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      Type 1 Diabetes Patients With Different Residual Beta-Cell Function but Similar Age, HBA1c, and Cardiorespiratory Fitness Have Differing Exercise-Induced Angiogenic Cell Mobilisation

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          Abstract

          Background

          Many individuals with type 1 diabetes retain residual beta-cell function. Sustained endogenous insulin and C-peptide secretion is associated with reduced diabetes related complications, but underlying mechanisms remain unclear. Lower circulating numbers of endothelial and hematopoietic progenitor cells (EPCs and HPCs), and the inability to increase the count of these cells in response to exercise, are also associated with increased diabetes complications and cardiovascular disease. It is unknown whether residual beta-cell function influences HPCs and EPCs. Thus, this study examined the influence of residual beta-cell function in type 1 diabetes upon exercise-induced changes in haematopoietic (HPCs) and endothelial progenitor cells (EPCs).

          Methods

          Participants with undetectable stimulated C-peptide (n=11; Cpep und), 10 high C-peptide (Cpep high; >200 pmol/L), and 11 non-diabetes controls took part in this observational exercise study, completing 45 minutes of intensive walking at 60% V ˙ O 2 p e a k . Clinically significant HPCs (CD34 +) and EPCs (CD34 +VEGFR2 +) phenotypes for predicting future adverse cardiovascular outcomes, and subsequent cell surface expression of chemokine receptor 4 (CXCR4) and 7 (CXCR7), were enumerated at rest and immediately post-exercise by flow cytometry.

          Results

          Exercise increased HPCs and EPCs phenotypes similarly in the Cpep high and control groups (+34-121% across phenotypes, p<0.04); but Cpep und group did not significantly increase from rest, even after controlling for diabetes duration. Strikingly, the post-exercise Cpep und counts were still lower than Cpep high at rest.

          Conclusions

          Residual beta-cell function is associated with an intact exercise-induced HPCs and EPCs mobilisation. As key characteristics (age, fitness, HbA1c) were similar between groups, the mechanisms underpinning the absent mobilisation within those with negative C-peptide, and the vascular implications, require further investigation.

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          Most cited references42

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          Isolation of Putative Progenitor Endothelial Cells for Angiogenesis

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            Residual Insulin Production and Pancreatic β-Cell Turnover After 50 Years of Diabetes: Joslin Medalist Study

            OBJECTIVE To evaluate the extent of pancreatic β-cell function in a large number of insulin-dependent diabetic patients with a disease duration of 50 years or longer (Medalists). RESEARCH DESIGN AND METHODS Characterization of clinical and biochemical parameters and β-cell function of 411 Medalists with correlation with postmortem morphologic findings of 9 Medalists. RESULTS The Medalist cohort, with a mean ± SD disease duration and age of 56.2 ± 5.8 and 67.2 ± 7.5 years, respectively, has a clinical phenotype similar to type 1 diabetes (type 1 diabetes): mean ± SD onset at 11.0 ± 6.4 years, BMI at 26.0 ± 5.1 kg/m2, insulin dose of 0.46 ± 0.2 u/kg, ∼94% positive for DR3 and/or DR4, and 29.5% positive for either IA2 or glutamic acid decarboxylase (GAD) autoantibodies. Random serum C-peptide levels showed that more than 67.4% of the participants had levels in the minimal (0.03–0.2 nmol/l) or sustained range (≥0.2 nmol/l). Parameters associated with higher random C-peptide were lower hemoglobin A1C, older age of onset, higher frequency of HLA DR3 genotype, and responsiveness to a mixed-meal tolerance test (MMTT). Over half of the Medalists with fasting C-peptide >0.17 nmol/l responded in MMTT by a twofold or greater rise over the course of the test compared to fasting. Postmortem examination of pancreases from nine Medalists showed that all had insulin+ β-cells with some positive for TUNEL staining, indicating apoptosis. CONCLUSIONS Demonstration of persistence and function of insulin-producing pancreatic cells suggests the possibility of a steady state of turnover in which stimuli to enhance endogenous β cells could be a viable therapeutic approach in a significant number of patients with type 1 diabetes, even for those with chronic duration.
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              Concise Review: Evidence for CD34 as a Common Marker for Diverse Progenitors

              CD34 is a transmembrane phosphoglycoprotein, first identified on hematopoietic stem and progenitor cells. Clinically, it is associated with the selection and enrichment of hematopoietic stem cells for bone marrow transplants. Due to these historical and clinical associations, CD34 expression is almost ubiquitously related to hematopoietic cells, and it is a common misconception that CD34-positive (CD34+) cells in nonhematopoietic samples represent hematopoietic contamination. The prevailing school of thought states that multipotent mesenchymal stromal cells (MSC) do not express CD34. However, strong evidence demonstrates CD34 is expressed not only by MSC but by a multitude of other nonhematopoietic cell types including muscle satellite cells, corneal keratocytes, interstitial cells, epithelial progenitors, and vascular endothelial progenitors. In many cases, the CD34+ cells represent a small proportion of the total cell population and also indicate a distinct subset of cells with enhanced progenitor activity. Herein, we explore common traits between cells that express CD34, including associated markers, morphology and differentiation potential. We endeavor to highlight key similarities between CD34+ cells, with a focus on progenitor activity. A common function of CD34 has yet to be elucidated, but by analyzing and understanding links between CD34+ cells, we hope to be able to offer an insight into the overlapping properties of cells that express CD34. Stem Cells 2014;32:1380–1389
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                Author and article information

                Contributors
                Journal
                Front Endocrinol (Lausanne)
                Front Endocrinol (Lausanne)
                Front. Endocrinol.
                Frontiers in Endocrinology
                Frontiers Media S.A.
                1664-2392
                11 February 2022
                2022
                : 13
                : 797438
                Affiliations
                [1] 1 Population Health Sciences Institute, Newcastle University , Newcastle upon Tyne, United Kingdom
                [2] 2 Nuffield Department of Primary Care Health Sciences, University of Oxford , Oxford, United Kingdom
                [3] 3 Faculty of Health Sciences and Wellbeing, University of Sunderland , Sunderland, United Kingdom
                [4] 4 Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds , Leeds, United Kingdom
                [5] 5 National Institute for Health Research Exeter Clinical Research Facility, University of Exeter Medical School , Exeter, United Kingdom
                [6] 6 Academic Department of Blood Sciences, Royal Devon and Exeter NHS Foundation Trust , Exeter, United Kingdom
                [7] 7 Translational and Clinical Research Institute, Newcastle University , Newcastle upon Tyne, United Kingdom
                [8] 8 Newcastle Centre for Diabetes Care, Newcastle upon Tyne Hospitals NHS Foundation Trust , Newcastle upon Tyne, United Kingdom
                [9] 9 School of Applied Sciences, Edinburgh Napier University , Edinburgh, United Kingdom
                Author notes

                Edited by: Lixin Li, Central Michigan University, United States

                Reviewed by: David H Wagner, University of Colorado Denver, United States; George L. King, Joslin Diabetes Center and Harvard Medical School, United States

                *Correspondence: Daniel J. West, Daniel.West@ 123456newcastle.ac.uk ; Guy S. Taylor, Guy.Taylor@ 123456newcastle.ac.uk

                This article was submitted to Clinical Diabetes, a section of the journal Frontiers in Endocrinology

                Article
                10.3389/fendo.2022.797438
                8874313
                ba7d37c1-4f04-4b8b-a6a8-6cca91368a4c
                Copyright © 2022 Taylor, Shaw, Scragg, Smith, Campbell, McDonald, Shaw, Ross and West

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 18 October 2021
                : 10 January 2022
                Page count
                Figures: 1, Tables: 1, Equations: 0, References: 42, Pages: 7, Words: 3248
                Funding
                Funded by: Diabetes Research and Wellness Foundation , doi 10.13039/501100000273;
                Award ID: SCA/OF/12/15
                Categories
                Endocrinology
                Original Research

                Endocrinology & Diabetes
                residual beta-cell function,haematopoietic progenitor cells,endothelial progenitor cells,exercise,exercise-induced mobilisation

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