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Beta Cells And Alpha Cells Of Pancreas

Beta Cells And Alpha Cells Of Pancreas

Feature papers represent the most advanced research with significant potential for high impact in the field. A Features Paper should be a substantial original Article that involves several techniques or approaches, provides an outlook for future research directions and describes possible research applications.

Diagram Of The Islets Of Langerhans. Shown Are The Acinar Cells, Beta Cells, Alpha Cells, Delta Cells And The Capillary Network Stock Photo

Functional papers are submitted on individual invitation or recommendation from the scientific editors and must receive positive feedback from the reviewers.

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By Eric Kalo Eric Kalo Scilit Google Scholar View Publications 1, * , Scott Read Scott Read Scilit Google Scholar View Publications 1, 2, 3, † and Golo Ahlenstiel Golo Ahlenstiel Scilit Google Scholar View Publications 1 , 2, 3, †

Submission received: August 13, 2022 / Revised: September 4, 2022 / Accepted: September 7, 2022 / Published: September 8, 2022

Distribution Of The Cells Of The Pancreatic Islet And Local Expression…

Numerous cell sources are being explored to enhance the mass of functional β cells, since the proof of concept for cell therapy of diabetes has been established by islet transplantation. Several of these cell sources have been shown to possess some degree of plasticity allowing differentiation along new lineages into insulin-secreting β cells. In this review, we explore emerging reprogramming pathways aimed at generating bone-specific insulin-producing cells. We focus on small molecules and key transcriptional regulators that orchestrate the phenotypic conversion and maintenance of engineered cells.

In recent years, the global incidence of diabetes mellitus has increased dramatically with the obesity epidemic. With more than 537 million people affected by the disease worldwide, it is expected to increase to more than half a billion by 2030 [1]. It has become an ever-growing burden that threatens to overwhelm many health care systems and economies around the world [2].

Diabetes is described as a group of heterogeneous metabolic diseases characterized by common elements of hyperglycemia and glucose intolerance due to defects in the section of insulin, improper effectiveness of insulin or both. In the progression of type 1 diabetes mellitus (T1DM) and type 2 DM (T2DM), there comes a point where a threshold percentage of β cells becomes dysfunctional, leading to a reliance on the administration of exogenous insulin to the treatment of patients with DM. .

Beta Cells And Alpha Cells Of Pancreas

Although the isolation of insulin in 1921 marked a panacea that radically transformed diabetes from a terminal disease to a treatable disease, the precise temporal control of glucose provided by endogenous insulin-producing β cells was not unmatched by current insulin delivery methods. As a result, exogenous insulin therapy can be a risk of hypoglycemia that can lead to a life-threatening coma and premature death [3]. Consequently, intensive insulin therapy that aims close to euglycemia can prevent the risk of long-term microvascular and macrovascular complications. Data from large population studies have consistently supported the notion that tight glycemic control can effectively reduce the development of diabetes complications and confer mortality and morbidity benefits [4, 5, 6].

A Natural Body Window To Study Human Pancreatic Islet Cell Function And Survival

Continuous monitoring of glucose and the administration of exogenous insulin are considered the mainstay of treatment for diabetes. While it leads significantly to the improvement of patient outcomes, it falls short of achieving optimal long-term blood glucose control, especially for T1DM patients [ 7 , 8 , 9 ]. In a recent randomized, multicenter trial, the results showed that the percentage of time that blood glucose remained in the target glycemic range (even with automated insulin delivery systems) was persistently suboptimal in patients with T1DM [ 10]. Consequently, therapies that result in the perpetual reconstitution of a physiological blood glucose setpoint are an extremely sought-after long-term approach.

Instead of modestly alleviating type 1 and type 2 diabetes, β-cell replacement has the potential to reverse these conditions. A successful pancreas transplant can provide a closed-loop system that restores euglycemia without the risk of severe hypoglycemia, thus stopping the development or progression of complications. However, the major risks associated with surgery, the chronic shortage of donor pancreas, graft rejection and the burden of life-long immunosuppression regimens place the usefulness of such an approach exclusively to a restricted group. of uremic patients with brittle diabetes.

To overcome the need for major surgery associated with pancreas transplantation, research has focused on developing protocols to isolate pancreatic islets. Despite the exceptional success of islet transplantation of Langerhans in decreasing insulin dependence for years in patients with T1DM, the widespread application of this approach has been hindered by the scarcity of donors, as well as by immunological challenges that are further exacerbated by long-term toxic effects. term of immunosuppressive drugs [11]. Despite the boys, the success of this approach fueled efforts for a mass generation of functional bone β cells that maintain the physiological oscillation of insulin secretion and the response to dysregulated glycemia. In addition, recent studies using autologous cell therapies may curb the need for lifelong immunosuppressive therapy.

Here, we review the cell sources, reprogramming tools, and emerging pathways envisioned in the mass generation of functional β cells for cell therapy of diabetes mellitus.

The Endocrine Pancreas

For the past 20 years, significant efforts have focused on the generation of human embryonic stem cells, hESC-derived β cells, that display sustained insulin secretion characteristics, which mainly reflect the dynamism of native human islets. By replicating the signaling events and physiologically relevant cues that dictated the fate transition through definitive endoderm and pancreatic endoderm to hormone-expressing cells during human pancreas development, β-like cells can be produced [ 12, 13, 14]. The particular interest in hESCs is supported by the fact that these cells have the capacity of extensive self-renewal and virtually can be differentiated into derivatives of all three germ layers.

Numerous studies have outlined protocols for the differentiation of insulin-producing cell types from hESCs [ 15 , 16 , 17 , 18 , 19 , 20 , 21 ]. However, the reconstruction of functionally equivalent mono-hormonal cells that produce insulin under cell culture conditions has been elusive. This is probably because the in vitro systems used lack critical signals present in vivo, including the close interaction between exocrine, ductal and endocrine cells [ 15 , 20 , 22 , 23 ]. Among the critical issues with hESC-derived therapeutic products is the occurrence of unwanted cell populations during in vitro differentiation that could interfere with the activity of the desired cell populations. Another concern is the risk of tumorigenicity. Furthermore, the wider use of ESCs for research purposes is still largely hindered by numerous governmental prohibitions regarding the use of human embryos in many countries, as well as ethical and religious sensitivities.

Compared to ESCs and induced pluripotent stem cells (iPSCs), stem-like adult mesenchymal stem cells (MSCs) are considered ideal candidates for generating functional beta cells for personalized medicine due to their anti-inflammatory, immunomodulatory properties and superior angiogenic. Numerous studies have shown that MSCs isolated from a wide range of tissues and organs, such as bone marrow, adipose tissue, Wharton’s jelly, umbilical cord matrix blood, placenta and dental pulp, possess a plasticity of development to differentiate into functional insulin-producing cells with similar cytoarchitecture and functionality. to β cells. Consequently, the use of MSC transplantation for the treatment of diabetes has been the focus of randomized controlled trials (RCTs) for the past few years. Although several clinical trials have shown that MSCs can reduce hyperglycemia by increasing insulin secretion in humans, the lack of control arms in some small sample sizes, inconsistent methods of isolation and delivery of MSCs, adverse effects and failure to sustain the therapeutic effect longitudinally by MSC. therapy were common limitations in almost all RCTs. Finally, genetically modified animals designed for xenotransplantation or human organs derived from interspecies chimeras, using the blastocyst complementation method, could offer unlimited sources of β cells. Figure 1 summarizes several strategies to generate bone-fidelity β-cells for diabetes replacement.

Beta Cells And Alpha Cells Of Pancreas

A logical place to start for β-cell generation is to use the plasticity of closely related endoderm-derived cell types, such as non-β pancreatic cells, and to persuade them to adopt a β-cell phenotype. Given the close ontogenetic relationship, functional similarity and dependency between these cells, the potential for interconversion is unequivocal [24]. Phenotypic plasticity between pancreatic α-cells and β-cells is particularly pronounced. A prominent study from several years ago showed that inter-endocrine plasticity and β-cell proliferation can be elicited upon increased metabolic demand or after a substantial diphtheria toxin-induced β-cell loss [ 25 ]. While this study was conducted in mice, there is no evidence to suggest that a similar event of intrinsic cell type interconversion may occur in other settings of β-cell damage in humans. Of note, a similar phenomenon of β-cell loss may occur naturally in mice that pass into adulthood.

And β Cells In Pancreatic Islet Of Langerhans (human)

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