ArticlePloS one2013
High beta-palmitate fat controls the intestinal inflammatory response and limits intestinal damage in mucin Muc2 deficient mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Regulation of Intestinal Inflammation by Dietary Fats.Frontiers in immunology · 2020Pooled it
- Development and large-scale production of human milk fat analog by fermentation of microalgae.Frontiers in nutrition · 2024Article
- Safety evaluation of INFAT® PLUS: Acute, genetic, teratogenic, and subchronic (90-day) toxicity studies.Toxicology reports · 2023Article
- Evaluation of Fatty Acid Distributions and Triacylglycerol Species in Sow Milk and Commercial Piglet Formulas: A Comparative Study Based on Fat Sources and Lactation Stages.Animals : an open access journal from MDPI · 2022Article
- The Role of Dietary Fats in the Development and Prevention of Necrotizing Enterocolitis.Nutrients · 2021Review
- Review
- Characterization and Analysis of the Temporal and Spatial Dynamic of Several Enteritis Modeling Methodologies.Frontiers in immunology · 2021Article
- Breast Milk Lipids and Fatty Acids in Regulating Neonatal Intestinal Development and Protecting against Intestinal Injury.Nutrients · 2020Review
- Negative Effects of a High-Fat Diet on Intestinal Permeability: A Review.Advances in nutrition (Bethesda, Md.) · 2020Review
- Inflammatory Links Between High Fat Diets and Diseases.Frontiers in immunology · 2018Review
- High Fat Diets Induce Colonic Epithelial Cell Stress and Inflammation that is Reversed by IL-22.Scientific reports · 2016Article
- Beta-palmitate - a natural component of human milk in supplemental milk formulas.Nutrition journal · 2016Review
- Deficiency of intestinal mucin-2 protects mice from diet-induced fatty liver disease and obesity.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Mucus mediated protection against acute colitis in adiponectin deficient mice.Journal of inflammation (London, England) · 2015Article
- Effect of chemotherapy on the microbiota and metabolome of human milk, a case report.Microbiome · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPalmitic-acid esterified to the sn-1,3 positions of the glycerol backbone (alpha, alpha'-palmitate), the predominant palmitate conformation in regular infant formula fat, is poorly absorbed and might cause abdominal discomfort. In contrast, palmitic-acid esterified to the sn-2 position (beta-palmitate), the main palmitate conformation in human milk fat, is well absorbed. The aim of the present study was to examine the influence of high alpha, alpha'-palmitate fat (HAPF) diet and high beta-palmitate fat (HBPF) diet on colitis development in Muc2 deficient (Muc2(-/-)) mice, a well-described animal model for spontaneous enterocolitis due to the lack of a protective mucus layer.
methodsMuc2(-/-) mice received AIN-93G reference diet, HAPF diet or HBPF diet for 5 weeks after weaning. Clinical symptoms, intestinal morphology and inflammation in the distal colon were analyzed.
resultsBoth HBPF diet and AIN-93G diet limited the extent of intestinal erosions and morphological damage in Muc2(-/-) mice compared with HAPF diet. In addition, the immunosuppressive regulatory T (Treg) cell response as demonstrated by the up-regulation of Foxp3, Tgfb1 and Ebi3 gene expression levels was enhanced by HBPF diet compared with AIN-93G and HAPF diets. HBPF diet also increased the gene expression of Pparg and enzymatic antioxidants (Sod1, Sod3 and Gpx1), genes all reported to be involved in promoting an immunosuppressive Treg cell response and to protect against colitis.
conclusionsThis study shows for the first time that HBPF diet limits the intestinal mucosal damage and controls the inflammatory response in Muc2(-/-) mice by inducing an immunosuppressive Treg cell response.
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