scholarly journals  -Score: An assessment of  -cell function after islet transplantation

Diabetes Care ◽  
2005 ◽  
Vol 28 (2) ◽  
pp. 343-347 ◽  
Author(s):  
E. A. Ryan ◽  
B. W. Paty ◽  
P. A. Senior ◽  
J. R.T. Lakey ◽  
D. Bigam ◽  
...  
Keyword(s):  
Islet Transplantation ◽  
Cell Function

CGM Shows Islet Transplantation Prevents Hypoglycemia, Correcting Time in Range and Reducing Glycemic Variability, Despite Subnormal Beta-Cell Function

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 143-OR ◽  
Author(s):  
SHAREEN FORBES ◽  
TOLU OLUTOYIN OLATEJU ◽  
ANNA LAM ◽  
JOHN CASEY ◽  
JOHN CAMPBELL ◽  
...  
Keyword(s):  
Beta Cell ◽  
Islet Transplantation ◽  
Beta Cell Function ◽  
Cell Function ◽  
Glycemic Variability ◽  
Time In Range

Effect of Exenatide on ?? Cell Function After Islet Transplantation in Type 1 Diabetes

2007 ◽  
Vol 83 (1) ◽  
pp. 24-28 ◽  
Author(s):  
Khalid Al Ghofaili ◽  
Michelle Fung ◽  
Ziliang Ao ◽  
Mark Meloche ◽  
R Jean Shapiro ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Islet Transplantation ◽  
Cell Function

scholarly journals Subcutaneous Transplantation of Islets into Streptozocin-Induced Diabetic Rats

2005 ◽  
Vol 14 (8) ◽  
pp. 595-605 ◽  
Author(s):  
Craig R. Halberstadt ◽  
Deana Williams ◽  
Dwaine Emerich ◽  
Moses Goddard ◽  
Alfred V. Vasconcellos ◽  
...  
Keyword(s):  
Islet Transplantation ◽  
Cell Function ◽  
Diabetic Rats ◽  
Diabetic Patients ◽  
Pancreatic Islet Transplantation ◽  
Minimally Invasive Surgical Procedure ◽  
Minimally Invasive Surgical ◽  
Ease Of Access ◽  
Syngeneic Islet Transplantation ◽  
Type 1 Diabetic Patients

Pancreatic islet transplantation into type 1 diabetic patients is currently being performed by intraportal infusion. This method, albeit reproducible, has some disadvantages including potential development of portal hypertension, hemorrhage, and an inability to retrieve or detect the transplanted tissue. Other transplant sites have been examined in animal models including the omentum, peritoneal cavity, and the spleen. A transplant site that has not been successful in supporting functional islet tissue transplantation in humans is the subcutaneous space due primarily to the lack of a well-defined vascular bed. This site has many favorable characteristics such as ease of access for transplantation and potential for removal of the transplanted tissue with a minimally invasive surgical procedure. This report addresses the evaluation of a subcutaneously placed device for the support of rat syngeneic islet transplantation in a streptozocin-induced diabetic model. The data generated support the use of this device for islet engraftment. In addition, beta cell function in this device compared favorably with the function of islets transplanted to the renal subcapsular space as well as islets within the native pancreas.

scholarly journals Beta-cell function and human islet transplantation: can we improve?

2021 ◽  
Author(s):  
Jennifer Chen ◽  
Jenny E Gunton
Keyword(s):  
Islet Transplantation ◽  
Cell Function ◽  
Therapeutic Option ◽  
Human Islets ◽  
Post Transplantation ◽  
Human Islet Transplantation ◽  
And Function ◽  
Islet Survival

Islet transplantation, a therapeutic option to treat type 1 diabetes, is not yet as successful as whole-pancreas transplantation as a treatment for diabetes. Mouse models are commonly used for islet research. However, it is clear disparities exist between islet transplantation outcomes in mice and humans. Given the shortage of transplant-grade islets, it is crucial that we further our understanding of factors that determine long-term islet survival and function post-transplantation. In turn, that may lead to new therapeutic targets and strategies that to improve transplant outcomes. Here, we summarise the current landscape in clinical transplantation, highlight underlying similarities and differences between mouse and human islets, and review interventions that are being considered to create a new pool of β-cells for clinical application.

Author response for "Donor insulin use predicts beta‐cell function after islet transplantation"

2020 ◽  
Author(s):  
Iestyn M Shapey ◽  
Angela Summers ◽  
Petros Yiannoullou ◽  
Hussein Khambalia ◽  
Catherine Fullwood ◽  
...  
Keyword(s):  
Beta Cell ◽  
Islet Transplantation ◽  
Beta Cell Function ◽  
Cell Function ◽  
Author Response ◽  
Insulin Use

scholarly journals Over-expression of AMP-activated protein kinase impairs pancreatic β-cell function in vivo

2005 ◽  
Vol 187 (2) ◽  
pp. 225-235 ◽  
Author(s):  
S K Richards ◽  
L E Parton ◽  
I Leclerc ◽  
G A Rutter ◽  
R M Smith
Keyword(s):  
Insulin Secretion ◽  
Protein Kinase ◽  
Islet Transplantation ◽  
Cell Function ◽  
Cell Mass ◽  
Β Cell ◽  
Over Expression ◽  
Β Cell Function ◽  
Amp Activated Protein Kinase

Treatment of type 1 diabetes by islet transplantation is currently limited by loss of functional β-cell mass after transplantation. We investigated here whether adenovirus-mediated changes in AMP-activated protein kinase (AMPK) activity, previously shown to affect insulin secretion in vitro, might affect islet graft function in vivo. In isolated mouse and rat islets, insulin secretion stimulated by 17 (vs 3) mmol/l glucose was inhibited by 36.5% (P<0.01) and 43% (P<0.02) respectively after over-expression of constitutively-active AMPK- (AMPK CA) versus null (eGFP-expressing) viruses, and glucose oxidation was decreased by 38% (P<0.05) and 26.6% (P<0.05) respectively. Increases in apoptotic index (terminal deoxynucleotide transferase-mediated deoxyuridine trisphosphate biotin nick end-labelling) (TUNEL)) were also observed in AMPK CA- (22.8 ± 3.6% TUNEL-positive cells, P<0.001), but not AMPK DN- (2.72 ± 3.9%, positive cells, P=0.05) infected islets, versus null adenovirus-treated islets (0.68 ± 0.36% positive cells). Correspondingly, transplantation of islets expressing AMPK CA into streptozotocin-diabetic C57 BL/6 mice improved glycaemic control less effectively than transplantation with either null (P<0.02) or AMPK-DN-infected (P<0.01) islets. We conclude that activation of AMPK inhibits β-cell function in vivo and may represent a target for therapeutic intervention during islet transplantation.

scholarly journals Low Dose IL-2 Combined with Rapamycin Led to an Expansion of CD4+CD25+FOXP3+ Tregs and Prolonged Human Islet-allograft Survival in Humanized Mice

2020 ◽  
Author(s):  
Ada Admin ◽  
Min Hu ◽  
Wayne J Hawthorne ◽  
Leigh Nicholson ◽  
Heather Burns ◽  
...  
Keyword(s):  
T Cells ◽  
Graft Survival ◽  
Islet Transplantation ◽  
Allograft Rejection ◽  
Low Dose ◽  
Mononuclear Cells ◽  
Cell Function ◽  
Human Islet ◽  
Allograft Survival ◽  
Islet Allograft

<a>Islet transplantation is an emerging therapy for type 1 diabetes (T1D) and hypoglycaemic unawareness. However, a key challenge for islet transplantation is cellular rejection and the requirement for long-term immunosuppression. In this study we established a diabetic-humanizedNOD-scidIL2Rnull(NSG) mouse model of T cell mediated human islet-allograft rejection and developed a therapeutic regimen of low-dose recombinant human interleukin2(IL-2) combined with low-dose rapamycin to prolong graft survival. NSG-mice that had received renal-subcapsular human islet-allografts and were transfused with 1×107 of human-spleen-mononuclear-cells (hSPMCs), reconstituted human CD45+ cells that were predominantly CD3+ T cells and rejected their grafts with a median survival time of 27 days. IL-2 alone (0.3×106 IU/m2 or 1×106 IU/m2), or rapamycin alone (0.5-1mg/kg) for 3 weeks did not prolong survival. However, the combination of rapamycin with IL-2 for 3 weeks significantly prolonged human islet-allograft survival. Graft survival was associated with expansion of CD4+CD25+FOXP3+ Tregs and enhanced TGF-β production by CD4+ T cells. CD8+ T cells showed reduced IFN-γ production and reduced expression of perforin-1. The combination of IL-2 and rapamycin has the potential to inhibit human islet-allograft rejection by expanding CD4+FOXP3+ Tregs in vivo and supressing effector cell function, and could be the basis of effective tolerance-based regimens.</a>

scholarly journals Low Dose IL-2 Combined with Rapamycin Led to an Expansion of CD4+CD25+FOXP3+ Tregs and Prolonged Human Islet-allograft Survival in Humanized Mice

2020 ◽  
Author(s):  
Ada Admin ◽  
Min Hu ◽  
Wayne J Hawthorne ◽  
Leigh Nicholson ◽  
Heather Burns ◽  
...  
Keyword(s):  
T Cells ◽  
Graft Survival ◽  
Islet Transplantation ◽  
Allograft Rejection ◽  
Low Dose ◽  
Mononuclear Cells ◽  
Cell Function ◽  
Human Islet ◽  
Allograft Survival ◽  
Islet Allograft

<a>Islet transplantation is an emerging therapy for type 1 diabetes (T1D) and hypoglycaemic unawareness. However, a key challenge for islet transplantation is cellular rejection and the requirement for long-term immunosuppression. In this study we established a diabetic-humanizedNOD-scidIL2Rnull(NSG) mouse model of T cell mediated human islet-allograft rejection and developed a therapeutic regimen of low-dose recombinant human interleukin2(IL-2) combined with low-dose rapamycin to prolong graft survival. NSG-mice that had received renal-subcapsular human islet-allografts and were transfused with 1×107 of human-spleen-mononuclear-cells (hSPMCs), reconstituted human CD45+ cells that were predominantly CD3+ T cells and rejected their grafts with a median survival time of 27 days. IL-2 alone (0.3×106 IU/m2 or 1×106 IU/m2), or rapamycin alone (0.5-1mg/kg) for 3 weeks did not prolong survival. However, the combination of rapamycin with IL-2 for 3 weeks significantly prolonged human islet-allograft survival. Graft survival was associated with expansion of CD4+CD25+FOXP3+ Tregs and enhanced TGF-β production by CD4+ T cells. CD8+ T cells showed reduced IFN-γ production and reduced expression of perforin-1. The combination of IL-2 and rapamycin has the potential to inhibit human islet-allograft rejection by expanding CD4+FOXP3+ Tregs in vivo and supressing effector cell function, and could be the basis of effective tolerance-based regimens.</a>

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