详细记录  
题名:gamma-Aminobutyric Acid Regulates Both the Survival and Replication of Human beta-Cells.
作者:TIAN J; DANG H; CHEN Z; GUAN A; JIN Y; ATKINSON MA; KAUFMAN DL;
来源:Diabetes. 2013 Nov;62(11):3760-5. doi: 10.2337/db13-0931. Epub 2013 Aug 30. [ IF= 7.89 ] ]
URL :10.2337/db13-0931
日期:20131203
摘要:gamma-Aminobutyric acid (GABA) has been shown to inhibit apoptosis of rodent
beta-cells in vitro. In this study, we show that activation of GABAA receptors
(GABAA-Rs) or GABAB-Rs significantly inhibits oxidative stress-related beta-cell
apoptosis and preserves pancreatic beta-cells in streptozotocin-rendered
hyperglycemic mice. Moreover, treatment with GABA, or a GABAA-R- or
GABAB-R-specific agonist, inhibited human beta-cell apoptosis following islet
transplantation into NOD/scid mice. Accordingly, activation of GABAA-Rs and/or
GABAB-Rs may be a useful adjunct therapy for human islet transplantation. GABA-R
agonists also promoted beta-cell replication in hyperglycemic mice. While a
number of agents can promote rodent beta-cell replication, most fail to provide
similar activities with human beta-cells. In this study, we show that GABA
administration promotes beta-cell replication and functional recovery in human
islets following implantation into NOD/scid mice. Human beta-cell replication was
induced by both GABAA-R and GABAB-R activation. Hence, GABA regulates both the
survival and replication of human beta-cells. These actions, together with the
anti-inflammatory properties of GABA, suggest that modulation of peripheral
GABA-Rs may represent a promising new therapeutic strategy for improving
beta-cell survival following human islet transplantation and increasing
beta-cells in patients with diabetes.

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