Researchers identify a metabolite as a biomarker of diabetes risk
Type 2 diabetes (T2D) is the most common form of diabetes and is associated with many complications. T2D is preventable through weight control and exercise; however, many individuals are unaware that they are at risk and do not change their lifestyle in time to avoid disease. In this issue of the Journal of Clinical Investigation , Robert Gerszten and colleagues at Massachusetts General Hospital identify the metabolite 2-aminoadipic acid (2-AAA) as a biomarker for T2D diabetes risk. Individuals with increased levels of 2-AAA had a much greater risk of developing diabetes than individuals with lower 2-AAA levels. The authors found that this metabolite was present in at-risk individuals up to 12 years before to T2D onset. Additionally, addition of 2-AAA to isolated pancreatic cells from both mice and humans enhanced insulin secretion. This study provides a biomarker of T2D risk that is a potential therapeutic target for the regulation of glucose homeostasis.
TITLE: 2-Aminoadipic acid is a biomarker for diabetes risk
AUTHOR CONTACT: Robert E. Gerszten
Massachusetts General Hospital, Charlestown, MA, USA
Phone: 617-724-8322; Fax: 617-726-1544; E-mail: RGERSZTEN@PARTNERS.ORG
View this article at: http://www.jci.org/articles/view/64801?key=174fdbca12771be4333b
Genotype influences muscle performance
Elite endurance athletes commonly have mutations that result in the loss of the protein α-actinin-3, which is a major component of fast-twitch muscle fibers. Loss of α-actinin-3 is associated with reduced power, increased endurance capacity, and enhanced response to endurance training. In this issue of the Journal of Clinical Investigation , Kathryn North and colleagues at the Murdoch Children's Research Institute report that the loss of α-actinin-3 in fast-twitch muscle fibers, results in compensation by α-actinin-2. The presence of α-actinin-2 in fast-twitch muscle contributed to reprogramming these muscles through increased calcineurin signaling. This study provides insight into how mutations in the gene encoding α-actinin-3 promote skeletal muscle adaptations that are advantageous to elite endurance athletes
TITLE: ACTN3 genotype influences muscle performance through the regulation of calcineurin signaling
AUTHOR CONTACT: Kathryn North
Murdoch Childrens Research Institute, Parkville, UNK, AUS
Phone: 61-3-8341-6226; Fax: 61-3-9348-1391; E-mail: kathryn.north@mcri.edu.au
View this article at: http://www.jci.org/articles/view/67691?key=56ae65251668e68f1365
ALSO IN THIS ISSUE
TITLE: Radiation-induced acid ceramidase confers prostate cancer resistance and tumor relapse
AUTHOR CONTACT: Xiang Liu
Medical University of South Carolina, Charleston, SC, USA
Phone: 843-792-8499; E-mail: liux@musc.edu
View this article at: http://www.jci.org/articles/view/64791?key=33fb88a91ba4be40201d
TITLE: Integrins protect cardiomyocytes from ischemia/reperfusion injury
AUTHOR CONTACT: Robert Ross
UCSD / VA Healthcare San Diego, San Diego, CA, USA
Phone: 858-642-1138; Fax: 858-642-1199; E-mail: rross@ucsd.edu
View this article at: http://www.jci.org/articles/view/64216?key=e8e6af4e23435ac156c4
TITLE: Pak and Rac GTPases promote oncogenic KIT-induced neoplasms
AUTHOR CONTACT: Reuben Kapur
Indiana University School of Medicine, Herman B Wells Center for Pediatric , Indianapolis, IN, USA
Phone: 317-274-4658; Fax: 317-274-8679; E-mail: rkapur@iupui.edu
View this article at: http://www.jci.org/articles/view/67509?key=24e726058175dbdba5b3
TITLE: Myeloid-derived suppressor cell development is regulated by a STAT-IRF-8 Axis
AUTHOR CONTACT: Scott Abrams
Roswell Park Cancer Institute, Buffalo, NY, USA
Phone: 716-845-4375; E-mail: Scott.Abrams@RoswellPark.org
View this article at: http://www.jci.org/articles/view/68189?key=80115473c2ff550aa400
TITLE: Maternal uterine NK cell–activating receptor KIR2DS1 enhances placentation
AUTHOR CONTACT: Ashley Moffett
Department of Pathology, Cambridge CB2 1QP, , GBR
Phone: 01223-333727; Fax: 01223-765065; E-mail: am485@cam.ac.uk
View this article at: http://www.jci.org/articles/view/68991?key=fc35e5ed4594967662fd
TITLE: p16 INK4a protects against dysfunctional telomere–induced ATR-dependent DNA damage responses
AUTHOR CONTACT: Sandy Chang
Yale University School Of Medicine, New Haven, CT, USA
Phone: 203-737-4667; E-mail: schang@yale.edu
View this article at: http://www.jci.org/articles/view/69574?key=ef90170fda08456e9bb8
TITLE: Inhibiting glycolytic metabolism enhances CD8+ T cell memory and antitumor function
AUTHOR CONTACT: Luca Gattinoni
NCI, Bethesda, MD, USA
Phone: 301-451-6914; E-mail: gattinol@mail.nih.gov
View this article at: http://www.jci.org/articles/view/69589?key=7e34837159d36216bbd4
TITLE: Blood pressure homeostasis is maintained by a P311–TGF-β axis
AUTHOR CONTACT: Lucia Schuger
The University of Chicago, Chicago, IL, USA
Phone: 773-702-4784; Fax: 773-795-6357; E-mail: lschuger@bsd.uchicago.edu
View this article at: http://www.jci.org/articles/view/69884?key=54f3c5a99261ca71485e
Journal of Clinical Investigation