Pathophysiological Mechanisms and Clinical Associations of Non-Alcoholic Fatty Pancreas Disease

Pagkali, Antonia; Makris, Anastasios; Brofidi, Kalliopi; Agouridis, Aris; Filippatos, Theodosios

doi:10.2147/dmso.s397643

Cited by 4 publications

(1 citation statement)

References 128 publications

(221 reference statements)

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“…However, the spectrum of ultrastructural changes observed in our case is comparable with the disordering of acinar cell ER, endolysosomal system, mitochondria, and autophagy observed in tissue sections from patients with pancreatitis ( Helin et al, 1980 ; Fortunato et al, 2009 ; Mareninova et al, 2009 ; Biczo et al, 2018 ), as well as in isolated human acinar cells ( Gukovskaya et al, 2016 ; Lugea et al, 2017 ; Gukovskaya et al, 2019 ) and acinar cells in tissue slices ( Xu et al, 2017 ; Dolai et al, 2018 ) subjected to pancreatitis insults in vitro. Moreover, our findings of both intra- and extracellular lipid material together with ultrastructural changes suggesting low grade pancreatitis in the setting of T2DM are consistent with similar findings in human patients with T2DM and pancreatitis ( Petroff et al, 2021 ; Caldart et al, 2023 ), as well as with the recently proposed hypothesis that these pancreatic diseases may originate from intrapancreatic fat or start with NAFPD ( Alempijevic et al, 2017 ; Petrov, 2023 ; Pagkali et al, 2024 ).…”

Section: Discussionsupporting

confidence: 91%

Western diet-induced ultrastructural changes in mouse pancreatic acinar cells

Lipovšek,

Dolenšek,

Dariš

et al. 2024

Front. Cell Dev. Biol.

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Mouse models of diet-induced type 2 diabetes mellitus provide powerful tools for studying the structural and physiological changes that are related to the disease progression. In this study, diabetic-like glucose dysregulation was induced in mice by feeding them a western diet, and light and transmission electron microscopy were used to study the ultrastructural changes in the pancreatic acinar cells. Acinar necrosis and vacuolization of the cytoplasm were the most prominent features. Furthermore, we observed intracellular and extracellular accumulation of lipid compounds in the form of lipid droplets, structural enlargement of the cisternae of the rough endoplasmic reticulum (RER), and altered mitochondrial morphology, with mitochondria lacking the typical organization of the inner membrane. Last, autophagic structures, i.e., autophagosomes, autolysosomes, and residual bodies, were abundant within the acinar cells of western diet-fed mice, and the autolysosomes contained lipids and material of varying electron density. While diets inducing obesity and type 2 diabetes are clearly associated with structural changes and dysfunction of the endocrine pancreas, we here demonstrate the strong effect of dietary intervention on the structure of acinar cells in the exocrine part of the organ before detectable changes in plasma amylase activity, which may help us better understand the development of non-alcoholic fatty pancreas disease and its association with endo- and exocrine dysfunction.

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Section: Discussionsupporting

confidence: 91%

Western diet-induced ultrastructural changes in mouse pancreatic acinar cells

Lipovšek,

Dolenšek,

Dariš

et al. 2024

Front. Cell Dev. Biol.

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Prevalence of Fatty Pancreas and its relation with anthropometric values on the Growth and Obesity Cohort Study

Alberti,

Cantillo,

Pereira

et al. 2024

Jornal de Pediatria

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Oxalate Nephropathy After Kidney Transplantation: Risk Factors and Outcomes of Two Phenotypes

Garg,

Nguyen,

Astor

et al. 2024

Clinical Transplantation

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Describing risk factors and outcomes in kidney transplant recipients with oxalate nephropathy (ON) may help elucidate the pathogenesis and guide treatment strategies. We used a large single‐center database to identify patients with ON and categorized them into delayed graft function with ON (DGF‐ON) and late ON. Incidence density sampling was used to select controls. A total of 37 ON cases were diagnosed between 1/2011 and 1/2021. DGF‐ON (n = 13) was diagnosed in 1.05% of the DGF population. Pancreatic atrophy on imaging (36.4% vs. 2.9%, p = 0.002) and gastric bypass history (7.7% vs. 0%; p = 0.06) were more common in DGF‐ON than with controls with DGF requiring biopsy but without evidence of ON. DGF‐ON was not associated with worse graft survival (p = 0.98) or death‐censored graft survival (p = 0.48). Late ON (n = 24) was diagnosed after a mean of 78.2 months. Late ON patients were older (mean age 55.1 vs. 48.4 years; p = 0.02), more likely to be women (61.7% vs. 37.5%; p = 0.03), have gastric bypass history (8.3% vs. 0.8%; p = 0.02) and pancreatic atrophy on imaging (38.9% vs. 13.3%; p = 0.02). Late ON was associated with an increased risk of graft failure (HR 2.0; p = 0.07) and death‐censored graft loss (HR 2.5; p = 0.10). We describe two phenotypes of ON after kidney transplantation: DGF‐ON and late ON. Our study is the first to our knowledge to evaluate DGF‐ON with DGF controls without ON. Although limited by small sample size, DGF‐ON was not associated with adverse outcomes when compared with controls. Late ON predicted worse allograft outcomes.

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Pathophysiological Mechanisms and Clinical Associations of Non-Alcoholic Fatty Pancreas Disease

Cited by 4 publications

References 128 publications

Western diet-induced ultrastructural changes in mouse pancreatic acinar cells

Western diet-induced ultrastructural changes in mouse pancreatic acinar cells

Prevalence of Fatty Pancreas and its relation with anthropometric values on the Growth and Obesity Cohort Study

Oxalate Nephropathy After Kidney Transplantation: Risk Factors and Outcomes of Two Phenotypes

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