Betatrophin The long awaited circulating factor from the liver promoting β-cell replication?

被引:10
作者
Ahnfelt-Ronne, Jonas [1 ]
Madsen, Ole D. [1 ]
机构
[1] Novo Nordisk AS, Diabet Res Unit, Malov, Denmark
关键词
AGNPTL8; betatrophin; Lipasin; RIFL; diabetes; INSULIN-RESISTANT STATES; GROWTH-FACTOR; RECEPTOR; HYPERPLASIA; GLUCOSE; MOUSE; IDENTIFICATION; METABOLISM;
D O I
10.4161/isl.28686
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Regenerative therapy in diabetes with the capacity to reconstitute a functional beta-cell mass sufficient for glycemic control holds the promise to effectively prevent the development of devastating late complications due to the unique ability of the beta-cell to sense and regulate blood-glucose levels. An ability that cannot be mimicked by insulin replacement therapy or any other means of current treatment regiments for very large patient populations. Recently, Douglas A. Melton's group from Harvard University reported the identification of a circulating protein secreted from the liver under insulin resistant states which is sufficient to dramatically and specifically increase the replication rate of beta-cells in the mouse resulting in an increased functional beta-cell mass over time. They re-named the factor betatrophin and described a number of exciting features of this molecule which suggested that it could be a potential candidate for development as a regenerative medicine in diabetes. 1 The official name of the gene encoding mouse betatrophin is Gm6484, but it has been annotated a number of times under different names: EG624219(2,3), RIFL4, Lipasin(5) and ANGPTL8.(6) The official human gene name is C19orf80, but it has also been annotated as TD26(7), LOC55908(8), as well as RIFL, Lipasin, ANGPTL8 and betatrophin.
引用
收藏
页码:e28686 / 1
页数:4
相关论文
共 22 条
[1]
Hepatocyte Growth Factor Plays a Key Role in Insulin Resistance-Associated Compensatory Mechanisms [J].
Araujo, Tiago G. ;
Oliveira, Alexandre G. ;
Carvalho, Bruno M. ;
Guadagnini, Dioze ;
Protzek, Andre O. P. ;
Carvalheira, Jose B. C. ;
Boschero, Antonio C. ;
Saad, Mario J. A. .
ENDOCRINOLOGY, 2012, 153 (12) :5760-5769
[2]
A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance [J].
Bruning, JC ;
Michael, MD ;
Winnay, JN ;
Hayashi, T ;
Horsch, D ;
Accili, D ;
Goodyear, LJ ;
Kahn, CR .
MOLECULAR CELL, 1998, 2 (05) :559-569
[3]
Identification of genes differentially expressed in human hepatocellular carcinoma by a modified suppression subtractive hybridization method [J].
Dong, XY ;
Pang, XW ;
Yu, ST ;
Su, YR ;
Wang, HC ;
Yin, YH ;
Wang, YD ;
Chen, WF .
INTERNATIONAL JOURNAL OF CANCER, 2004, 112 (02) :239-248
[4]
Liver-Derived Systemic Factors Drive β Cell Hyperplasia in Insulin-Resistant States [J].
El Ouaamari, Abdelfattah ;
Kawamori, Dan ;
Dirice, Ercument ;
Liew, Chong Wee ;
Shadrach, Jennifer L. ;
Hu, Jiang ;
Katsuta, Hitoshi ;
Hollister-Lock, Jennifer ;
Qian, Wei-Jun ;
Wagers, Amy J. ;
Kulkarni, Rohit N. .
CELL REPORTS, 2013, 3 (02) :401-410
[5]
Espes D, 2013, DIABETES
[6]
Evidence for a circulating islet cell growth factor in insulin-resistant states [J].
Flier, SN ;
Kulkarni, RN ;
Kahn, CR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (13) :7475-7480
[7]
Adaptive changes of human islets to an obesogenic environment in the mouse [J].
Gargani, S. ;
Thevenet, J. ;
Yuan, J. E. ;
Lefebvre, B. ;
Delalleau, N. ;
Gmyr, V. ;
Hubert, T. ;
Duhamel, A. ;
Pattou, F. ;
Kerr-Conte, J. .
DIABETOLOGIA, 2013, 56 (02) :350-358
[8]
Lower blood glucose, hyperglucagonemia, and pancreatic α cell hyperplasia in glucagon receptor knockout mice [J].
Gelling, RW ;
Du, XQ ;
Dichmann, DS ;
Romer, J ;
Huang, H ;
Cui, L ;
Obici, S ;
Tang, B ;
Holst, JJ ;
Fledelius, C ;
Johansen, PB ;
Rossetti, L ;
Jelicks, LA ;
Serup, P ;
Nishimura, E ;
Charron, MJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (03) :1438-1443
[9]
Regulation of Pancreatic β Cell Mass by Neuronal Signals from the Liver [J].
Imai, Junta ;
Katagiri, Hideki ;
Yamada, Tetsuya ;
Ishigaki, Yasushi ;
Suzuki, Toshinobu ;
Kudo, Hirohito ;
Uno, Kenji ;
Hasegawa, Yutaka ;
Gao, Junhong ;
Kaneko, Keizo ;
Ishihara, Hisamitsu ;
Niijima, Akira ;
Nakazato, Masamitsu ;
Asano, Tomoichiro ;
Minokoshi, Yasuhiko ;
Oka, Yoshitomo .
SCIENCE, 2008, 322 (5905) :1250-1254
[10]
Liver-Specific Disruption of the Murine Glucagon Receptor Produces α-Cell Hyperplasia Evidence for a Circulating α-Cell Growth Factor [J].
Longuet, Christine ;
Robledo, Ana M. ;
Dean, E. Danielle ;
Dai, Chunhua ;
Ali, Safina ;
McGuinness, Ian ;
de Chavez, Vincent ;
Vuguin, Patricia M. ;
Charron, Maureen J. ;
Powers, Alvin C. ;
Drucker, Daniel J. .
DIABETES, 2013, 62 (04) :1196-1205