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Adiponectin (ADIPOQ) gene regulates the glucose metabolism, insulin sensitivity, fatty acid oxidation, immunity and reproduction. In the present investigation, PCR-RFLP method was conducted to identify the genetic polymorphism in intron 2 region of adiponectin (ADIPOQ) gene in Indian Sahiwal cattle. PCR of intron 2 of ADIPOQ gene fragment produced amplicon of 961 bp which was subsequently digested with RsaI restriction enzyme. The RsaI/PCR-RFLP assay revealed monomorphic pattern only, TT genotype (wild type homozygote) in Sahiwal cattle population which was confirmed by sequencing. The obtained sequences of ADIPOQ after aligning revealed absence of RsaI recognition site GTAC and consequently, the association study with economic traits could not be performed
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Objective@#The aim of the study was to investigate the association between single nucleotide polymorphisms (SNP) at rs 1501299 (SNP+276 G>T) of the adiponectin gene and plasma adiponectin levels in type 2 diabetes mellitus (T2DM) patients in Myanmar.@*Methodology@#One hundred T2DM patients and 104 non-diabetic subjects were included in this cross-sectional analytical study. Genotype frequencies were determined by polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP) method. Plasma adiponectin level was measured by enzyme-linked immunosorbent assay (ELISA). @*Result@#Genotype frequencies (GG, GT, TT) of SNP+276 in diabetic patients were 39%, 48% and 13%, respectively. The GT and TT genotypes were more frequent in T2DM patients (OR 1.98, 95% CI, 1.10-3.55; p=0.02 and OR 4.07, 95% CI, 1.34-12.3; p=0.01), respectively. The T allele of SNP+276 was significantly associated with T2DM (OR 1.96, 95% CI, 1.27-3.01; p=0.002). Mean plasma adiponectin level was significantly lower than in T2DM patients (27.41±16.7 μg/mL) compared to non-diabetic subjects (37.19±26.77 μg/mL) (p=0.002)@*Conclusion@#SNP+276 at rs 1501299 of the adiponectin gene was associated with type 2 diabetes and low plasma adiponectin levels in this Myanmar population.
Subject(s)
Diabetes Mellitus, Type 2ABSTRACT
Numerous epidemiological studies have studied the association of adiponectin (ADIPOQ) gene and adiponectin receptor (ADIPOR) gene polymorphisms with risk of colorectal cancer (CRC),but the outcomes were incomplete and inconsistent.Therefore,we conducted a meta-analysis to assess the associations systematically.All eligible case-control studies published up to Jan.2015 were searched from PubMed,the Cochrane library,Elsevier,Wiley Online library,China National Knowledge Infrastructure,WanFang data and Chongqing VIP.Effect sizes of odds ratio (OR) and 95％ confidence interval (95％CI) were calculated by using a fixed-or random-effect model.Twelve case-control studies including 6141 cases and 7398 controls were selected.Significant differences in the distributions of allele frequency with CRC risk were directly present in ADIPOQ variants rs2241766,rs1501299 and ADIPOR variant rs1342387.In stratified analysis for different populations,significant differences were present in ADIPOQ variant rs822396 for Ashkenazi Jewish,in ADIPOQ variant rs1501299 and ADIPOR variant rs1342387 for Chinese and in ADIPOQ variant rs 2241766 for Ashkenazi Jewish and Chinese.In addition,the factors correlated with insulin resistance had synergistic effect with ADIPOQ variants rs2241766 T/G and rs1501299 G/T on risk of CRC.ADIPOQ variants rs2241766 T/G,rs1501299 G/T and ADIPOR variant ADIPOR rs1342387 G/A had a population specific correlation with CRC risk,which may be mediated by insulin resistance.And large well-designed studies are still needed for further evaluation of rs822396 and rs1063538,especially for their interaction and combined effect in the correlation with CRC risk.
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Objective To investigate the adiponectin(ADIPOQ)gene polymorphisms and which association with colorectal cancer(CRC).Methods Genotyping of blood samples were performed for 250 case-control pairs.Taqman real-time PCR was used to test the three single nucleotide polymorphisms(SNPs),namely rs266729,rs2441 766,rs1 501299.Logistic regression was applied to assess the effects of three SNPs,the gene-gene,and gene-environment interactions on CRC risk.Results The ADIPOQ rs266729 GG and CG+GG genotype had a higher CRC risk than those carrying the CC genotype[OR (95%CI ):1.87 (1.01 - 3.47),1.63 (1.14-2.32),respectively].The same results was observed in cases who carried TG+GG genotype vs .TT genotype in rs2441 766 [OR(95%CI ):1.45(1.02-2.06)].The rs1 501299 GT+TT genotype had a lower CRC risk than those carrying the GG genotype [OR(95%CI ):0.61(0.43-0.88)].Furthermore,in two-factor gene-environment interaction analyses,rs266729 presented signifi-cant interactions with Body mass index (BMI),with OR of 1.1 6 (95%CI :1.03-1.30).Conclusion The results suggest that vari-ants in ADIPOQ may contribute to increased colorectal cancer risk and this contribution may be modified by BMI.
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Background: Insulin resistance and central adiposity are frequent disorders in PCOS women, which are marked by biological marker dysregulation related to this metabolic abnormalities. Association between adiponectin and insulin resistance has been investigated in many studies, while only a few studies were done in PCOS patients. This study is to determine the association of T45G polymorphisms in Indonesian population with PCOS biological markers and their influence to adiponectin serum. Methods: Fifty-two PCOS patients and 52 normal ovulatory women without hyperandrogenism as control subjects were included. Blood samples were collected between day 3 and 5 of a spontaneous menstrual cycle at 7 to 9 am, after overnight fasting. Serum levels of FSH, LH, testosterone, SHBG, glucose, insulin, lipid profile and adiponectin were measured. Insulin resistance was estimated by HOMA-IR, HOMA-β, and SHBG. T45G gene polymorphisms were determined by PCR after genomic DNA was obtained from peripheral blood of patients and control subjects. Results: There were significant difference between PCOS and control group in term of BMI, LH, testosterone, SHBG, and FAI, but not significant to T45G gene polymorphisms frequency distribution. Adiponectin levels were lower in PCOS patients than control. There was an association between insulin resistance with PCOS. Among PCOS patients, no association between adiponectin LH, testosterone, SHBG, and FAI with T45G gene polymorphisms. T45G gene polymorphisms were more frequent in PCOS with low adiponectin levels compared to those with high adiponectin levels, although not significant statistically. Conclusion: T45G gene polymorphisms has no direct association with PCOS biological markers, but its association with adiponectin needs further study.
Subject(s)
Polycystic Ovary Syndrome , Adiponectin , Biomarkers , Insulin ResistanceABSTRACT
Objective: To investigate the correlation between the single nucleotide polymorphism (SNP) of adiponectin (APM1) gene and type 2 diabetes mellitus. Methods: Three common binding sites (-11377C>G, +45T>G, and +276G> T) of SNP on the APM1 gene were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay in 75 pedigrees (337 individuals) of type 2 diabetes mellitus. Genehunt software was used to analyze the transmission-disequilibrium (TDT) and to calculate SNP combining haplotypes. Meanwhile, the physiological and biochemical parameters were also determined in the pedigrees of type 2 diabetes mellitus. Results: We found no preferential transmission in the tested binding sites or any haplotypes of SNP in the APM1 gene in the filial generation of type 2 diabetes mellitus. In type 2 diabetes mellitus group, GG genotype had higher body mass index (BMD (P=O.032) and waist circumference (WC) (P= 0.030) compared to CC genotype in the patients with SNP-11377 binding site; patients with G allele had lower levels of high-density lipoprotein cholesterol (HDL-C) (P = 0.006) and higher levels of fasting plasma insulin (FINS) (P = 0.011) as compared to CC genotype. However, FINS levels (P=O.021) in subjects with CC genotype were significantly lower than those with G allele in healthy control group. For patients with SNP+45 binding site, those with GG genotypes had higher BMI (P= 0.036) and lower levels of FINS (P = 0.014) than those with TT genotypes in both groups. For patients with SNP + 276 binding site, those with GG genotypes had higher BMI(P = 0.043) than those with T allele in the control group. Conclusion: The SNP of the APM1 gene is not associated with the pedigrees of type 2 diabetes mellitus, but APMl gene has influence on the function of insulin B cells and the development of obesity.
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@#: ObjectiveTo study the effect of acupuncture on resistin and adiponectin and its gene expression in type 2 diabetic rats.MethodsThe rats of type 2 diabetes model were randomly divided into acupuncture group, rosiglitazone group and model control group, meanwhile 8 normal rats were assigned as the normal control group. The changes of total cholesterol(TC), triglycerides(TG), high density lipoprotein-cholesterol(HDL-C) and fasting plasma glucose (FPG) were measured. The expression of resistin gene and adiponectin gene in the adipose tissue was determined with RT-PCR. The level of serum resistin and adiponectin in type 2 diabetes rats were observed before and after acupuncture.ResultsThe levels of TC, TG, FPG resistin lowered obviously, and the levels of HDL-C adiponectin raised significantly. The expression of resistin gene lowered obviously. The expression of adiponectin gene significantly raised in acupuncture group, compared with the model control(P＜0.01, P＜0.05).ConclusionAcupuncture can decrease resistin gene expression, raise adiponectin gene expression, accordingly release insulin resistance.
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We investigated the association between two single nucleotide polymorphisms (SNPs) in the adiponectin gene (rs822395 and rs266729) and coronary artery disease (CAD) in a case-control study of 198 unrelated Chinese CAD patients (with ; 70 percent coronary stenosis or previous myocardial infarction) and 237 non-CAD controls. The ligase reaction was used to detect SNPs rs822395 and rs266729, and the allelic association of these SNPs with the occurrence and severity of CAD was assessed. There were no significant differences in the genotypic or allelic frequencies of the two SNPs between control and CAD individuals. In addition, there was no association between the two SNPs and the severity of CAD based on the number of diseased vessels. The frequencies of alleles C and G at rs266729 differed significantly between females in the CAD and control groups, but not between males. Female carriers of allele G at rs266729 had a higher risk of CAD compared with allele C carriers (OR = 1.30, 95 percent CI: 1.09-2.64, p = 0.02). These results indicate a gender-specific effect of the adiponectin gene rs266729 variant in modulating the risk of CAD in women.
Subject(s)
Humans , Animals , Male , Female , Adult , Middle Aged , Aged, 80 and over , Adiponectin/genetics , Coronary Artery Disease/genetics , China , Gene Frequency , Genotype , Polymorphism, Single NucleotideABSTRACT
Adiponectin is an adipocyte-derived secretory protein. It was found to be associated with insulin resistance, inflammation and arteriosclerosis. To further study the biological function and expression of adiponection in vivo, adipoenctin gene knock-out and LacZ gene knock-in mouse model was constructed. Gene targeting strategy was designed to replace part of exon 2 and exon 3 of adiponectin gene with full length LacZ gene in frame with remaining upstream ATG and signal peptide sequence of exon 2. The targeting vector (Adipo-LacZ-XpPNT) was constructed and verified by restriction enzyme digestion and sequencing. CJ7 ES cells were transfected with targeting vector linearized by NotⅠ digestion, selected in the medium containing both G418 and ganciclovoir. Resistant clones were screened by PCR and further confirmed by Southern blot for correct homologous recombinants. Chimera mice were obtained by routing microinjection of homologous recombined ES cells into blastocysts. After mating, mice heterozygous and further homozygous for adiponectin knockout and LacZ gene knock-in were established. Expression of both endogenous adiponectin and exogenous LacZ gene in mouse tissues and sera were detected by RT-PCR, Northern-blot, Western blot and ELISA. The results show that adiponectin was disrupted at both mRNA and protein levels. LacZ gene is expressed exclusively in adipose tissue of mutant mice. Its expression profile is identical to endogenous adiponection. Unexpectedly, LacZ activity could not be detected in both adipose tissue and serum although LacZ protein can be detected in adipose tissue but not in serum of mutant mice. In conclusion, mice homozygous for adiponectin knockout and LacZ gene knock-in have been successfully constructed. Mutant mice display LacZ expression profile identical to endogenous adiponectin albeit neither LacZ activity nor protein can be detected in serum of mutant mice.
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T) of SNP on the APM1 gene were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay in 75 pedigrees (337 individuals) of type 2 diabetes mellitus. Genehunt software was used to analyze the transmission-disequilibrium (TDT) and to calculate SNP combining haplotypes. Meanwhile, the physiological and biochemical parameters were also determined in the pedigrees of type 2 diabetes mellitus. Results: We found no preferential transmission in the tested binding sites or any haplotypes of SNP in the APM1 gene in the filial generation of type 2 diabetes mellitus. In type 2 diabetes mellitus group, GG genotype had higher body mass index (BMI)(P=0.032) and waist circumference (WC)(P=0.030) compared to CC genotype in the patients with SNP-11377 binding site; patients with G allele had lower levels of high-density lipoprotein cholesterol (HDL-C)(P=0.006)and higher levels of fasting plasma insulin (FINS) (P=0.011) as compared to CC genotype. However, FINS levels (P=0.021) in subjects with CC genotype were significantly lower than those with G allele in healthy control group. For patients with SNP+45 binding site, those with GG genotypes had higher BMI (P=0.036) and lower levels of FINS (P=0.014) than those with TT genotypes in both groups. For patients with SNP+276 binding site, those with GG genotypes had higher BMI(P=0.043) than those with T allele in the control group. Conclusion: The SNP of the APM1 gene is not associated with the pedigrees of type 2 diabetes mellitus, but APM1 gene has influence on the function of insulin B cells and the development of obesity.