Alterations in Beta Cell Identity in Type 1 and Type 2 Diabetes

<p>To discuss the current understanding of “β cell identity” and factors underlying altered identity of pancreatic β cells in diabetes, especially in humans. Altered identity of β cells due to dedifferentiation and/or transdifferentiation has been proposed as a mechanism of loss of β cells in...

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محفوظ في:
التفاصيل البيبلوغرافية
المؤلف الرئيسي: Abu Saleh Md Moin (6189512) (author)
مؤلفون آخرون: Alexandra E. Butler (6189536) (author)
منشور في: 2019
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author Abu Saleh Md Moin (6189512)
author2 Alexandra E. Butler (6189536)
author2_role author
author_facet Abu Saleh Md Moin (6189512)
Alexandra E. Butler (6189536)
author_role author
dc.creator.none.fl_str_mv Abu Saleh Md Moin (6189512)
Alexandra E. Butler (6189536)
dc.date.none.fl_str_mv 2019-08-10T06:00:00Z
dc.identifier.none.fl_str_mv 10.1007/s11892-019-1194-6
dc.relation.none.fl_str_mv https://figshare.com/articles/journal_contribution/Alterations_in_Beta_Cell_Identity_in_Type_1_and_Type_2_Diabetes/21597642
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Biomedical and clinical sciences
Clinical sciences
Medical biochemistry and metabolomics
Medical biotechnology
β Cell
Dedifferentiation
Transdifferentiation
Type 1 diabetes
Type 2 diabetes
Pancreas
dc.title.none.fl_str_mv Alterations in Beta Cell Identity in Type 1 and Type 2 Diabetes
dc.type.none.fl_str_mv Text
Journal contribution
info:eu-repo/semantics/publishedVersion
text
contribution to journal
description <p>To discuss the current understanding of “β cell identity” and factors underlying altered identity of pancreatic β cells in diabetes, especially in humans. Altered identity of β cells due to dedifferentiation and/or transdifferentiation has been proposed as a mechanism of loss of β cells in diabetes. In dedifferentiation, β cells do not undergo apoptosis; rather, they lose their identity and function. Dedifferentiation is well characterized by the decrease in expression of key β cell markers such as genes encoding major transcription factors, e.g., MafA, NeuroD1, Nkx6.1, and Foxo1, and an increase in atypical or “disallowed” genes for β cells such as lactate dehydrogenase, monocarboxylate transporter MCT1, or progenitor cell genes (Neurog3, Pax4, or Sox9). Moreover, altered identity of mature β cells in diabetes also involves transdifferentiation of β cells into other islet hormone producing cells. For example, overexpression of α cell specific transcription factor Arx or ablation of Pdx1 resulted in an increase of α cell numbers and a decrease in β cell numbers in rodents. The frequency of α-β double-positive cells was also prominent in human subjects with T2D. These altered identities of β cells likely serve as a compensatory response to enhance function/expand cell numbers and may also camouflage/protect cells from ongoing stress. However, it is equally likely that this may be a reflection of new cell formation as a frank regenerative response to ongoing tissue injury. Physiologically, all these responses are complementary. In diabetes, (1) endocrine identity recapitulates the less mature/less-differentiated fetal/neonatal cell type, possibly representing an adaptive mechanism; (2) residual β cells may be altered in their subtype proportions or other molecular features; (3) in humans, “altered identity” is a preferable term to dedifferentiation as their cellular fate (differentiated cells losing identity or progenitors becoming more differentiated) is unclear as yet.</p><h2>Other Information</h2> <p> Published in: Current Diabetes Reports<br> License: <a href="https://creativecommons.org/licenses/by/4.0" target="_blank">https://creativecommons.org/licenses/by/4.0</a><br>See article on publisher's website: <a href="http://dx.doi.org/10.1007/s11892-019-1194-6" target="_blank">http://dx.doi.org/10.1007/s11892-019-1194-6</a></p>
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spelling Alterations in Beta Cell Identity in Type 1 and Type 2 DiabetesAbu Saleh Md Moin (6189512)Alexandra E. Butler (6189536)Biomedical and clinical sciencesClinical sciencesMedical biochemistry and metabolomicsMedical biotechnologyβ CellDedifferentiationTransdifferentiationType 1 diabetesType 2 diabetesPancreas<p>To discuss the current understanding of “β cell identity” and factors underlying altered identity of pancreatic β cells in diabetes, especially in humans. Altered identity of β cells due to dedifferentiation and/or transdifferentiation has been proposed as a mechanism of loss of β cells in diabetes. In dedifferentiation, β cells do not undergo apoptosis; rather, they lose their identity and function. Dedifferentiation is well characterized by the decrease in expression of key β cell markers such as genes encoding major transcription factors, e.g., MafA, NeuroD1, Nkx6.1, and Foxo1, and an increase in atypical or “disallowed” genes for β cells such as lactate dehydrogenase, monocarboxylate transporter MCT1, or progenitor cell genes (Neurog3, Pax4, or Sox9). Moreover, altered identity of mature β cells in diabetes also involves transdifferentiation of β cells into other islet hormone producing cells. For example, overexpression of α cell specific transcription factor Arx or ablation of Pdx1 resulted in an increase of α cell numbers and a decrease in β cell numbers in rodents. The frequency of α-β double-positive cells was also prominent in human subjects with T2D. These altered identities of β cells likely serve as a compensatory response to enhance function/expand cell numbers and may also camouflage/protect cells from ongoing stress. However, it is equally likely that this may be a reflection of new cell formation as a frank regenerative response to ongoing tissue injury. Physiologically, all these responses are complementary. In diabetes, (1) endocrine identity recapitulates the less mature/less-differentiated fetal/neonatal cell type, possibly representing an adaptive mechanism; (2) residual β cells may be altered in their subtype proportions or other molecular features; (3) in humans, “altered identity” is a preferable term to dedifferentiation as their cellular fate (differentiated cells losing identity or progenitors becoming more differentiated) is unclear as yet.</p><h2>Other Information</h2> <p> Published in: Current Diabetes Reports<br> License: <a href="https://creativecommons.org/licenses/by/4.0" target="_blank">https://creativecommons.org/licenses/by/4.0</a><br>See article on publisher's website: <a href="http://dx.doi.org/10.1007/s11892-019-1194-6" target="_blank">http://dx.doi.org/10.1007/s11892-019-1194-6</a></p>2019-08-10T06:00:00ZTextJournal contributioninfo:eu-repo/semantics/publishedVersiontextcontribution to journal10.1007/s11892-019-1194-6https://figshare.com/articles/journal_contribution/Alterations_in_Beta_Cell_Identity_in_Type_1_and_Type_2_Diabetes/21597642CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/215976422019-08-10T06:00:00Z
spellingShingle Alterations in Beta Cell Identity in Type 1 and Type 2 Diabetes
Abu Saleh Md Moin (6189512)
Biomedical and clinical sciences
Clinical sciences
Medical biochemistry and metabolomics
Medical biotechnology
β Cell
Dedifferentiation
Transdifferentiation
Type 1 diabetes
Type 2 diabetes
Pancreas
status_str publishedVersion
title Alterations in Beta Cell Identity in Type 1 and Type 2 Diabetes
title_full Alterations in Beta Cell Identity in Type 1 and Type 2 Diabetes
title_fullStr Alterations in Beta Cell Identity in Type 1 and Type 2 Diabetes
title_full_unstemmed Alterations in Beta Cell Identity in Type 1 and Type 2 Diabetes
title_short Alterations in Beta Cell Identity in Type 1 and Type 2 Diabetes
title_sort Alterations in Beta Cell Identity in Type 1 and Type 2 Diabetes
topic Biomedical and clinical sciences
Clinical sciences
Medical biochemistry and metabolomics
Medical biotechnology
β Cell
Dedifferentiation
Transdifferentiation
Type 1 diabetes
Type 2 diabetes
Pancreas