|CSC-DC001849||Panoply™ Human C19ORF80 Knockdown Stable Cell Line||Inquriy|
|CSC-SC001849||Panoply™ Human C19ORF80 Over-expressing Stable Cell Line||Inquriy|
Recent Research Progress
Lipasin, also known as TD26 / RIFL / Betatrophin / ANGPTL8 / C19orf80, is located on chromosome 19p13.2, a locus associated with serum high-density lipoprotein (HDL) levels. The lipasin gene is embedded on the strand opposite that of the host gene dedicator of cytokinesis 6 (DOCK6), suggesting tissue-specific expression. The mouse lipasin gene has been identified as the Gm6484 gene located on chromosome 9. To date, several lipasin orthologs have been identified in mammals. There is growing evidence of an association between the expression of lipasin and serum lipid profiles, especially in patients with obesity or diabetes.
Metabolic syndrome is a group of metabolic disorders, including glucose intolerance and dyslipidemia, which increase the risk of atherosclerotic cardiovascular disease and diabetes. The prevalence of metabolic syndrome, a major public health problem, has been growing steadily, leading to a growing interest in developing drugs to correct dyslipidemia and hyperglycemia. Lipasin has been shown to have a dual role in lipid metabolism and glucose homeostasis. Lipasin is secreted from the liver into the circulation, involved in triglyceride metabolism and promotes pancreatic beta cell proliferation. Active as a dimmer, lipoprotein lipase (LPL) binds to heparan sulfate proteoglycans (HSPG) and glycosylphosphatidylinositol anchored high density lipoprotein binding protein 1(GPIHPB1) on the surface of capillary microvascular endothelial cells. LPL hydrolyzes triglyceride (TAG) in chylomicrons and very low-density lipoprotein (VLDL) to produce free fatty acid (FFAs), which is then absorbed by peripheral tissues, including fat, muscle and heart. Both angiopoietin-like 3 (Angptl3) and Angptl4 need to be cleaved to release the functional N-terminus to inhibit LPL, respectively, reversibly or irreversibly disrupting dimer formation. Lipasin may directly or indirectly inhibit LPL by promoting Angptl3 cleavage. Food intake significantly induces lipoprotein expression, while fasting induced Angptl4. Therefore, Lipasin are important regulators of lipid metabolism. The results of Fu et al. showed that fasting serum Lipasin levels in non-diabetic lean subjects were approximately 2 ng/ mL, and increased in patients with type2 diabetes and obesity. Lipasin levels increased 2 hours following the defined diet, and therefore, Lipasin is a nutritionally regulated hepatocyte factor. The increased levels of lipoproteins in type2 diabetes and obesity provide a potential mechanism for explaining hypertriglyceridemia in both pathological conditions due to the dual effects of triglyceride metabolism and glucose homeostasis.
Figure 1: Roles of lipasin (Angptl8) in regulating triglyceride metabolism and pancreatic beta-cell proliferation (Ren Zhang, et al. Cardiovascular Diabetology, 2014)
Currently, Lipasin has been identified and characterized by several groups, and shows promise as a therapeutic agent for metabolic syndrome and Type 2 diabetes. However, the physiological functions and molecular targets of this protein are still largely unknown, and the lipasin function remains controversial. Consequently, further study of lipasin function is undoubtedly valuable and meaningful for future research work and clinical treatment.
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