Anti-ADIPOQ (full length) polyclonal antibody

Adiponectin has been schown to protect from insulin resistance, demonstrate anti-inflammatory and anti-atherosclerotic effects and be involved in the pathogenesis of metabolic syndrome (MS). We aimed to assess the association between serum adiponectin concentration, insulin resistance and various risk factors of MS and to investigate the relationship between the single nucleotide polymorphism (SNP) + 45 T>G (rs 2241766) in the adiponectin (ADIPOQ) gene and the risk of MS. 200 patients with MS and 250 healthy controls were enrolled in this study. The level of fasting serum insulin, glucose, and lipid levels were measured. Insulin resistance was estimated using homeostasis model of assessment for insulin resistance (HOMA-IR). Serum adiponectin levels were measured by enzyme-linked immunosorbent assay and the SNP + 45 T>G in the ADIPOQ gene was performed by the polymerase chain reaction-restriction fragment length polymorphism method. MS patients had a significantly higher levels of HOMA-IR (p<0.001) and lower serum adiponectin concentrations (p<0.001) compared to controls. Multiple regression analysis showed that serum adiponectin levels was associated negatively with HOMA-IR (r=-0.307; p=0.001) and positively with high-density lipoprotein cholesterol (HDL-C) (r=0.369; p=0.000) in MS patients. In addition, there was no significant association between genotypes of rs 2241766 and the risk of MS. In conclusion, adiponectin is known to play key regulator of insulin sensitivity, endothelial function and lipid metabolism. Our findings confirm the associations of hypoadiponectinemia with MS and gave evidence that the SNP+45 T>G polymorphism in the gene of ADIPOQ is not associated with MS.

Higher levels of circulating adiponectin have been related to lower risk of colorectal cancer in several prospective cohort studies, but it remains unclear whether this association may be causal. We aimed to improve causal inference in a Mendelian Randomization meta-analysis using nested case-control studies of the European Prospective Investigation into Cancer and Nutrition (EPIC, 623 cases, 623 matched controls), the Health Professionals Follow-up Study (HPFS, 231 cases, 230 controls) and the Nurses' Health Study (NHS, 399 cases, 774 controls) with available data on pre-diagnostic adiponectin concentrations and selected single nucleotide polymorphisms in the ADIPOQ gene. We created an ADIPOQ allele score that explained approximately 3% of the interindividual variation in adiponectin concentrations. The ADIPOQ allele score was not associated with risk of colorectal cancer in logistic regression analyses (pooled OR per score-unit unit 0.97, 95% CI 0.91, 1.04). Genetically determined twofold higher adiponectin was not significantly associated with risk of colorectal cancer using the ADIPOQ allele score as instrumental variable (pooled OR 0.73, 95% CI 0.40, 1.34). In a summary instrumental variable analysis (based on previously published data) with higher statistical power, no association between genetically determined twofold higher adiponectin and risk of colorectal cancer was observed (0.99, 95% CI 0.93, 1.06 in women and 0.94, 95% CI 0.88, 1.01 in men). Thus, our study does not support a causal effect of circulating adiponectin on colorectal cancer risk. Due to the limited genetic determination of adiponectin, larger Mendelian Randomization studies are necessary to clarify whether adiponectin is causally related to lower risk of colorectal cancer.