Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2023 Feb;72(2):409-410.
doi: 10.1136/gutjnl-2022-327601. Epub 2022 May 16.

Modelling chronic pancreatitis as a complex genetic disease in mice

Zsanett Jancsó  1 , Alexandra Demcsák  1 , Miklós Sahin-Tóth  2
Affiliations
Comment

Modelling chronic pancreatitis as a complex genetic disease in mice

Zsanett Jancsó et al. Gut. 2023 Feb.
No abstract available

Keywords: ACUTE PANCREATITIS; CHRONIC PANCREATITIS; PANCREATIC DISORDERS; TRYPSINOGEN.

PubMed Disclaimer

Conflict of interest statement

Competing interests: None declared.

Figures

Figure 1.
Figure 1.
Body weight and pancreas weight of T7K24R × Ctrb1-del mice at 3, 4, and 6 weeks of age. For comparison, age-matched data for C57BL/6N mice and the parent strains T7K24R and Ctrb1-del are also shown. A, Body weight. B, Pancreas weight in mg units. C, Pancreas weight as percent of body weight. Individual data points were graphed with the mean and SD indicated. The differences of means between the groups were analyzed by one-way ANOVA followed by Tukey’s post-hoc test. P < 0.05 was considered statistically significant.
Figure 2.
Figure 2.
Histology of the pancreas from T7K24R × Ctrb1-del mice at 3, 4, and 6 weeks of age. For comparison, pancreas section from a 6-week-old C57BL/6N mouse is shown. Representative hematoxylin-eosin stained pancreas sections are shown. The scale bars correspond to 50 μm. Note that the phenotype at 3 weeks of age was variable, see text for details. Although not shown, pancreas histology of 6-week-old T7K24R and Ctrb1-del mice was normal, indistinguishable from that of C57BL/6N controls.
See this image and copyright information in PMC

Comment on

References

    1. Wang YC, Mao XT, Yu D, Mao SH, Li ZS, Zou WB, Liao Z. Alcohol amplifies the association between common variants at PRSS1-PRSS2 locus and chronic pancreatitis in a dose-dependent manner. Gut 2022. Jan 7. gutjnl-2021-326670 - PubMed
    1. Génin E, Cooper DN, Masson E, Férec C, Chen JM. NGS mismapping confounds the clinical interpretation of the PRSS1 p.Ala16Val (c.47C>T) variant in chronic pancreatitis. Gut 2022, 71:841–842 - PubMed
    1. Sun C, Liu M, An W, Mao X, Jiang H, Zou W, Wu H, Liao Z, Li Z. Heterozygous Spink1 c.194+2T>C mutant mice spontaneously develop chronic pancreatitis. Gut 2020, 69:967–968 - PubMed
    1. Németh BC, Orekhova A, Zhang W, Nortman SA, Thompson T, Hegyi P, Abu-El-Haija M. Novel p.K374E variant of CPA1 causes misfolding-induced hereditary pancreatitis with autosomal dominant inheritance. Gut 2020, 69:790–792 - PMC - PubMed
    1. Mayerle J, Sendler M, Hegyi E, Beyer G, Lerch MM, Sahin-Tóth M. Genetics, cell biology, and pathophysiology of pancreatitis. Gastroenterology 2019, 156:1951–1968 - PMC - PubMed

Publication types