A dual role of lipasin (betatrophin) in lipid metabolism and glucose homeostasis: consensus and controversy. Review uri icon

Overview

abstract

  • Metabolic syndrome includes glucose intolerance and dyslipidemia, both of which are strong risk factors for developing diabetes and atherosclerotic cardiovascular diseases. Recently, multiple groups independently studied a previously uncharacterized gene, officially named C19orf80 (human) and Gm6484 (mouse), but more commonly known as RIFL, Angptl8, betatrophin and lipasin. Both exciting and conflicting results have been obtained, and significant controversy is ongoing. Accumulating evidence from genome wide association studies and mouse genetic studies convincingly shows that lipasin is involved in lipid regulation. However, the mechanism of action, the identity of transcription factors mediating its nutritional regulation, circulating levels, and relationship among lipasin, Angptl3 and Angptl4, remain elusive. Betatrophin represents a promising drug target for replenishing β-cell mass, but current results have not been conclusive regarding its potency and specificity. Here, we summarize the consensus and controversy regarding functions of lipasin/betatrophin based on currently available evidence.

publication date

  • September 13, 2014

Research

keywords

  • Glucose
  • Homeostasis
  • Lipid Metabolism
  • Peptide Hormones

Identity

PubMed Central ID

  • PMC4172915

Scopus Document Identifier

  • 84908120785

Digital Object Identifier (DOI)

  • 10.1007/s00125-014-3346-1

PubMed ID

  • 25212743

Additional Document Info

volume

  • 13