMED]  [FULLTEXT]
39.Al-Yahyaee SA, Ganguly SS, Al Kindi MN, Al-Bahrani AI. Apolipoprotein E polymorphism in Omani dyslipidemic patients with and without coronary artery disease. Hum Biol 2007;79:93-102.   Back to cited text no. 39  [PUBMED]  
40.Saidi S, Slamia LB, Ammou SBnone , Mahjoub T, Almawi WY. Association of apolipoprotein E gene polymorphism with ischemic stroke involving large-vessel disease and its relation to serum lipid levels. J Stroke Cerebrovasc Dis 2007;16:160-6.  Back to cited text no. 40    
41.Mendes-Lana A, Pena GG, Freitas SN, Lima AA, Nicolato RL, Nascimento-Neto RM, et al. Apolipoprotein E polymorphism in Brazilian dyslipidemic individuals: Ouro Preto study. Braz J Med Biol Res 2007;40:49-56.  Back to cited text no. 41  [PUBMED]  [FULLTEXT]


  [Figure 1]

  [Table 1], [Table 2], [Table 3]

This article has been cited by
1 Genetics of coronary artery disease A clinician perspective
Manda V. Sasidhar,Satyajit Reddy,Ashutosh Naik,Sudhir Naik
Indian Heart Journal. 2014;
[Pubmed] | [DOI]
2 Relationship of apolipoprotein E polymorphism with lipid profiles in atherosclerotic coronary artery disease
Ibrahim Elmadbouh,Yasser Elghobashy,Eman Abd-Allah,Ahmad-Ashraf Reda,Adnan Fathe,Safaa Tayel,Tarek Abd-Elhakim
The Egyptian Heart Journal. 2013; 65(2): 71
[Pubmed] | [DOI]
3 Relationship of apolipoprotein E polymorphism with lipid profiles in atherosclerotic coronary artery disease
Elmadbouh, I. and Elghobashy, Y. and Abd-Allah, E. and Reda, A.-A. and Fathe, A. and Tayel, S. and Abd-Elhakim, T.
Egyptian Heart Journal. 2013; 65(2): 71-78
4 Inflammatory gene variants in the tsimane, an indigenous bolivian population with a high infectious load
Vasunilashorn, S. and Finch, C.E. and Crimmins, E.M. and Vikman, S.A. and Stieglitz, J. and Gurven, M. and Kaplan, H. and Allayee, H.
Biodemography and Social Biology. 2011; 57(1): 33-52
5 APOE, MTHFR, LDLR and ACE Polymorphisms Among Angami and Lotha Naga Populations of Nagaland, India
Benrithung Murry, Neikethono Vakha, Nongthombam Achoubi, M. P. Sachdeva, K. N. Saraswathy
Journal of Community Health. 2011;
[VIEW] | [DOI]
6 Different associations of apolipoprotein E polymorphism with metabolic syndrome by sex in an elderly Chinese population
Meng Hua Tao, Jian Wei Liu, Michael J. LaMonte, Jing Liu, Lei Wang, Yao He, Xiao Ying Li, Lu Ning Wang, Ling Ye
Metabolism. 2011;
[VIEW] | [DOI]
7 Factor analysis of risk variables associated with metabolic syndrome in adult Asian Indians
Das, M. and Pal, S. and Ghosh, A.
Journal of Cardiovascular Disease Research. 2010; 1(2): 86-91
8 Synergistic effects of ACE (I/D) and ApoE (HhaI) gene polymorphisms among the adult Asian Indians with and without metabolic syndrome
Das, M., Pal, S., Ghosh, A.
Diabetes Research and Clinical Practice. 2009; 86(3): e58-e61
9 Synergistic effects of ACE (I/D) and ApoE (HhaI) gene polymorphisms among the adult Asian Indians with and without metabolic syndrome
Mithun Das,Susil Pal,Arnab Ghosh
Diabetes Research and Clinical Practice. 2009; 86(3): e58
[Pubmed] | [DOI]


Print this article  Email this article
          Previous article         Next article


   Next article
   Previous article 
   Table of Contents
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Article in PDF (192 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  

    Materials and Me...
    Article Figures
    Article Tables

 Article Access Statistics
    PDF Downloaded218    
    Comments [Add]    
    Cited by others 9    

Recommend this journal