Journals / Trakya University Journal of Natural Sciences / 2019 / Cilt: 20 - Sayı: Kök Hücre

CONCISE REVIEW: β CELL REPLACEMENT THERAPIES IN TREATMENT OF DIABETES MELLITUS

Pages
45–54
Publication Date
2022-10-18
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

This review is carrying a novel potential for enlightening the current treatments and future-based therapies.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Metabolic rate of glucose uptake is generally controlled by a feedback mechanism covering islet β cells and insulinsensitive tissues, wherein tissue sensitivity to insulin influences the level of β-cell comeback.
📊
Key Findings & Data:Latest discoveriesfrom clinical research deliver significant information about approaches to stop and treat diabetes and some of the adversativeproperties of these interferences.
💡
Conclusion & Impact:This review is carrying a novel potential for enlightening the current treatments and future-based therapies.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Metabolic rate of glucose uptake is generally controlled by a feedback mechanism covering islet β cells and insulinsensitive tissues, wherein tissue sensitivity to insulin influences the level of β-cell comeback. In case of insulin presence, βcells preserve standard glucose tolerance via enhancing insulin production. Even though β-cell dysfunction has a stronghereditary component, environmental alterations carry an important part as well. Current research methods have facilitated toestablish the important part of hexoses, amino acids, and fatty acids in the development of insulin resistance and β-celldysfunction, therefore more operative treatments to slow the progressive loss of β-cell function are required. Latest discoveriesfrom clinical research deliver significant information about approaches to stop and treat diabetes and some of the adversativeproperties of these interferences. Generation of satisfactory numbers of pancreatic endocrine cells that work in the same wayas primary islets is of supreme prominence for the expansion of cell treatments to cure. In this study, we focused on differenttechniques starting from islet and pancreas transplantations individually and ending on new therapies such as stem celltechnology and bioengineering. We aimed to establish a comprehensive and detailed explanation of treatment perspectives forislet cell loss. This review is carrying a novel potential for enlightening the current treatments and future-based therapies.

Özet

Glikoz alımının metabolik oranı, genellikle adacık hücrelerini ve insüline duyarlı dokuları kapsayan bir geri bildirim mekanizması ile kontrol edilir. İnsülin varlığında β hücreleri insülin üretimini artırarak standart glikoz toleransını korurlar. βhücre disfonksiyonunda kalıtsal bileşenlerin etkileri yüksek olsa da, çevresel değişikliklerin de önemli bir rol oynadığı gösterilmiştir. Güncel araştırma yöntemleri, insülin direnci ve β-hücre disfonksiyonunun oluşmasında heksozların, amino asitlerin ve yağ asitlerinin etkilerinin varlığını göstermekle birlikte, hücre fonksiyonunun aşamalı kaybını yavaşlatmak için daha etkili tedavilerin gerekliliğini de göstermektedir. Klinik araştırmalardan elde edilen sonuçlar diyabetin durdurulması ve tedavi edilmesi ve bu müdahalelerin olumsuz özelliklerinden bazıları ile ilgili önemli bilgiler sunmaktadır. Birincil adacık hücreleri ile aynı şekilde çalışan pankreatik endokrin hücrelerinin yeterli sayıda üretilmesi, iyileştirilmesi için hücre tedavilerinin genişletilmesi büyük öneme sahiptir. Bu derlemede, adacık ve pankreas transplantasyonlarından başlayıp kök hücre teknolojisi ve biyomühendislik odaklı yeni tedavi tekniklerinin incelenmesine odaklandık. Adacık hücre kaybı için tedavi perspektiflerinin kapsamlı ve ayrıntılı bir açıklamasını yapmayı amaçladık. Dolayısıyla bu inceleme, mevcut tedavileri ve geleceğe dayalı tedavileri aydınlatmak için açıklayıcı bir potansiyel taşımaktadır.

🔖

Cite This Article

ERGÜN, B., ARPALI, E., SOMUNCU, Ö. S., ÇELİK, U. (2022). CONCISE REVIEW: β CELL REPLACEMENT THERAPIES IN TREATMENT OF DIABETES MELLITUS. Trakya University Journal of Natural Sciences, Cilt: 20 - Sayı: Kök Hücre, 45–54. https://ajindex.com/articles/598582

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (13)

  1. Akinci, E., Banga, A., Greder, L.V., Dutton, J.R. & Slack, J.M.W. 2012. Reprogramming of pancreatic exocrine cells towards a beta (beta) cell character using Pdx1, Ngn3 and MafA. Biochemical Journal, 442: 539-550
  2. Burns, C.J., Persaud, S.J. & Jones, P.M. 2004. Stem cell therapy for diabetes: do we need to make beta cells? Journal of Endocrinology, 183: 437-443
  3. Calafiore, R., Basta, G., Luca, G., Calvitti, M., Calabrese, G., Racanicchi, L., Macchiarulo, G., Mancuso, F., Guido, L. & Brunetti, P. 2004. Grafts of microencapsulated pancreatic islet cells for the therapy of diabetes mellitus in non-immunosuppressed animals. Biotechnology and Applied Biochemistry, 39: 159-164
  4. Cheung, A.T., Dayanandan, B., Lewis, J.T., Korbutt, G.S., Rajotte, R.V., Bryer-Ash, M., Boylan, M.O., Wolfe, M.M. & Kieffer, T.J. 2000. Glucose-dependent insulin release from genetically engineered K cells. Science, 290: 1959- 1962
  5. Cui, W., Kim, D.H., Imamura, M., Hyon, S.H. & Inoue, K. 2001. Tissue-engineered pancreatic islets: culturing rat islets in the chitosan sponge. Cell Transplantation, 10: 499- 502
  6. Dean, P.G., Kukla, A., Stegall, M.D. & Kudva, Y.C. 2017. Pancreas transplantation. British Medical Journal, 357pp
  7. Ellis, C., Ramzy, A. & Kieffer, T.J. 2017. Regenerative medicine and cell-based approaches to restore pancreatic function. Nature Reviews Gastroenterology & Hepatology, 14: 612-628
  8. Fioretto, P., Steffes, M.W., Sutherland, D.E.R., Goetz, F.C. & Mauer, M. 1998. Reversal of lesions of diabetic nephropathy after pancreas transplantation. New England Journal of Medicine, 339: 69-75
  9. Green, A.D., Vasu, S. & Flatt, P.R. 2018. Cellular models for beta-cell function and diabetes gene therapy. Acta physiologica, 222.
  10. Hafiz, M.M., Faradji, R.N., Froud, T., Pileggi, A., Baidal, D.A., Cure, P., Ponte, G., Poggioli, R., Cornejo, A., Messinger, S., Ricordi, C. & Alejandro, R. 2005. Immunosuppression and procedure-related complications in 26 patients with type 1 diabetes mellitus receiving allogeneic islet cell transplantation. Transplantation, 80: 1718-1728
  11. Halpin, A., Floora, H., Hidalgo, L., Shapiro, J., Senior, P., Bigam, D. & Campbell, P. 2017. Patient Tailored Crossmatch, Do Islet Cell and Pancreas Transplants Call for a Different Fit? Transplantation, 101: 29
  12. Hammerman, M.R. 2007. Organogenesis of kidney and endocrine pancreas: the window opens. Organogenesis, 3: 59-66
  13. Hussain, M.A. & Theise, N.D. 20