Absorption Studies in Patients With Crohn's Disease and in Patients With Ulcerative Colitis

Andersson, H; Dotevall, G; Gillberg, R; Jagenburg, Rudolf; Kock, N. G.

doi:10.1111/j.0954-6820.1971.tb07450.x

Cited by 23 publications

(2 citation statements)

References 7 publications

(5 reference statements)

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“…59 Impaired dietary lipid absorption also has been described in patients with UC. [60][61][62] Future studies will investigate the mechanisms underlying the relationship between intestinal inflammation and dietary lipid malabsorption in CTa IKO mice.…”

Section: Q18mentioning

confidence: 99%

Intestinal Phospholipid Disequilibrium Initiates an ER Stress Response That Drives Goblet Cell Necroptosis and Spontaneous Colitis in Mice

Kennelly¹,

Carlin²,

Ju³

et al. 2021

Cellular and Molecular Gastroenterology and Hepatology

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Using mice with impaired intestinal de novo phosphatidylcholine (PC) synthesis, we found that maintaining the PC content of intestinal epithelial cell membranes is crucial to prevent endoplasmic reticulum stress and colitis development, showing an important role for PC in colonic function. BACKGROUND & AIMS: Patients with ulcerative colitis have low concentrations of the major membrane lipid phosphatidylcholine (PC) in gastrointestinal mucus, suggesting that defects in colonic PC metabolism might be involved in the development of colitis. To determine the precise role that PC plays in colonic barrier function, we examined mice with intestinal epithelial cell (IEC)-specific deletion of the rate-limiting enzyme in the major pathway for PC synthesis: CTP Q6 :phosphocholine cytidylyltransferase-a (CTa IKO mice). METHODS: Colonic tissue of CTa IKO mice and control mice was analyzed by histology, immunofluorescence, electron microscopy, quantitative polymerase chain reaction, Western blot, and thin-layer chromatography. Histopathologic colitis scores were assigned by a pathologist blinded to the experimental groupings. Intestinal permeability was assessed by fluorescein isothiocyanate-dextran gavage and fecal microbial composition was analyzed by sequencing 16s ribosomal RNA amplicons. Subsets of CTa IKO mice and control mice were treated with dietary PC supplementation, antibiotics, or 4-phenylbutyrate. RESULTS: Inducible loss of CTa in the intestinal epithelium reduced colonic PC concentrations and resulted in rapid and spontaneous colitis with 100% penetrance in adult mice. Colitis development in CTa IKO mice was traced to a severe and unresolving endoplasmic reticulum stress response in IECs with altered membrane phospholipid composition. This endoplasmic reticulum stress response was linked to the necroptotic death of IECs, leading to excessive loss of goblet cells, formation of a thin mucus barrier, increased intestinal permeability, and infiltration of the epithelium by microbes. CONCLUSIONS: Maintaining the PC content of IEC membranes protects against colitis development in mice, showing a crucial role for IEC phospholipid composition in colonic homeostasis.

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Section: Q18mentioning

confidence: 99%

Intestinal Phospholipid Disequilibrium Initiates an ER Stress Response That Drives Goblet Cell Necroptosis and Spontaneous Colitis in Mice

Kennelly¹,

Carlin²,

Ju³

et al. 2021

Cellular and Molecular Gastroenterology and Hepatology

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“…Renal complications are often detected in patients with inflammatory bowel disease (IBD) (Rothfuss et al, 2006), characterized by renal tubular damage (Fraser et al, 2001;Kreisel et al, 1996). In humans (Andersson et al, 1971) and experimental animals (Barada et al, 2001), colitis is associated with large intestinal dysfunction, leading to malabsorbed fats which in turn, cause a high urinary concentration of oxalate (Andersson and Bosaeus, 1981). Oikonomou et al (2011) showed that renal oxalate stones are well-known extraintestinal manifestations of IBD.…”

Section: Introductionmentioning

confidence: 99%

Early detection of renal injury using urinary vanin‐1 in rats with experimental colitis

Hosohata

Ando

Fujimura

2013

J of Applied Toxicology

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Renal complications are often detected in patients with inflammatory bowel disease (IBD). Because conventional markers such as serum creatinine and β2-microglobulin are not sensitive and/or specific, a new renal biomarker is needed. We have recently identified urinary vanin-1 as an early biomarker for the detection of nephrotoxicant-induced renal injury. In this study, we compared the usefulness of urinary vanin-1 with other newly developed biomarkers [urinary monocyte chemoattractant protein-1 (MCP-1), kidney injury molecule-1 (Kim-1) and N-acetyl-beta-D-glucosaminidase (NAG)] for the detection of renal complications in rats with experimental colitis. On day 2 after intracolonic injection of 2,4,6-trinitrobenzene sulfonic acid (TNBS), male Wistar rats developed not only colitis, but histologically evident renal injury. Urinary vanin-1 started to elevate on day 1, whereas serum creatinine and urinary excretions of glucose, total protein, albumin, Kim-1, MCP-1 and NAG significantly increased only on day 2. The mRNA expressions of vanin-1 and Kim-1 significantly increased in the kidney, but not in the colon. In addition, vanin-1 did not appear in the blood. On the other hand, colonic mRNA expression and the serum concentration of MCP-1 were significantly higher in the TNBS-treated rats than in the control animals. These results suggest that, in contrast to MCP-1, urinary vanin-1 and Kim-1 mainly originated from the kidney rather than the colon in this model. Compared with Kim-1 and MCP-1, vanin-1 might be an earlier biomarker for the detection of renal injury in rats with experimental colitis.

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Remediable Defects in Crohn Disease

Beeken¹

1975

Arch Intern Med

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Absorption Studies in Patients With Crohn's Disease and in Patients With Ulcerative Colitis

Cited by 23 publications

References 7 publications

Intestinal Phospholipid Disequilibrium Initiates an ER Stress Response That Drives Goblet Cell Necroptosis and Spontaneous Colitis in Mice

Intestinal Phospholipid Disequilibrium Initiates an ER Stress Response That Drives Goblet Cell Necroptosis and Spontaneous Colitis in Mice

Early detection of renal injury using urinary vanin‐1 in rats with experimental colitis

Remediable Defects in Crohn Disease

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