β-Cell Secretory Capacity and Demand in Recipients of Islet, Pancreas, and Kidney Transplants

Rickels, Michael R.; Mueller, Rebecca; Teff, Karen L.; Naji, Ali

doi:10.1210/jc.2009-2289

Cited by 48 publications

(45 citation statements)

References 42 publications

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“…Interestingly, the proinsulin/ C-peptide ratio is particularly elevated in islet transplant recipients who fail to maintain insulin independence (21)(22)(23), suggesting an association with graft failure. One study reported no difference in proinsulin/insulin ratio among islet transplant recipients, normal control subjects, and immunosuppressed recipients of other organ transplants in patients with lower HbA 1c and at earlier time points posttransplant (24). Taken together, these findings suggest that defective proinsulin processing may be a marker of graft dysfunction and eventual failure and may be exacerbated by hyperglycemia (25).…”

Section: Impaired Proinsulin Processingmentioning

confidence: 98%

Death and Dysfunction of Transplanted β-Cells: Lessons Learned From Type 2 Diabetes?

et al. 2013

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β-Cell replacement by islet transplantation is a potential curative therapy for type 1 diabetes. Despite advancements in islet procurement and immune suppression that have increased islet transplant survival, graft function progressively declines, and many recipients return to insulin dependence within a few years posttransplant. The progressive loss of β-cell function in islet transplants seems unlikely to be explained by allo- and autoimmune-mediated mechanisms alone and in a number of ways resembles β-cell failure in type 2 diabetes. That is, both following transplantation and in type 2 diabetes, islets exhibit decreased first-phase glucose-stimulated insulin secretion, impaired proinsulin processing, inflammation, formation of islet amyloid, signs of oxidative and endoplasmic reticulum stress, and β-cell death. These similarities suggest common mechanisms may underlie loss of insulin production in both type 2 diabetes and islet transplantation and point to the potential for therapeutic approaches used in type 2 diabetes that target the β-cell, such as incretin-based therapies, as adjuncts for immunosuppression in islet transplantation.

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Section: Impaired Proinsulin Processingmentioning

confidence: 98%

Death and Dysfunction of Transplanted β-Cells: Lessons Learned From Type 2 Diabetes?

et al. 2013

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“…In addition to impaired glucagon responsiveness, islet engraftment in the liver is also associated with a deficiency of pancreatic polypeptide (PP) release (53); a loss of nutrient-stimulated PP secretion in CP contributes to hepatic insulin resistance. The combined deficiency of glucagon and PP responsiveness in transplanted islets recapitulates the defect seen in other versions of pancreatogenic or type 3c diabetes.…”

Section: Improving Success Of Islet Auto-transplantationmentioning

confidence: 99%

Total Pancreatectomy With Islet Autotransplantation

Bellin¹,

Gelrud²,

Arreaza-Rubín³

et al. 2014

Pancreas

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A workshop sponsored by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) focused on research gaps and opportunities in total pancreatectomy with islet autotransplantation (TPIAT) for the management of chronic pancreatitis (CP). The session was held on July 23, 2014 and structured into five sessions: (1) patient selection, indications, and timing; (2) technical aspects of TPIAT; (3) improving success of islet autotransplantation; (4) improving outcomes after total pancreatectomy; and (5) registry considerations for TPIAT. The current state of knowledge was reviewed; knowledge gaps and research needs were specifically highlighted. Common themes included the need to identify which patients best benefit from and when to intervene with TPIAT, current limitations of the surgical procedure, diabetes remission and the potential for improvement, opportunities to better address pain remission, GI complications in this population, and unique features of children with CP considered for TPIAT. The need for a multicenter patient registry that specifically addresses the complexities of CP and total pancreatectomy outcomes as well as post-surgical diabetes outcomes was repeatedly emphasized.

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“…Вопросы патогенеза нормальной у реципиентов с трансплантатом почки или сочетанной трансплантацией, которые получали низкую дозу глюкокортикоидов (5 мг ежедневно) и уме-ренную дозу такролимуса (концентрация в крови была в пределах от 6 до 10 мкг/л) [44]. Митохондрии играют ключевую роль в секреции ин-сулина.…”

Post-transplantation diabetes mellitus: an overview

et al. 2015

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© Сахарный диабет, 2015Вопросы патогенеза осттрансплантационный сахарный диабет (ПТСД) -частое осложнение после транс-плантации солидных органов. Пациенты с развившимся ПТСД имеют повышенный риск острого отторжения, инфекций, кардиоваскулярных событий, снижения долгосрочной выживаемости [1]. В США ме-дицинские затраты на реципиента почечного трансплан-тата с развившимся ПТСД увеличиваются на $21 500 [2].

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β-Cell Secretory Capacity and Demand in Recipients of Islet, Pancreas, and Kidney Transplants

Abstract: Impaired beta-cell secretory capacity in islet transplantation is best explained by a low engrafted beta-cell mass and not by a deleterious effect of tacrolimus.

Cited by 48 publications

References 42 publications

Death and Dysfunction of Transplanted β-Cells: Lessons Learned From Type 2 Diabetes?

Death and Dysfunction of Transplanted β-Cells: Lessons Learned From Type 2 Diabetes?

Total Pancreatectomy With Islet Autotransplantation

Post-transplantation diabetes mellitus: an overview

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