Resistin – 420 C/G polymorphism and serum resistin level in Iranian patients with gestational diabetes mellitus
© Takhshid and Zare; licensee BioMed Central. 2015
Received: 11 July 2014
Accepted: 21 April 2015
Published: 28 April 2015
Resistin is a circulating adipokine with insulin-antagonizing effects. The aim of this study was to investigate the relationship between the single nucleotide polymorphism (SNP) -420C > G in the resistin gene with serum resistin levels, insulin resistance, and risk of gestational diabetes (GDM) in Iranian population.
75 GDM patients and 70 healthy pregnant women were enrolled in this study. Genotyping for SNP- 420C > G in the resistin gene was performed by the polymerase chain reaction- restriction fragment length polymorphism (PCR-RFLP) method. Serum resistin and insulin were measured by immunoassay. Blood glucose levels and lipid profile were measured by enzymatic methods. Homeostasis model of assessment for insulin resistance (HOMA-IR) were calculated.
GG genotype and G allele of SNP-420C > G were more frequent in GDM patients compared to non-GDM subjects. Serum resistin level was similar in GDM and non-GDM patients. The serum levels of resistin in GDM and non-GDM women with GG genotype were similar to those with GC + CC genotype. Multivariate logistic regression analysis after adjusting for confounding factors showed a higher susceptibility to GDM in patients with GG genotype compared to subjects with GG + GT genotype (odds ratio = 4.59, 95% CI; 1.96-10.71, p = 0.00). Serum resistin level was correlated with serum triglyceride, total and low density lipoprotein (LDL) cholesterol (p < 0.05) in GDM patients. No significant association was found between serum resistin, insulin resistance, and SNP-420C > G.
The SNP-420C/G of resistin gene is associated with genetic susceptibility to GDM in our population. Further studies are necessary to confirm the role of this polymorphism in pathogenesis of GDM and to explore potential mechanisms by which it modulates susceptibility to GDM.
KeywordsGestational diabetes Resistin Single nucleotide polymorphism- 420C/G
Gestational diabetes mellitus (GDM) is a type of glucose intolerance that occurs during pregnancy . GDM and type 2 diabetes (T2D) are closely related disorders with a common pathogenesis . Ethnicity, family history, dietary habit, physical inactivity and obesity are among risk factors implicated in susceptibility to both T2D and GDM [2,3]. Insulin resistance is an important characteristic of both T2D and GDM . Several adipokines including leptin, visfatin, adiponectin and resistin are reported to be involved in development of insulin resistance [4,5].
Resistin is a cysteine-rich polypeptide with 108 amino acid residues synthesized and secreted by adiopcytes, immune and endothelial cells . In pregnancy, the placenta is a major source of maternal circulating resistin . Initial studies in rodent animal models suggested that resistin involves in insulin resistance and T2D. Indeed, up-regulation of resistin in obese animal rodent models, decrease in its circulating level by thiazolidinediones (TZDs), and decrease in plasma glucose level in response to anti-resistin antibody administration in obese animals have been reported . However, the exact role of resistin in the pathogenesis of insulin resistance and T2D in humans is still unclear. Although the association between elevated circulating resistin and insulin resistance has been suggested in some studies [9,10], other studies fail to detect such an association [11,12]. Several inconsistent findings have also been reported from serum resistin levels in patients with GDM. Most of these findings showed no difference in the serum resistin level between GDM and normal glucose tolerant (NGT) subjects [13,14]. However, there are other reports indicating increased [15,16] or decreased  serum resistin concentrations in women with GDM compared with NGT pregnant women.
The gene encoded resistin (RETN gene) is located on 19p3.2 and composed of four exons and three introns. It is a polymorphic gene with several single nucleotide polymorphism (SNPs) in its promoter, introns and 3′-UTR (3′-untranslated region) regions . Because of its possible influence on RETN gene expression and circulating resistin concentration, SNP-420C > G (rs 1862513) in the promoter is one of the most studied SNPs of RETN gene [17-20]. It has been reported that the promoter activity of RETN is higher in individuals with GG genotype of SNP-420C > G compared to CC/GC genotype . The association of SNP-420C > G genotype with T2D has been shown in some previous studies [19,21]. Because of the close relationship between T2D and GDM, it is reasonable to evaluate the association between this SNP and susceptibility to GDM. Thus, the first aim of our study was to evaluate the association of SNP- 420C > G with risk of GDM in Iranian population. We also aimed to compare serum resistin level between GDM and non-GDM subjects, as well as its association with genotypes of SNP-420C > G. Furthermore, we examined possible associations between serum resistin levels with obesity, insulin resistance and serum biochemical abnormalities related to GDM.
All subjects enrolled in the present study were Iranian and recruited from outpatient clinic of Hafez and Zinabieh Hospitals in Shiraz, Iran, between September 2011 and May 2013. The subjects were firstly screened for presence of GDM, using 50-g glucose challenge test (GCT) at 24-28th weeks of gestation. For the pregnant women with positive results of GCT (plasma glucose ≥140 mg/dl), 100-g three hour oral glucose tolerance test (3 hrs - OGTT) was performed and the subjects with at least two results higher than normal values (fasting < 95 mg/dl, 1 h <180 mg/dl, 2 h <155 mg/dl and 3 < 140 mg/dl ) were diagnosed as GDM . Seventy healthy pregnant women and seventy five pregnant women who had GDM were enrolled in this study. The absence of family history for the T2D, absence of clinical evidence of any major disease and absence of medication use that may alter glucose tolerance were the inclusion criteria for the control pregnant women. The inclusion criteria for the pregnant women with GDM were: (1) newly diagnosed cases, and (2) no previous use of oral hypoglycemic agents. The exclusion criteria from the study were the presence of type-1 or type-2 diabetes mellitus and other known major diseases. Maternal BMI (kg/m2) was calculated as the ratio of the weight (kg) to the square of the height (m). The study protocol was approved by the ethics committee at Shiraz university of Medical Sciences, Shiraz, Iran. Informed written consent was obtained from all participants.
Fasting venous maternal blood sample was collected in both groups, after an overnight 12 hour fasting. Sera were separated immediately and stored at −70 C until biochemical analyses were performed. Fasting plasma glucose (FPG), total cholesterol (TC), triglyceride (TG) and high-density lipoprotein cholesterol (HDL-C) were measured by using commercially available kits. Fasting plasma low-density lipoprotein cholesterol (LDL C) was calculated using the formula of Friedewald et al. ; LDL-C = total cholesterol (TC) – (HDL-C) - [triglycerides (TG) ÷ 5]. HbA1C was measured by ion-exchange high performance liquid chromatography. Serum insulin levels were measured by radioimmunoassay using available commercial kits. Serum resistin concentration was measured by immunoassay using a commercially human resistin ELISA kit (Biovendor, Czech Republic) according to the manufacturer’s instructions. The lowest detectable level of serum resistin was 0.012 ng/ml and intra- and inter-assay coefficients of variation of the assay were 5.9% and 7.6%, respectively. In this study, HOMA-IR (homeostasis model of assessment for insulin resistance) was used for evaluation of insulin sensitivity. HOMA-IR is defined as follows: ([fasting glucose] × [fasting insulin])/22.5 .
RETEN gene SNP −420 C/G genotyping
All statistical analyses were performed using SPSS 15.0 software (SPSS Inc., Chicago, IL, USA). The normality of distribution of the continuous variables in groups was assessed by the Shapiro–Wilk test. The normally distributed variables were analyzed applying the Student’s t-test, and the variables that did not show a normal distribution were compared using Mann–Whitney U-test. The data were presented in mean ± standard deviation (SD) or ratio and percent. Bivariate correlation (computing Pearson’s coefficient with their significance levels) between maternal serum resistin levels and maternal blood insulin, FPG, HOMA-IR, BMI, gestational age, maternal age in the GDM and non-GDM subjects was calculated. Multiple linear regression analysis was conducted using the stepwise method to determine which factors were significantly and independently associated with maternal serum resistin. The differences in serum resistin levels between GDM and Non- GDM subjects were analyzed using ANCOVA after adjustment for covariates (maternal age, gestational age, BMI, and HOMA-ir).The Chi-square test was used to compare frequencies of allele and genotypes. To examine the independent association of the SNP -420C > G with GDM, univariate and multivariate logistic regression analysis was conducted. In the regression models, GDM status was chosen as the dependent variable and GG and GC + CC genotypes as the independent variable. Confounding variables including maternal BMI, maternal age, and maternal HOMA-index were later included in the model. For all comparisons, the statistical significance was defined by a P < 0.05.
Comparison of baseline characteristics between subjects with and without GDM
Demographic characteristics and biochemical measurements in the GDM patients and Non- GDM subjects
GDM group(n = 75)
Non-GDM group(n = 70)
29.4 ± 4.9
26.7 ± 5.0
29.9 ± 3.4
29.6 ± 3.1
BMI(Kg/m 2 )
28.2 ± 4.5
28.1 ± 4.4
87.9 ± 22.4
78.7 ± 11.3
5.80 ± 0.95
5.08 ± 0.37
18.2 ± 11.6
17.5 ± 7.4
4.6 ± 3.1
3.4 ± 1.6
267.3 ± 121.2
267.8 ± 101.9
230.7 ± 50.9
240.0 ± 51.1
52.4 ± 13.6
52.6 ± 12.4
113.6 ± 28.7
118.7 ± 27.6
13.0 ± 6.6
11.4 ± 6.9
Correlation between serum resistin and clinical parameters
Serum resistin concentration did not show any significant correlation with GDM related risk factors including maternal age(r = 0.053; p = 522), BMI(r = 0.051; p < 0.538), and HOMA-IR(r = 0.006; p < 0.946), in entire cohort. Pearson correlation analysis showed that fasting serum resistin concentrations were positively correlated with TG (r = 0.293; p < 0.03), TC(r = 0.288; p = 0.032), LDL-C (r = 0.353; p = 0.011) in GDM patients. Stepwise linear regression analysis revealed that TG (β = 0.353, P = 0.002) was the independent predictor of serum resistin and accounted for 12.5% of the variance.
Genotype and allele analysis of SNP -420C > G
Genotype and allele frequencies of RETN gene SNP −420 C/G in the non – GDM (control) and GDM patients
GC + CC
OR (95% CI), 4.0 (1. 8–8.8)
OR (95% CI), 2.4 (1.48 -3.96)
Multivariate logistic regression analysis for gestational diabetes
SNP - 420 C/G
Variations in serum resistin concentration (ng/ml) and BMI (kg/mg 2 ) by genotypes of the SNP −420 C/G
GDM patients genotype
Non-GDM subjects genotype
GC + CC
GC + CC
13.8 ± 5.3
12.5 ± 7.2
13.7 ± 2.9
11.9 ± 7.7
(10.3 - 14.7)
(9.8 - 13.9)
BMI(Kg/m 2 )
28.2 ± 5.3
28.2 ± 3.3
28.2 ± 4.4
27.9 ± 4.1
(26.6 – 29.9)
(27.0 – 29.4)
(27.0 – 29.3)
(25.3 – 30.6)
The findings of this study showed that GG genotype and G- allele of SNP- 420C/G in the RETN gene is associated with genetic susceptibility to GDM in our population. The second finding of this study was the positive correlation between the serum concentration of atherogenic lipids and serum resistin. However, no significant associations were observed between serum resistin levels, SNP- 420C/G in the patients with GDM.
Allelic and genotypic frequencies of SNP- 420C/G (rs1862513) show ethnic variation . In this study, the frequency of rare G/G genotypes and G allele among the control NGT women was 16.4% and 51.5%, respectively. This is closely comparable with another Iranian data by Emamogolipour, et al.  but higher than those reported for healthy Caucasian, Chinese, Korean and Japanese subject (24% to 30%) [18,27,28]. Previous studies have shown an association between G allele of SNP- 420C/G and T2D in Iranian and other population [19,26]. To best of our knowledge, this is the first study that revealed the association of SNP- 420C/G with GDM. Our data showed that the frequency of GG genotype and G allele was significantly higher in the GDM patients compared to normal pregnant group. The exact molecular mechanisms that link this polymorphism with GDM are not known at present. It has been previously reported that G allele of SNP- 420 in the promoter of RETN gene was associated with increase in circulating resistin [18,19]. According to the authors, this could be related to specific recognition of – 420G by Sp 1/3, which increases RETN promoter activity, leading to enhanced serum resistin levels. In this study, we did not observe any association between serum resistin levels and SNP- 420G. It has been reported that resistin gene expression is controlled by genetics and environmental factors such as dietary habits [29,30]. Indeed, an ethnic specific resistin gene expression has been suggested . Onum et al.  suggested that this ethnic difference may be related to SNP-385 in the RETN gene. They showed that combination of A allele of SNP- 358 with the G allele of SNP-420 in subjects with G-A haplotype conferred the highest circulating resistin concentration. On the basis of onum et al.’s hypothesis, the ethnic differences in SNP- 358 might account for the discrepancy observed in association of SNP- 420 with serum resistin in different population . We did not evaluate SNP-358 in this study; hence, it is not clear whether the A of SNP- 358 indeed accounts for of any association between plasma rsistin and SPN-420 in our population.
In agreement with the results of two previous studies [33,34], our findings showed that serum resistin levels were similar in the GDM and non- GDM subjects. By contrast, other studies have found lower  or higher [15,16] resistin levels in GDM patients compared to healthy pregnant women. These discrepancies mostly arise from the presence of heterogeneities in the several aspects of aforementioned studies. One of the causes of these heterogeneities among studies is the application of different GDM diagnostic methods, i.e., National Diabetes Data Group (NDDG, 100 g 3 hrs OGTT), Carpenter and Coustan (100 g 3 hrs OGTT), and WHO criteria (75 g 2 hrs OGTT) . Since these methods had different criteria for diagnosis of GDM, the population of GDM patients as well as control subjects that enrolled in the aforementioned studies substantially different in aspect of level of hyperglycemia and severity of GDM. Moreover, it has been reported that the maternal serum resisin is increased in concomitant with the increase in the gestational age . Therefore, difference in the gestational age of the subjects at the time blood sampling for resistin assay is the second cause of heterogeneity between these studies. The discrepancies between the studies may also be a reflection of genetic and anthropometric variations among ethnic groups that enrolled in these studies, as some functional polymorphism in the resistin gene as well as obesity has been showed that influenced on the expression of resistin in some ethnic group. Finally, difference in preparation of sample (serum/plasma), conditions of sample storage, and assay methods which used for the quantification of resistin may also consider as a plausible explanation for difference among studies, as variable results has been reported for the concentration circulating resistin in these studies .
Resistin has been reported to be related to obesity and insulin in patients with T2D [20,37]. Similar to T2D insulin resistance and obesity are involved in the etiology of GDM . Increases in HOMA-ir and serum insulin concentration are the representative parameter of insulin resistance . Consistent with other studies, the results of the present study revealed that HOMA- ir was significantly higher in GDM patients compared to healthy pregnant women. However, serum resistin levels in GDM group did not show any correlation with HOMA-ir, serum insulin concentration. These results are in line with other studies [13,34], suggesting that serum resistin levels may not be associated with insulin resistance in GMD patients.
The increase in serum TG, total cholesterol, LDL cholesterol concentration and high TG/HDL-C ratio are atherogenic markers that correlate with insulin resistance . Similar to other studies [30,40], a strong positive correlation was found among serum resistin, serum TG, total cholesterol, LDL cholesterol concentration, and TG/ HDL ratio in the present study. Our results also demonstrated that the serum levels of atherogenic lipids were elevated in GDM patients with the highest quartile resistin, which suggested that increase in resistin concentration might be closely associated with modulation of lipid metabolism and may play a role in dyslipidemia in GDM patients.
Several SNPs were known in the RETN gene but we considered only the SNP-420C > G in the promoter of gene because of its possible influence on RETN gene expression and circulating resistin concentration. Hence, further studies will be required to clarify the association among resistin gene polymorphisms, circulating resistin and GDM.
In conclusion, the findings of the present study suggest that GG genotype of SNP- 420C/G in the promoter of RETN associated with genetic susceptibility to GDM in our population. However, we failed to show any association between this polymorphism and known risk factors of GDM. Thus, further studies are necessary to confirm the role of this polymorphism in the pathogenesis of GDM and to explore the potential mechanisms by which it modulates susceptibility to GDM.
This research was financially supported by a research grant from Shiraz University of Medical Sciences.
- Metzger BE, Buchanan TA, Coustan DR, de Leiva A, Dunger DB, Hadden DR, et al. Summary and recommendations of the fifth international workshop-conference on gestational diabetes mellitus. Diabetes Care. 2007;30 Suppl 2:S251–60.View ArticlePubMedGoogle Scholar
- Ben-Haroush A, Yogev Y, Hod M. Epidemiology of gestational diabetes mellitus and its association with type 2 diabetes. Diabet Med. 2004;21(2):103–13.View ArticlePubMedGoogle Scholar
- Konig M, Shuldiner AR. The genetic interface between gestational diabetes and type 2 diabetes. J Matern Fetal Neonatal Med. 2012;25(1):36–40.View ArticlePubMedGoogle Scholar
- Raucci R, Rusolo F, Sharma A, Colonna G, Castello G, Costantini S. Functional and structural features of adipokine family. Cytokine. 2013;61(1):1–14.View ArticlePubMedGoogle Scholar
- Sahin-Efe A, Katsikeris F, Mantzoros CS. Advances in adipokines. Metabolism. 2012;61(12):1659–65.View ArticlePubMedGoogle Scholar
- Park HK, Ahima RS. Resistin in rodents and humans. Diab Metab J. 2013;37(6):404–14.View ArticleGoogle Scholar
- Megia A, Vendrell J, Gutierrez C, Sabate M, Broch M, Fernandez-Real JM, et al. Insulin sensitivity and resistin levels in gestational diabetes mellitus and after parturition. Eur J Endocrinol. 2008;158(2):173–8.View ArticlePubMedGoogle Scholar
- Steppan CM, Bailey ST, Bhat S, Brown EJ, Banerjee RR, Wright CM, et al. The hormone resistin links obesity to diabetes. Nature. 2001;409(6818):307–12.View ArticlePubMedGoogle Scholar
- Gharibeh MY, Al Tawallbeh GM, Abboud MM, Radaideh A, Alhader AA, Khabour OF. Correlation of plasma resistin with obesity and insulin resistance in type 2 diabetic patients. Diabetes Metab. 2010;36(6 Pt 1):443–9.View ArticlePubMedGoogle Scholar
- Tsiotra PC, Tsigos C, Anastasiou E, Yfanti E, Boutati E, Souvatzoglou E, et al. Peripheral mononuclear cell resistin mRNA expression is increased in type 2 diabetic women. Mediators Inflamm. 2008;2008:892864.View ArticlePubMed CentralPubMedGoogle Scholar
- Lee JH, Chan JL, Yiannakouris N, Kontogianni M, Estrada E, Seip R, et al. Circulating resistin levels are not associated with obesity or insulin resistance in humans and are not regulated by fasting or leptin administration: cross-sectional and interventional studies in normal, insulin-resistant, and diabetic subjects. J Clin Endocrinol Metab. 2003;88(10):4848–56.View ArticlePubMedGoogle Scholar
- Pfutzner A, Langenfeld M, Kunt T, Lobig M, Forst T. Evaluation of human resistin assays with serum from patients with type 2 diabetes and different degrees of insulin resistance. Clin Lab. 2003;49(11–12):571–6.PubMedGoogle Scholar
- Akdeniz N, Kuyumcuoglu U, Kale A, Arikan S, Kale E, Erdemoglu M. Resistin may not associate with gestational diabetes mellitus although insulin resistance. Clin Exp Obstet Gynecol. 2011;38(3):236–8.PubMedGoogle Scholar
- Kulik-Rechberger B, Mora-Janiszewska O. Serum resistin concentrations in cases of gestational diabetes mellitus with good glycemic control and in cord blood. Ginekol Pol. 2009;80(6):432–6.PubMedGoogle Scholar
- Chen D, Fang Q, Chai Y, Wang H, Huang H, Dong M. Serum resistin in gestational diabetes mellitus and early postpartum. Clin Endocrinol (Oxf). 2007;67(2):208–11.View ArticleGoogle Scholar
- Vitoratos N, Deliveliotou A, Dimitrakaki A, Hassiakos D, Panoulis C, Deligeoroglou E, et al. Maternal serum resistin concentrations in gestational diabetes mellitus and normal pregnancies. J Obstet Gynaecol Res. 2011;37(2):112–8.View ArticlePubMedGoogle Scholar
- Hivert MF, Manning AK, McAteer JB, Dupuis J, Fox CS, Cupples LA, et al. Association of variants in RETN with plasma resistin levels and diabetes-related traits in the framingham offspring study. Diabetes. 2009;58(3):750–6.View ArticlePubMed CentralPubMedGoogle Scholar
- Cho YM, Youn BS, Chung SS, Kim KW, Lee HK, Yu KY, et al. Common genetic polymorphisms in the promoter of resistin gene are major determinants of plasma resistin concentrations in humans. Diabetologia. 2004;47(3):559–65.View ArticlePubMedGoogle Scholar
- Osawa H, Yamada K, Onuma H, Murakami A, Ochi M, Kawata H, et al. The G/G genotype of a resistin single-nucleotide polymorphism at −420 increases type 2 diabetes mellitus susceptibility by inducing promoter activity through specific binding of Sp1/3. Am J Hum Genet. 2004;75(4):678–86.View ArticlePubMed CentralPubMedGoogle Scholar
- Ukkola O, Kunnari A, Kesaniemi YA. Genetic variants at the resistin locus are associated with the plasma resistin concentration and cardiovascular risk factors. Regul Pept. 2008;149(1–3):56–9.View ArticlePubMedGoogle Scholar
- Wen Y, Lu P, Dai L. Association between resistin gene −420 C/G polymorphism and the risk of type 2 diabetes mellitus: a meta-analysis. Acta Diabetol. 2013;50(2):267–72.View ArticlePubMedGoogle Scholar
- Association AD. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2008;31(Supplement 1):S55–60.View ArticleGoogle Scholar
- Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem. 1972;18(6):499–502.PubMedGoogle Scholar
- Kirwan JP, Huston-Presley L, Kalhan SC, Catalano PM. Clinically useful estimates of insulin sensitivity during pregnancy: validation studies in women with normal glucose tolerance and gestational diabetes mellitus. Diabetes Care. 2001;24(9):1602–7.View ArticlePubMedGoogle Scholar
- El-Shal AS, Pasha HF, Rashad NM. Association of resistin gene polymorphisms with insulin resistance in Egyptian obese patients. Gene. 2013;515(1):233–8.View ArticlePubMedGoogle Scholar
- Emamgholipour SH-n, Najmafshar A. Promoter resistin gene polymorphism in patients with type 2 diabetes and its influence on concerned metabolic phenotypes. Iran J Diabetes Lipid Disord. 2009;8:150–6.Google Scholar
- Chi S, Lan C, Zhang S, Liu H, Wang X, Chen Y, et al. Association of -394C > G and -420C > G polymorphisms in the RETN gene with T2DM and CHD and a new potential SNP might be exist in exon 3 of RETN gene in Chinese. Mol Cell Biochem. 2009;330(1–2):31–8.View ArticlePubMedGoogle Scholar
- Ochi M, Osawa H, Hirota Y, Hara K, Tabara Y, Tokuyama Y, et al. Frequency of the G/G genotype of resistin single nucleotide polymorphism at −420 appears to be increased in younger-onset type 2 diabetes. Diabetes. 2007;56(11):2834–8.View ArticlePubMedGoogle Scholar
- Yoshimura Y, Nishii S, Zaima N, Moriyama T, Kawamura Y. Ellagic acid improves hepatic steatosis and serum lipid composition through reduction of serum resistin levels and transcriptional activation of hepatic ppara in obese, diabetic KK-A(y) mice. Biochem Biophys Res Commun. 2013;434(3):486–91.View ArticlePubMedGoogle Scholar
- Cabrera de Leon A, Almeida Gonzalez D, Gonzalez Hernandez A, Dominguez Coello S, Marrugat J, Juan Aleman Sanchez J, et al. Relationships between serum resistin and fat intake, serum lipid concentrations and adiposity in the general population. J Atheroscler Thromb. 2014;21(5):454–62.View ArticlePubMedGoogle Scholar
- Menzaghi C, Trischitta V. Genetics of serum resistin: a paradigm of population-specific regulation? Diabetologia. 2010;53(2):226–8.View ArticlePubMedGoogle Scholar
- Onuma H, Tabara Y, Kawamura R, Tanaka T, Ohashi J, Nishida W, et al. A at single nucleotide polymorphism-358 is required for G at −420 to confer the highest plasma resistin in the general Japanese population. PLoS One. 2010;5(3), e9718.View ArticlePubMed CentralPubMedGoogle Scholar
- Karatas A, Tuncay Isikkent N, Ozlu T, Demirin H. Relationship of maternal serum resistin and visfatin levels with gestational diabetes mellitus. Gynecol Endocrinol. 2014;30(5):355–8.View ArticlePubMedGoogle Scholar
- Lobo TF, Torloni MR, Gueuvoghlanian-Silva BY, Mattar R, Daher S. Resistin concentration and gestational diabetes: a systematic review of the literature. J Reprod Immunol. 2013;97(1):120–7.View ArticlePubMedGoogle Scholar
- Lobo TF, Torloni Mr Fau - Gueuvoghlanian-Silva BY, Gueuvoghlanian-Silva By Fau - Mattar R, Mattar R Fau - Daher S, Daher S: Resistin concentration and gestational diabetes: a systematic review of the literature. (1872–7603 (Electronic)).Google Scholar
- Chen D, Fang Q Fau - Chai Y, Chai Y Fau - Wang H, Wang H Fau - Huang H, Huang H Fau - Dong M, Dong M: Serum resistin in gestational diabetes mellitus and early postpartum. (0300–0664 (Print)).Google Scholar
- Ukkola O. Resistin - a mediator of obesity-associated insulin resistance or an innocent bystander? Eur J Endocrinol. 2002;147(5):571–4.View ArticlePubMedGoogle Scholar
- Borai A, Livingstone C, Kaddam I, Ferns G. Selection of the appropriate method for the assessment of insulin resistance. BMC Med Res Methodol. 2011;11:158.View ArticlePubMed CentralPubMedGoogle Scholar
- Pacifico L, Bonci E, Andreoli G, Romaggioli S, Di Miscio R, Lombardo CV, et al. Association of serum triglyceride-to-HDL cholesterol ratio with carotid artery intima-media thickness, insulin resistance and nonalcoholic fatty liver disease in children and adolescents. Nutr Metab Cardiovasc Dis. 2014;24(7):737–43.View ArticlePubMedGoogle Scholar
- Osawa H, Ochi M, Tabara Y, Kato K, Yamauchi J, Takata Y, et al. Serum resistin is positively correlated with the accumulation of metabolic syndrome factors in type 2 diabetes. Clin Endocrinol (Oxf). 2008;69(1):74–80.View ArticleGoogle Scholar
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.