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Pancreatic islet

Islet Cell Transplantation After Pancreas Removal May Help Preserve Normal Blood Sugar

Pancreatic isletSurgery to remove all or part of the pancreas and then transplant a patient’s own insulin-producing islet cells appears to be a safe and effective final measure to alleviate pain from severe chronic pancreatitis and to help prevent surgically induced diabetes, according to a report published online by JAMA Surgery.

Chronic pancreatitis (CP) is an inflammatory disease that over time leads to loss of function of the pancreas and manifests with intractable pain, malabsorption and diabetes. While medical management and pain control are the initial approaches to CP, some patients need to undergo more invasive procedures to relieve ductal pressure in the pancreas. If those measures fail, surgical options can include total removal of the pancreas (total pancreatectomy, TP) or the Whipple procedure to remove part of the pancreas. Total pancreas removal produces diabetes because insulin-secreting cells are removed. Autologous islet transplantation (AIT) was first described in the 1970s as a potential way to preserve normal blood glucose levels after near-total or total pancreas removal. However, few medical centers worldwide offer such treatment for patients with CP, according to background information in the study.Denise S. Tai, M.D., of the University of California, Los Angeles, and co-authors examined the outcomes of nine patients (5 male) who underwent pancreatic resection and AIT at the UCLA Center for Pancreatic Diseases between March 2007 and December 2013. It was a two-center collaboration with the University of California, San Francisco, handling isolation of the islet cells from the pancreatic tissue after removal.

Results show that eight of nine patients had successful procedures to isolate islet cells after their total or partial pancreas removal. Two of the patients did not require insulin and one required a low dose. All nine patients had less pain or were pain free two months after surgery.

“Pancreatic resection with AIT for severe CP is a safe and effective final alternative to ameliorate debilitating pain and to help prevent the development of surgical diabetes. It is practiced at only a few specialized centers worldwide because of the need for multidisciplinary coordination and care of these patients. … However, with the practice of geographically remote islet isolation by means of institutional collaboration, many more patients with CP may have access to and may greatly benefit from this procedure,” the authors conclude.


Story Source:

The above story is based on materials provided by The JAMA Network Journals.Note: Materials may be edited for content and length.


Journal Reference:

  1. Denise S. Tai, Na Shen, Gregory L. Szot, Andrew Posselt, Nicholas J. Feduska, Andrew Habashy, Barbara Clerkin, Erin Core, Ronald W. Busuttil, O. Joe Hines, Howard A. Reber, Gerald S. Lipshutz. Autologous Islet Transplantation With Remote Islet Isolation After Pancreas Resection for Chronic Pancreatitis.JAMA Surgery, 2014; DOI: 10.1001/jamasurg.2014.932

Cite This Page:

The JAMA Network Journals. “Islet cell transplantation after pancreas removal may help preserve normal blood sugar.” ScienceDaily. ScienceDaily, 10 December 2014. <www.sciencedaily.com/releases/2014/12/141210162322.htm>.

 

 

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Enterovirus

Detection of Enterovirus Infection in Insulin Producing Cells in Patients Newly Diagnosed with Type 1 Diabetes

EnterovirusNorwegian scientists with European partners have found evidence for the presence of Enterovirus in pancreatic islets of type 1 diabetic patients. This provides evidence consistent with the theory that a low-grade Enteroviral infection in the pancreatic islets contribute to disease progression in humans.

The discovery provides possibility for both antiviral treatment and vaccine of type 1 diabetes, according to a press release from The University of Oslo. Type 1 diabetes affects young people and children. Unlike type 2, type 1 cannot be treated by diet changes and exercise Insulin is needed. Only 29 % of the patients reach the recommended goals for treatment to prevent disabling late diabetes complications.

The Diabetes Virus Detection study (DiViD) is the first to examine fresh pancreatic tissue at the diagnosis of type 1 diabetes for the presence of viruses. Minimal pancreatic tail resection was performed 3-9 weeks after onset of type 1 diabetes in 6 adult patients (age 24-35 years).

The presence of enteroviral capsid protein 1 (VP1) and the expression of class I HLA were investigated by immunohistochemistry. Enterovirus RNA was analyzed from isolated pancreatic islets and from fresh frozen whole pancreatic tissue using PCR and sequencing. Non-diabetic organ donors served as controls. VP1 was detected in the islets of all type 1 diabetes patients (2 of 9 controls).

Hyperexpression of class I HLA molecules was found in the islets of all patients (1 of 9 controls).

Enterovirus specific RNA sequences were detected in 4 of 6 cases (0 of 6 controls). The results were confirmed in different laboratories. Only 1.7 % of the islets contained VP1 positive cells and the amount of enterovirus RNA was low. The results provides evidence for the presence of enterovirus in pancreatic islets of type 1 diabetic patients, being consistent with the possibility that a low grade enteroviral infection in the pancreatic islets contribute to disease progression in humans.


Story Source:

The above story is based on materials provided by Oslo University HospitalNote: Materials may be edited for content and length.


Journal Reference:

  1. L. Krogvold, B. Edwin, T. Buanes, G. Frisk, O. Skog, M. Anagandula, O. Korsgren, D. Undlien, M. Eike, S. J. Richardson, P. Leete, N. G. Morgan, S. Oikarinen, M. Oikarinen, J. E. Laiho, H. Hyoty, J. Ludvigsson, K. F. Hanssen, K. Dahl-Jorgensen. Detection of a low-grade enteroviral infection in the islets of Langerhans of living patients newly diagnosed with type 1 diabetesDiabetes, 2014; DOI: 10.2337/db14-1370

Cite This Page:

Oslo University Hospital. “Detection of enterovirus infection in insulin producing cells in patients newly diagnosed with type 1 diabetes.” ScienceDaily. ScienceDaily, 15 December 2014. <www.sciencedaily.com/releases/2014/12/141215114103.htm>.

 

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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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