Relevant bibliographies by topics / Islet/β-cell replacement

Academic literature on the topic 'Islet/β-cell replacement'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Islet/β-cell replacement"

1

Da Silva Xavier, Gabriela. "The Cells of the Islets of Langerhans." Journal of Clinical Medicine 7, no. 3 (March 12, 2018): 54. http://dx.doi.org/10.3390/jcm7030054.

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Islets of Langerhans are islands of endocrine cells scattered throughout the pancreas. A number of new studies have pointed to the potential for conversion of non-β islet cells in to insulin-producing β-cells to replenish β-cell mass as a means to treat diabetes. Understanding normal islet cell mass and function is important to help advance such treatment modalities: what should be the target islet/β-cell mass, does islet architecture matter to energy homeostasis, and what may happen if we lose a particular population of islet cells in favour of β-cells? These are all questions to which we will need answers for islet replacement therapy by transdifferentiation of non-β islet cells to be a reality in humans. We know a fair amount about the biology of β-cells but not quite as much about the other islet cell types. Until recently, we have not had a good grasp of islet mass and distribution in the human pancreas. In this review, we will look at current data on islet cells, focussing more on non-β cells, and on human pancreatic islet mass and distribution.
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2

Quizon, Michelle J., and Andrés J. García. "Engineering β Cell Replacement Therapies for Type 1 Diabetes: Biomaterial Advances and Considerations for Macroscale Constructs." Annual Review of Pathology: Mechanisms of Disease 17, no. 1 (January 24, 2022): 485–513. http://dx.doi.org/10.1146/annurev-pathol-042320-094846.

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While significant progress has been made in treatments for type 1 diabetes (T1D) based on exogenous insulin, transplantation of insulin-producing cells (islets or stem cell–derived β cells) remains a promising curative strategy. The current paradigm for T1D cell therapy is clinical islet transplantation (CIT)—the infusion of islets into the liver—although this therapeutic modality comes with its own limitations that deteriorate islet health. Biomaterials can be leveraged to actively address the limitations of CIT, including undesired host inflammatory and immune responses, lack of vascularization, hypoxia, and the absence of native islet extracellular matrix cues. Moreover, in efforts toward a clinically translatable T1D cell therapy, much research now focuses on developing biomaterial platforms at the macroscale, at which implanted platforms can be easily retrieved and monitored. In this review, we discuss how biomaterials have recently been harnessed for macroscale T1D β cell replacement therapies.
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3

Stephens, Clarissa Hernandez, Rachel A. Morrison, Madeline McLaughlin, Kara Orr, Sarah A. Tersey, J. Catharine Scott-Moncrieff, Raghavendra G. Mirmira, Robert V. Considine, and Sherry Voytik-Harbin. "Oligomeric collagen as an encapsulation material for islet/β-cell replacement: effect of islet source, dose, implant site, and administration format." American Journal of Physiology-Endocrinology and Metabolism 319, no. 2 (August 1, 2020): E388—E400. http://dx.doi.org/10.1152/ajpendo.00066.2020.

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Replacement of islets/β-cells that provide long-lasting glucose-sensing and insulin-releasing functions has the potential to restore extended glycemic control in individuals with type 1 diabetes. Unfortunately, persistent challenges preclude such therapies from widespread clinical use, including cumbersome administration via portal vein infusion, significant loss of functional islet mass upon administration, limited functional longevity, and requirement for systemic immunosuppression. Previously, fibril-forming type I collagen (oligomer) was shown to support subcutaneous injection and in situ encapsulation of syngeneic islets within diabetic mice, with rapid (<24 h) reversal of hyperglycemia and maintenance of euglycemia for beyond 90 days. Here, we further evaluated this macroencapsulation strategy, defining effects of islet source (allogeneic and xenogeneic) and dose (500 and 800 islets), injection microenvironment (subcutaneous and intraperitoneal), and macrocapsule format (injectable and preformed implantable) on islet functional longevity and recipient immune response. We found that xenogeneic rat islets functioned similarly to or better than allogeneic mouse islets, with only modest improvements in longevity noted with dosage. Additionally, subcutaneous injection led to more consistent encapsulation outcomes along with improved islet health and longevity, compared with intraperitoneal administration, whereas no significant differences were observed between subcutaneous injectable and preformed implantable formats. Collectively, these results document the benefits of incorporating natural collagen for islet/β-cell replacement therapies.
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4

Burns, Christopher J., Shanta J. Persaud, and Peter M. Jones. "Stem cell therapy for diabetes: do we need to make beta cells?" Journal of Endocrinology 183, no. 3 (December 2004): 437–43. http://dx.doi.org/10.1677/joe.1.05981.

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Type 1 diabetes can now be ameliorated by islet transplantation, although this treatment is restricted by the insufficient supply of islet tissue. The need for an essentially limitless supply of a substitute for primary human islets of Langerhans has led to research into the suitability of stem/progenitor cells to generate insulin-producing cells to use in replacement therapies for diabetes. Although there has been much research in this area, an efficient and reproducible protocol for the differentiation of stem cells into functional insulin-secreting β-cells that are suitable for transplantation has yet to be reported. In this commentary we examine the minimum requirements for replacement β-cells and outline some of the potential sources of these cells. We also argue that the generation of the ‘perfect’ beta-cell may not necessarily lead to the most suitable tissue for transplantation.
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5

Brusko, Todd M., Holger A. Russ, and Cherie L. Stabler. "Strategies for durable β cell replacement in type 1 diabetes." Science 373, no. 6554 (July 29, 2021): 516–22. http://dx.doi.org/10.1126/science.abh1657.

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Technological advancements in blood glucose monitoring and therapeutic insulin administration have improved the quality of life for people with type 1 diabetes. However, these efforts fall short of replicating the exquisite metabolic control provided by native islets. We examine the integrated advancements in islet cell replacement and immunomodulatory therapies that are coalescing to enable the restoration of endogenous glucose regulation. We highlight advances in stem cell biology and graft site design, which offer innovative sources of cellular material and improved engraftment. We also cover cutting-edge approaches for preventing allograft rejection and recurrent autoimmunity. These insights reflect a growing understanding of type 1 diabetes etiology, β cell biology, and biomaterial design, together highlighting therapeutic opportunities to durably replace the β cells destroyed in type 1 diabetes.
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6

Carlotti, Françoise, Arnaud Zaldumbide, Johanne H. Ellenbroek, H. Siebe Spijker, Rob C. Hoeben, and Eelco J. de Koning. "β-Cell Generation: Can Rodent Studies Be Translated to Humans?" Journal of Transplantation 2011 (2011): 1–15. http://dx.doi.org/10.1155/2011/892453.

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β-cell replacement by allogeneic islet transplantation is a promising approach for patients with type 1 diabetes, but the shortage of organ donors requires new sources ofβcells. Islet regenerationin vivoand generation ofβ-cellsex vivofollowed by transplantation represent attractive therapeutic alternatives to restore theβ-cell mass. In this paper, we discuss different postnatal cell types that have been envisaged as potential sources for futureβ-cell replacement therapy. The ultimate goal being translation to the clinic, a particular attention is given to the discrepancies between findings from studies performed in rodents (bothex vivoon primary cells andin vivoon animal models), when compared with clinical data and studies performed on human cells.
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7

Ermakova, P. S., E. I. Cherkasova, N. A. Lenshina, A. N. Konev, M. A. Batenkin, S. A. Chesnokov, D. M. Kuchin, E. V. Zagainova, V. E. Zagainov, and A. V. Kashina. "Modern pancreatic islet encapsulation technologies for the treatment of type 1 diabetes." Russian Journal of Transplantology and Artificial Organs 23, no. 4 (October 22, 2021): 95–109. http://dx.doi.org/10.15825/1995-1191-2021-4-95-109.

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The review includes the results of analytical research on the problem of application of pancreatic islet encapsulation technologies for compensation of type 1 diabetes. We present a review of modern encapsulation technologies, approaches to encapsulation strategies, insulin replacement technologies: auto-, allo- and xenotransplantation; prospects for cell therapy for insulin-dependent conditions; modern approaches to β-cell encapsulation, possibilities of optimization of encapsulation biomaterials to increase survival of transplanted cells and reduce adverse consequences for the recipient. The main problems that need to be solved for effective transplantation of encapsulated islets of Langerhans are identified and the main strategies for translating the islet encapsulation technology into medical reality are outlined.
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8

Berney, Thierry, Olle Korsgren, Andrew Posselt, and Antonello Pileggi. "Islet Transplantation &β-Cell Replacement Therapies for Diabetes." Journal of Transplantation 2011 (2011): 1–2. http://dx.doi.org/10.1155/2011/157840.

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9

Shinzato, Misaki, Chika Miyagi-Shiohira, Kazuho Kuwae, Kai Nishime, Yoshihito Tamaki, Tasuku Yonaha, Mayuko Sakai-Yonaha, et al. "AP39, a Mitochondrial-Targeted H2S Donor, Improves Porcine Islet Survival in Culture." Journal of Clinical Medicine 11, no. 18 (September 14, 2022): 5385. http://dx.doi.org/10.3390/jcm11185385.

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The rapid deterioration of transplanted islets in culture is a well-established phenomenon. We recently reported that pancreas preservation with AP39 reduces reactive oxygen species (ROS) production and improves islet graft function. In this study, we investigated whether the addition of AP39 to the culture medium could reduce isolated islet deterioration and improve islet function. Isolated islets from porcine pancreata were cultured with 400 nM AP39 or without AP39 at 37 °C. After culturing for 6–72 h, the islet equivalents of porcine islets in the AP39(+) group were significantly higher than those in the AP39(−) group. The islets in the AP39(+) group exhibited significantly decreased levels of ROS production compared to the islets in the AP39(−) group. The islets in the AP39(+) group exhibited significantly increased mitochondrial membrane potential compared to the islets in the AP39(−) group. A marginal number (1500 IEs) of cultured islets from each group was then transplanted into streptozotocin-induced diabetic mice. Culturing isolated islets with AP39 improved islet transplantation outcomes in streptozotocin-induced diabetic mice. The addition of AP39 in culture medium reduces islet deterioration and furthers the advancements in β-cell replacement therapy.
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10

Niu, Guoguang, John P. McQuilling, Yu Zhou, Emmanuel C. Opara, Giuseppe Orlando, and Shay Soker. "In VitroProliferation of Porcine Pancreatic Islet Cells forβ-Cell Therapy Applications." Journal of Diabetes Research 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/5807876.

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β-Cell replacement through transplantation is the only curative treatment to establish a long-term stable euglycemia in diabetic patients. Owing to the shortage of donor tissue, attempts are being made to develop alternative sources of insulin-secreting cells. Stem cells differentiation and reprograming as well as isolating pancreatic progenitors from different sources are some examples; however, no approach has yet yielded a clinically relevant solution. Dissociated islet cells that are cultured in cell numbers byin vitroproliferation provide a promising platform for redifferentiation towardsβ-cells phenotype. In this study, we cultured islet-derived cellsin vitroand examined the expression ofβ-cell genes during the proliferation. Islets were isolated from porcine pancreases and enzymatically digested to dissociate the component cells. The cells proliferated well in tissue culture plates and were subcultured for no more than 5 passages. Only 10% of insulin expression, as measured by PCR, was preserved in each passage. High glucose media enhanced insulin expression by about 4–18 fold, suggesting a glucose-dependent effect in the proliferated islet-derived cells. The islet-derived cells also expressed other pancreatic genes such as Pdx1, NeuroD, glucagon, and somatostatin. Taken together, these results indicate that pancreatic islet-derived cells, proliferatedin vitro, retained the expression capacity for key pancreatic genes, thus suggesting that the cells may be redifferentiated into insulin-secretingβ-like cells.
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