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JCI early table of contents for Sept. 16, 2013

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

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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

Murdoch Childrens Research Institute, Parkville, UNK, AUS
Phone: 61-3-8341-6226; Fax: 61-3-9348-1391; E-mail:

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TITLE: Radiation-induced acid ceramidase confers prostate cancer resistance and tumor relapse

Medical University of South Carolina, Charleston, SC, USA
Phone: 843-792-8499; E-mail:

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TITLE: Integrins protect cardiomyocytes from ischemia/reperfusion injury

UCSD / VA Healthcare San Diego, San Diego, CA, USA
Phone: 858-642-1138; Fax: 858-642-1199; E-mail:

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TITLE: Pak and Rac GTPases promote oncogenic KIT-induced neoplasms

Indiana University School of Medicine, Herman B Wells Center for Pediatric , Indianapolis, IN, USA
Phone: 317-274-4658; Fax: 317-274-8679; E-mail:

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TITLE: Myeloid-derived suppressor cell development is regulated by a STAT-IRF-8 Axis

Roswell Park Cancer Institute, Buffalo, NY, USA
Phone: 716-845-4375; E-mail:

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TITLE: Maternal uterine NK cellactivating receptor KIR2DS1 enhances placentation

AUTHOR CONTACT: Ashley Moffett
Department of Pathology, Cambridge CB2 1QP, , GBR
Phone: 01223-333727; Fax: 01223-765065; E-mail:

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TITLE: p16INK4a protects against dysfunctional telomereinduced ATR-dependent DNA damage responses

Yale University School Of Medicine, New Haven, CT, USA
Phone: 203-737-4667; E-mail:

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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:

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TITLE: Blood pressure homeostasis is maintained by a P311TGF-β axis

The University of Chicago, Chicago, IL, USA
Phone: 773-702-4784; Fax: 773-795-6357; E-mail:

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Contact: Corinne Williams
Journal of Clinical Investigation

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