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Journal of Diabetes Research
Volume 2016 (2016), Article ID 4860595, 7 pages
Review Article

The Rise and the Fall of Betatrophin/ANGPTL8 as an Inducer of β-Cell Proliferation

1Biochemistry and Molecular Biology Unit, Dasman Diabetes Institute, Kuwait City, Kuwait
2Research Division, Dasman Diabetes Institute, Kuwait City, Kuwait

Received 15 June 2016; Revised 16 August 2016; Accepted 17 August 2016

Academic Editor: Daisuke Yabe

Copyright © 2016 Mohamed Abu-Farha et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Diabetes is a global health problem that is caused by impaired insulin production from pancreatic β-cells. Efforts to regenerate β-cells have been advancing rapidly in the past two decades with progress made towards identifying new agents that induce β-cells regeneration. ANGPTL8, also named betatrophin, has been recently identified as a hormone capable of inducing β-cells proliferation and increasing β-cells mass in rodents. Its discovery has been cherished as a breakthrough and a game changer in the field of β-cells regeneration. Initially, ANGPTL8 has been identified as atypical member of the angiopoietin-like protein family as a regulator of triglyceride in plasma through its interaction with ANGPTL3 and its regulation of lipoprotein lipase activity. In this review, we will review literature on the proposed role of ANGPTL8 in β-cells proliferation, the controversy regarding this role, and the emerging data questioning its involvement in β-cells proliferation. Additionally we will discuss new clinical data that describes its role in diabetes and the putative therapeutic targeting of this protein.