Literature DB >> 26829442

β-cell Mass in Nondiabetic Autoantibody-Positive Subjects: An Analysis Based on the Network for Pancreatic Organ Donors Database.

Marc Diedisheim1, Roberto Mallone1, Christian Boitard1, Etienne Larger1.   

Abstract

CONTEXT: Little information is available about β-cell mass in antibody-positive (Ab+) nondiabetic subjects.
OBJECTIVE: We have investigated whether the publicly available virtual slides of the Network for Pancreatic Organ Donors with Diabetes (nPOD) project can be used to assess β-cell mass and distribution in nondiabetic antibody-negative (Ab−) and antibody-positive (Ab+) subjects and in patients with recent-onset type 1 diabetes (T1D). SUBJECTS AND METHODS: We developed a semi-automated quantification method and applied it to 415 insulin-stained slides from 69 Ab− subjects, 101 slides from 18 Ab+ subjects, and 46 slides from eight recent-onset (<3 y) T1D subjects. Among these subjects, 48, 17, and seven had an available pancreatic mass, respectively, and were used for the quantification of β-cell mass.
RESULTS: In Ab− subjects, the β-cell and endocrine mass were 0.66 ± 0.42 and 1.0 ± 0.65 g, respectively. Nonexocrine tissue represented 29% of pancreatic area, a proportion that increased with age. Proportional β-cell area relative to total pancreatic area was higher in the tail compared with head (0.83 vs 0.71%; P < .001). In Ab+ subjects, β-cell mass and β-cell area were similar to those of Ab− individuals, whereas these parameters were dramatically decreased in recent-onset T1D patients.
CONCLUSION: The virtual slides of the nPOD project can be used for quantification projects. In Ab+ nondiabetic subjects, the β-cell mass was not decreased. However, as this cohort is largely composed of donors from the general population, with a single autoantibody, future studies with a larger number of donors with multiple autoantibodies and predisposing human leucocyte antigen genes are required to better define the dynamics of β-cell destruction in the preclinical phases of T1D.

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Year:  2016        PMID: 26829442     DOI: 10.1210/jc.2015-3756

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


  15 in total

1.  Increased Hormone-Negative Endocrine Cells in the Pancreas in Type 1 Diabetes.

Authors:  Abu Saleh Md Moin; Sangeeta Dhawan; Christine Shieh; Peter C Butler; Megan Cory; Alexandra E Butler
Journal:  J Clin Endocrinol Metab       Date:  2016-06-14       Impact factor: 5.958

Review 2.  Structure and function of the exocrine pancreas in patients with type 1 diabetes.

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Journal:  Rev Endocr Metab Disord       Date:  2019-06       Impact factor: 6.514

3.  Assessment of β Cell Mass and Function by AIRmax and Intravenous Glucose in High-Risk Subjects for Type 1 Diabetes.

Authors:  Wei Hao; Alyssa Woodwyk; Craig Beam; Henry T Bahnson; Jerry P Palmer; Carla J Greenbaum
Journal:  J Clin Endocrinol Metab       Date:  2017-12-01       Impact factor: 5.958

4.  β Cells Persist in T1D Pancreata Without Evidence of Ongoing β-Cell Turnover or Neogenesis.

Authors:  Carol J Lam; Daniel R Jacobson; Matthew M Rankin; Aaron R Cox; Jake A Kushner
Journal:  J Clin Endocrinol Metab       Date:  2017-08-01       Impact factor: 5.958

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Authors:  Teresa Rodriguez-Calvo; Mark Atkinson; Matthias von Herrath
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6.  Strength in Numbers: Opportunities for Enhancing the Development of Effective Treatments for Type 1 Diabetes-The TrialNet Experience.

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Review 7.  Nucleic acid biomarkers of β cell stress and death in type 1 diabetes.

Authors:  Farooq Syed; Carmella Evans-Molina
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Review 8.  Autoreactive T cells in type 1 diabetes.

Authors:  Alberto Pugliese
Journal:  J Clin Invest       Date:  2017-08-01       Impact factor: 14.808

9.  Immunoregulated insulitis and slow-progressing type 1 diabetes after duodenopancreatectomy.

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Review 10.  Insulitis in the pathogenesis of type 1 diabetes.

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