Anti-RETN monoclonal antibody

Previous research has found a correlation between resistin and lipid level variations. Polymorphisms in the resistin gene (RETN) could be involved in this relationship, but the results of the different studies are contradictory. The aim of this study was to examine the association between resistin and lipid levels, and to determine whether resistin polymorphisms are associated with resistin levels and lipid profile in prepubertal children and adolescents. The single nucleotide polymorphisms (SNPs) rs1862513 and rs10401670 were analyzed in 442 randomly selected 6- to 8-year-old children and 827 children aged 12-16 years. Anthropometric data were recorded. Lipid profile was determined using standard methods. Serum resistin levels were measured using a multiplexed bead immunoassay. Resistin polymorphisms were determined by TaqMan (R) allelic discrimination assays. A relationship was found between serum levels of resistin and the SNP rs10401670 in 6- to 8-year-old boys. SNP rs10401670 was also related to TC and LDL-cholesterol in 12- to 16-year-old boys and to HDL-C in 12- to 16-year-old girls. SNP rs1862513 was not related to any of the studied variables. Serum resistin levels were significantly and negatively associated with ApoAI levels in 12-to 16-year-old girls. A SNP in the 3'UTR region of RETN (rs10401670) is associated with resistin levels and lipid profile in children, showing different associations depending on age and gender.

Adipose tissue is the primary source of the adipokines resistin and fasting-induced adipose factor (FIAF). We reported that the brain is also a site of adipokine expression, although their function there is unknown. Peripheral resistin and fasting-induced adipose factor are reported to be inflammatory markers, and we hypothesized that they would be induced in the brain by hypoxia/ischaemia. We show that neonatal hypoxia/ischaemia rapidly increased flaf mRNA in the injured cortex and hippocampus at 2 and 7 days after hypoxia/ischaemia. In contrast, resistin (retn) mRNA was increased in the cortex only at 21 days after hypoxia/ischaemia. As a lipopolysaccharide-induced inflammatory response did not increase brain fiaf and retn mRNA levels, we conclude that brain injury may be responsible for the novel hypoxia/ischaemia-induced changes in adipokine gene expression. In summary, our results indicate that brain injury, or an inflammatory stimulus, regulates the central expression of two genes normally considered to be adipose tissue-specific. These observations add to our previous evidence that the brain is an important site of adipokine gene expression.