Human Total Betatrophin ELISA Kit

The thyroid hormone, T-3, regulates cell growth, differentiation and development through binding to the nuclear thyroid hormone receptor (THR), a member of the steroid/TR superfamily of ligand-dependent transcriptional factors. T-3 modulates lipid metabolism in liver, although the detailed molecular mechanisms are unclear at present. Here, by a microarray analysis, we identified a novel chromosome 19 open reading frame 80 (C19orf80) which was activated by T-3. T-3 stimulation led to upregulation of both mRNA and protein levels of C19orf80. Immunofluorescence analysis revealed a vesicle-like pattern of C19orf80 around lipid droplets or within the lysosome-associated compartment in cells. Furthermore, T-3 treatment as well as C19orf80 overexpression specifically activated the autophagic response and lipid metabolism, as observed from lipidated LC3 (LC3-II) and levels of oxygen consumption rate, respectively. Reciprocally, knockdown of C19orf80 obstructed T-3-activated autophagy and lipolysis. Moreover, treatment with autolysosome maturation inhibitors, ammonium chloride and chloroquine, not only suppressed the T-3-activated autophagic process but also lipid metabolism. Our results collectively suggested that T-3 regulates lipid metabolism through a C19orf80-activated autophagic process.

This computational material-based study aimed to provide a comprehensive data with the molecular interaction between betatrophin and its target as the confirmation of the primary role of betatrophin on serological lipid profile alteration and metabolic syndrome progression. We analyzed the binding behavior of betatrophin and LPL using docking model. The underlying molecular interaction between betatrophin and lipoprotein lipase (LPL) binding site results in the inhibitory activity of betatrophin on LPL. Our in Silico data showed that betatrophin could regulate that essential enzyme and suggested indirectly to restrict TG level during the circadian cycle in the human circulation. To sum up, betatrophin or RIFL shows as a promising future early biomarker for obesity and cancer linked metabolic syndrome. Hence, this preliminary computational material analysis data provided a hallmark for the future development of betatrophin as the clinical biomaterial marker in metabolic syndrome and gastrointestinal cancer.