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GABA Hormone

Understanding the Impact of GABA on Insulin Secretion and Regulation

In order to manage blood glucose levels, pancreatic beta cells release insulin in pulses. These bursts of insulin help the body to regulate and stabilize blood sugar. In individuals with type 1 diabetes, however, the pancreatic beta cells that normally secrete insulin are mistakenly destroyed by the body. This leaves the body unable to effectively regulate blood sugar on its own. Understanding the interaction between insulin-producing beta cells and other processes in the body may help researchers improve treatment and prevention options when it comes to diabetes.

A recent study examined the different roles gamma amino-butyric acid (GABA) plays in cell activity. In the brain, GABA is released from nerve cell vesicles each time a nerve impulse occurs. The GABA prepares cells for subsequent impulses by working as a calming agent. Researchers previously believed that this process worked in much the same way in the pancreas.

However, in the pancreas, GABA is evenly distributed throughout the beta cells rather than contained within small vesicles, and it is transported via the volume regulatory anion channel. This is the same channel that helps stabilize pressure inside and outside of cells so that they maintain their shape. Furthermore, research showed that GABA is released in a similar pattern and frequency as pulsatile in vivo insulin secretion. Just like in the brain, GABA plays an integral role in preparing and calming cells to make them more receptive to subsequent insulin pulses.

Scientists are interested in learning more about how GABA signaling can support the regulation of insulin secretion and potentially protect cells from autoimmune activity. This opens new doors for biomedical research that has the ability to impact diabetes care.

It is encouraging to see different types of researchers all coming together and learning from and building upon one another’s work in order to advance understanding, prevention, and treatment of various diseases, including diabetes.

Diabetes Research Connection stays abreast of the latest discoveries in the field and supports early career scientists in contributing to this body of work by providing critical funding for their projects. It is essential that scientists have the resources to pursue novel research in order to develop improved prevention, treatment, and management options for type 1 diabetes. Learn more and support current projects by visiting https://diabetesresearchconnection.org.

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Lab Mouse

Novel Type 1 Diabetes Treatment Shown to Work on Human Beta Cells Transplanted Into Mice

Lab MouseA chemical produced in the pancreas that prevented and even reversed type 1 diabetes in mice had the same effect on human beta cells transplanted into mice, new research has found.

 

GABA, or gamma-aminobutryic acid, is an amino acid produced by the same beta cells that make and secrete insulin.

Drs. Gerald Prud’homme and Qinghua Wang of the Keenan Research Centre for Biomedical Sciences of St. Michael’s Hospital published a paper in 2011 showing for the first time that GABA injections not only prevented type 1 diabetes in mice, but even reversed the disease.

A new paper published (Nov. 29) in the December issue of Diabetes shows GABA does the same thing in mice who have been injected with human pancreatic cells.

Type 1 diabetes, formerly known as juvenile diabetes, is characterized by the immune system’s destruction of the beta cells in the pancreas. As a result, the body makes little or no insulin. The only conventional treatment for type 1 diabetes is insulin injection, but insulin is not a cure as it does not prevent or reverse the loss of beta cells.

Drs. Prud’homme and Wang also found that GABA vastly improved the survival rate of pancreatic cells when they were being transplanted into mice. About 70 per cent of pancreatic cells die between the time the organ is harvested and transplanted. The researchers said their finding could lead to future research specifically related to pancreatic transplants.

GABA has been known for decades to be a key neurotransmitter in the brain, a chemical that nerve cells use to communicate with each other, but its role in the pancreas was unknown until the 2011 paper by Drs. Prud’homme and Wang.

GABA and related therapies would have to be tested in human clinical trials, a process that could take several years, the researchers said, noting that many treatments that work in mice do not always translate into effective human therapies.


Story Source:

The above story is based on materials provided by St. Michael’s Hospital. The original article was written by Leslie Shepherd. Note: Materials may be edited for content and length.


Journal Reference:

  1. I. Purwana, J. Zheng, X. Li, M. Deurloo, D. O. Son, Z. Zhang, C. Liang, E. Shen, A. Tadkase, Z.-P. Feng, Y. Li, C. Hasilo, S. Paraskevas, R. Bortell, D. L. Greiner, M. Atkinson, G. J. Prud’homme, Q. Wang. GABA Promotes Human  -Cell Proliferation and Modulates Glucose HomeostasisDiabetes, 2014; 63 (12): 4197 DOI: 10.2337/db14-0153

Cite This Page:

St. Michael’s Hospital. “Novel type 1 diabetes treatment shown to work on human beta cells transplanted into mice.” ScienceDaily. ScienceDaily, 25 November 2014. <www.sciencedaily.com/releases/2014/11/141125154733.htm>.
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OUR PROJECTS

See our approved research projects and campaigns.

Role of the integrated stress response in type 1 diabetes pathogenesis
In individuals with type 1 diabetes (T1D), the insulin-producing beta cells are spontaneously destroyed by their own immune system. The trigger that provokes the immune system to destroy the beta cells is unknown. However, accumulating evidence suggest that signals are perhaps first sent out by the stressed beta cells that eventually attracts the immune cells. Stressed cells adapt different stress mitigation systems as an adaptive response. However, when these adaptive responses go awry, it results in cell death. One of the stress response mechanisms, namely the integrated stress response (ISR) is activated under a variety of stressful stimuli to promote cell survival. However, when ISR is chronically activated, it can be damaging to the cells and can lead to cell death. The role of the ISR in the context of T1D is unknown. Therefore, in this DRC funded study, we propose to study the ISR in the beta cells to determine its role in propagating T1D.
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