Islet morphologic changes

Gepts, W; Veld, Pieter In 'T

doi:10.1002/dmr.5610030403

Cited by 23 publications

(4 citation statements)

References 86 publications

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“…Earlier human islet cell morphology studies have also shown evidence of beta cell regeneration or neotransformation in patients with diabetes of varying duration 6 . It was recognised that islet cells in diabetes were not atrophic, as previously thought, but "pseudo-atrophic" containing glucagonand somatostatin-containing cells, in addition to atypical regeneration with pancreatic-polypeptide-containing cells 23 . There were also various forms of regeneration, including new hyperactive beta cells from proliferation of excretory duct epithelial cells and islet cell hyperplasia with large beta cells containing immunoreactive insulin in "pseudo-atrophic" pancreas 23 .…”

Section: Discussionmentioning

confidence: 87%

Insulin micro-secretion in Type 1 diabetes and related microRNA profiles

Januszewski

Cho

Joglekar

et al. 2021

Sci Rep

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The aim of this cross-sectional study was to compare plasma C-peptide presence and levels in people without diabetes (CON) and with Type 1 diabetes and relate C-peptide status to clinical factors. In a subset we evaluated 50 microRNAs (miRs) previously implicated in beta-cell death and associations with clinical status and C-peptide levels. Diabetes age of onset was stratified as adult (≥ 18 y.o) or childhood (< 18 y.o.), and diabetes duration was stratified as ≤ 10 years, 10–20 years and > 20 years. Plasma C-peptide was measured by ultrasensitive ELISA. Plasma miRs were quantified using TaqMan probe-primer mix on an OpenArray platform. C-peptide was detectable in 55.3% of (n = 349) people with diabetes, including 64.1% of adults and 34.0% of youth with diabetes, p < 0.0001 and in all (n = 253) participants without diabetes (CON). C-peptide levels, when detectable, were lower in the individuals with diabetes than in the CON group [median lower quartile (LQ)–upper quartile (UQ)] 5.0 (2.6–28.7) versus 650.9 (401.2–732.4) pmol/L respectively, p < 0.0001 and lower in childhood versus adult-onset diabetes [median (LQ–UQ) 4.2 (2.6–12.2) pmol/L vs. 8.0 (2.3–80.5) pmol/L, p = 0.02, respectively]. In the childhood-onset group more people with longer diabetes duration (> 20 years) had detectable C-peptide (60%) than in those with shorter diabetes duration (39%, p for trend < 0.05). Nine miRs significantly correlated with detectable C-peptide levels in people with diabetes and 16 miRs correlated with C-peptide levels in CON. Our cross-sectional study results are supportive of (a) greater beta-cell function loss in younger onset Type 1 diabetes; (b) persistent insulin secretion in adult-onset diabetes and possibly regenerative secretion in childhood-onset long diabetes duration; and (c) relationships of C-peptide levels with circulating miRs. Confirmatory clinical studies and related basic science studies are merited.

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Section: Discussionmentioning

confidence: 87%

Insulin micro-secretion in Type 1 diabetes and related microRNA profiles

Januszewski

Cho

Joglekar

et al. 2021

Sci Rep

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“…The cellular and molecular mechanisms behind the ␤-cell death is not yet clarified, although it is suggested that the infiltration of immune cells (termed insulitis), in and around pancreatic islets early in the pathogenesis, is a crucial step (3,4). Proinflammatory cytokines secreted by invading macrophages and T-cells is believed to be important in the process of ␤-cell impairment (5)(6)(7).…”

mentioning

confidence: 97%

Cytokine-Induced Inhibition of Insulin Release from Mouse Pancreatic β-Cells Deficient in Inducible Nitric Oxide Synthase

Andersson

Flodström

Sandler

2001

Biochemical and Biophysical Research Communications

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“…From an immunological perspective, the association of T1DM with specific HLA alleles has not been demonstrated in secondary diabetes of chronic pancreatitis. This aspect was also able to support the fact that patients with chronic pancreatitis reach late (in the stages of disease evolution) absolute insulin, secondary diabetes being successfully treated with oral antidiabetics (10).…”

Section: Introductionmentioning

confidence: 71%

Pancreatogenic type 3C diabetes

Stoian¹,

Ditu²,

Diculescu³

et al. 2018

JMMS

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Background. The relationship between chronic pancreatitis and diabetes is well established. This form of diabetes is secondary to exocrine pancreatic disorder and is known as diabetes mellitus type 3c (T3cDM). Materials and Methods. In this retrospective study we included 261 patients, 59 patients being diagnosed with chronic pancreatitis and secondary diabetes mellitus, and admitted in the Fundeni Clinical Institute, 2nd

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Islet morphologic changes

Cited by 23 publications

References 86 publications

Insulin micro-secretion in Type 1 diabetes and related microRNA profiles

Insulin micro-secretion in Type 1 diabetes and related microRNA profiles

Cytokine-Induced Inhibition of Insulin Release from Mouse Pancreatic β-Cells Deficient in Inducible Nitric Oxide Synthase

Pancreatogenic type 3C diabetes

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