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

Alexandre‐Heymann, Laure; Mallone, Roberto; Scharfmann, Raphaël; Larger, Étienne

doi:10.1007/s11154-019-09501-3

Cited by 43 publications

(46 citation statements)

References 192 publications

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“…Furthermore, the traditional idea that pancreatic damage is a mere consequence of autoimmune progression has been shaken by evidence for a whole-pancreas disease, characterized by throughout structural and functional alterations as well as immune cell infiltration already present in early disease stages. Extensive fibrosis, arteriosclerosis, acinar atrophy, and leucocytic infiltration are common histological abnormalities found in T1D subjects, suggesting that widespread pancreatic inflammation caused by a non-antigen specific pathogenesis may importantly concur to β cell destruction by the immune system [44,45]. Questions certainly remain concerning the pathogenetic implications of cell-cell communication within the pancreatic islets as well as the regeneration/proliferation and apoptosis of the β cells for T1D [46,47].…”

Section: Discussionmentioning

confidence: 99%

Blood Co-Circulating Extracellular microRNAs and Immune Cell Subsets Associate with Type 1 Diabetes Severity

Garavelli

Bruzzaniti

Tagliabue

et al. 2020

IJMS

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Immune cell subsets and microRNAs have been independently proposed as type 1 diabetes (T1D) diagnostic and/or prognostic biomarkers. Here, we aimed to analyze the relationships between peripheral blood circulating immune cell subsets, plasmatic microRNAs, and T1D. Blood samples were obtained from both children with T1D at diagnosis and age-sex matched healthy controls. Then, immunophenotype assessed by flow cytometry was coupled with the quantification of 60 plasmatic microRNAs by quantitative RT-PCR. The associations between immune cell frequency, plasmatic microRNAs, and the parameters of pancreatic loss, glycemic control, and diabetic ketoacidosis were assessed by logistic regression models and correlation analyses. We found that the increase in specific plasmatic microRNAs was associated with T1D disease onset (let-7c-5p, let-7d-5p, let-7f-5p, let-7i-5p, miR-146a-5p, miR-423-3p, and miR-423-5p), serum C-peptide concentration (miR-142-5p and miR-29c-3p), glycated hemoglobin (miR-26a-5p and miR-223-3p) and the presence of ketoacidosis (miR-29c-3p) more strongly than the evaluated immune cell subset frequency. Some of these plasmatic microRNAs were shown to positively correlate with numbers of blood circulating B lymphocytes (miR-142-5p) and CD4+CD45RO+ (miR-146a-5p and miR-223-3p) and CD4+CD25+ cells (miR-423-3p and miR-223-3p) in children with T1D but not in healthy controls, suggesting a disease-specific microRNA association with immune dysregulation in T1D. In conclusion, our results suggest that, while blood co-circulating extracellular microRNAs and immune cell subsets may be biologically linked, microRNAs may better provide powerful information about T1D onset and severity.

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Section: Discussionmentioning

confidence: 99%

Blood Co-Circulating Extracellular microRNAs and Immune Cell Subsets Associate with Type 1 Diabetes Severity

Garavelli

Bruzzaniti

Tagliabue

et al. 2020

IJMS

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“…Besides, we compared the pancreas volume in patients with type 2 diabetes and in control subjects. The pancreas volume is known to be lower in patients with type 1 diabetes as compared to control subjects [42]. However, studies are discordant concerning the pancreas volume of patients with type 2 diabetes [43][44][45][46][47][48].…”

Section: Discussionmentioning

confidence: 99%

Patients with type 2 diabetes present with multiple anomalies of the pancreatic arterial tree on abdominal computed tomography: comparison between patients with type 2 diabetes and a matched control group

Alexandre‐Heymann

Barral

Dohan

et al. 2020

Cardiovasc Diabetol

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Background: Studies suggest that cardio-vascular risk factors could foster the development of type 2 diabetes (T2D). This could partly be mediated by pancreatic atherosclerosis resulting in pancreatic ischemia. We hypothesized that patients with T2D present with more severe atherosclerosis of pancreas-bound arteries than control patients without T2D. Methods: We performed a retrospective study comparing the abdominal computed tomography of patients with T2D and of control subjects matched for gender and for age. We performed a multivariate logistic regression with adjustment for age, gender, BMI and the presence or absence of hypertension. Results: Forty-eight patients with T2D and 48 control subjects were included. A calcification score of the splenic artery was defined (from 0: no calcification to 3: continuous linear calcifications). Seventeen percent of the patients with T2D presented with a high calcification score (i.e. 2 or 3), versus only 2% of the control subjects (p = 0.04). The mean number of pancreas-bound branches among the greater pancreatic artery, dorsal pancreatic artery and inferior pancreatic artery (from 0 to 3) was lower in patients with T2D than in control subjects (1.1 vs 1.7, p = 0.003). The mean number of visible intrapancreatic arterial subdivisions (from 0 to 2) was lower in patients with T2D than in control subjects (0.7 vs 1.3, p = 0.0017). All these differences hold true using multivariate logistic regression. None of these differences correlated with the duration of diabetes. The relationship between pancreas volume and BMI seen in control subjects was not confirmed in patients with T2D. Conversely, in patients with T2D but not in control subjects, the splenic artery diameter correlated with the pancreas volume. Conclusions: Patients with T2D present with more calcifications of the splenic artery and with a less dense pancreatic arterial tree than control subjects.

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“…Stimulated tests, such as secretin or cholecystokinin testing, are the gold standard for diagnosis of PEI. However, these difficult tests require duodenal intubation for hours (8,11,12,18,23,39,65,66). Newer, less invasive testing has been developed to assess PEI involving enzyme levels in serum, saliva, urine, or stool, with fecal elastase concentration (FEC) being the most studied and clinically available (67)(68)(69)(70)(71).…”

Section: Evaluation and Management Of Exocrine Insufficiency In T1dmentioning

confidence: 99%

“…PEI in T1D clinically presents with diarrhea, bloating, cramping, and/or weight loss largely from steatorrhea (74). However, these symptoms can be attributed to other complications of diabetes such as gastrointestinal autonomic neuropathy (i.e., gastroparesis), steatorrhea from celiac disease, or bacterial overgrowth of the proximal small bowel (65,67).…”

Section: Evaluation and Management Of Exocrine Insufficiency In T1dmentioning

confidence: 99%

Exocrine Pancreas Dysfunction in Type 1 Diabetes

et al. 2020

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

Cited by 43 publications

References 192 publications

Blood Co-Circulating Extracellular microRNAs and Immune Cell Subsets Associate with Type 1 Diabetes Severity

Blood Co-Circulating Extracellular microRNAs and Immune Cell Subsets Associate with Type 1 Diabetes Severity

Patients with type 2 diabetes present with multiple anomalies of the pancreatic arterial tree on abdominal computed tomography: comparison between patients with type 2 diabetes and a matched control group

Exocrine Pancreas Dysfunction in Type 1 Diabetes

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