التفاصيل البيبلوغرافية
| العنوان: |
Increased Proliferation of the Pancreatic Duct Gland Compartment in Type 1 Diabetes. |
| المؤلفون: |
Moin, Abu Saleh Md, Butler, Peter C, Butler, Alexandra E |
| المصدر: |
The Journal of Clinical Endocrinology & Metabolism, vol 102, iss 1 |
| بيانات النشر: |
eScholarship, University of California |
| سنة النشر: |
2017 |
| المجموعة: |
University of California: eScholarship |
| مصطلحات موضوعية: |
Stem Cell Research, Pediatric, Autoimmune Disease, Cancer, Regenerative Medicine, Clinical Research, Digestive Diseases, Pancreatic Cancer, Stem Cell Research - Nonembryonic - Non-Human, Rare Diseases, Diabetes, 2.1 Biological and endogenous factors, Aetiology, Metabolic and endocrine, Adolescent, Adult, Aged, 80 and over, Biomarkers, Case-Control Studies, Cell Proliferation, Child, Preschool, Diabetes Mellitus, Type 1, Female, Follow-Up Studies, Humans, Islets of Langerhans, Male |
| جغرافية الموضوع: |
200 - 209 |
| الوصف: |
ContextPancreatic duct glands (PDGs) have been proposed as a source of regeneration in response to exocrine pancreas injury, and thus may serve as an organ stem cell niche. There is evidence to suggest ongoing β-cell formation in longstanding type 1 diabetes (T1D), but the source is unknown.ObjectiveTo investigate the PDG compartment of the pancreas in humans with T1D for evidence of an active regenerative signature (presence of progenitor cells and increased proliferation) and, in particular, as a potential source of β-cells.Design, setting, and participantsPancreases from 46 brain dead organ donors (22 with T1D, 24 nondiabetic controls) were investigated for activation (increased proliferation) and markers of pancreatic exocrine and endocrine progenitors.ResultsPDG cell replication was increased in T1D (6.3% ± 1.6% vs 0.6% ± 0.1%, P < 0.001, T1D vs nondiabetic), most prominently in association with pancreatic inflammation. There were increased progenitor-like cells in PDGs of T1D, but predominantly with an exocrine fate.ConclusionThe PDG compartment is activated in T1D consistent with a response to ongoing inflammation, and via resulting ductal hyperplasia may contribute to local obstructive pancreatitis and eventual pancreatic atrophy characteristic of T1D. However, there is no evidence of effective endocrine cell formation from PDGs. |
| نوع الوثيقة: |
article in journal/newspaper |
| وصف الملف: |
application/pdf |
| اللغة: |
unknown |
| العلاقة: |
qt9zp026zx; https://escholarship.org/uc/item/9zp026zxTest |
| الإتاحة: |
https://escholarship.org/uc/item/9zp026zxTest |
| حقوق: |
public |
| رقم الانضمام: |
edsbas.ABA5D5ED |
| قاعدة البيانات: |
BASE |
