Catechin supplemented in a FOS diet induces weight loss by altering cecal microbiota and gene expression of colonic epithelial cells

2018 ◽  
Vol 9 (5) ◽  
pp. 2962-2969 ◽  
Author(s):  
Jianming Luo ◽  
Lulu Han ◽  
Liu Liu ◽  
Lijuan Gao ◽  
Bin Xue ◽  
...  
Keyword(s):  
Gene Expression ◽  
Weight Loss ◽  
Epithelial Cells ◽  
Gut Microbiota ◽  
Colonic Epithelial Cells ◽  
Body Weights ◽  
Cecal Microbiota

The present study showed that catechin controlled rats’ body weights by altering gut microbiota and gene expression of colonic epithelial cells when supplemented into a high-fructo-oligosaccharide (FOS) diet.

Soybean Diacylglycerol Regulates Lipid Metabolism in D-galactose induced Aging Rats by Altering Gut Microbiota and Gene Expression of Colonic Epithelial Cells

2022 ◽  
Author(s):  
Lulu Han ◽  
Rongrong Sun ◽  
Yong Wang ◽  
Jianming Luo ◽  
Xichun Peng
Keyword(s):  
Gene Expression ◽  
Lipid Metabolism ◽  
Cardiovascular Diseases ◽  
Epithelial Cells ◽  
Gut Microbiota ◽  
Chronic Diseases ◽  
Dietary Fat ◽  
Colonic Epithelial Cells ◽  
Aging Rats

Lipid metabolism is closely related to the health of aging bodies, and its disorder often leads to cardiovascular diseases and chronic diseases. Dietary fat is one of the important sources...

scholarly journals Ganoderma lucidum polysaccharide improves rat DSS-induced colitis by altering cecal microbiota and gene expression of colonic epithelial cells

2019 ◽  
Vol 63 (0) ◽  
Author(s):  
Jinli Xie ◽  
Yanghanxiu Liu ◽  
Bohui Chen ◽  
Guangwen Zhang ◽  
Shiyi Ou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Ganoderma Lucidum ◽  
Colonic Epithelial Cells ◽  
Cecal Microbiota

Alliin protects against inflammatory bowel disease by preserving the gene expression in colonic epithelial cells rather than altering gut microbiota

2019 ◽  
Vol 59 ◽  
pp. 309-318
Author(s):  
Xuanwei Li ◽  
Jianming Luo ◽  
Cheng Zhang ◽  
Liu Liu ◽  
Shiyi Ou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Bowel Disease ◽  
Epithelial Cells ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Colonic Epithelial Cells ◽  
Inflammatory Bowel

scholarly journals Regulation of Gene Expression through Gut Microbiota-Dependent DNA Methylation in Colonic Epithelial Cells

2020 ◽  
Vol 4 (4) ◽  
pp. 178-190 ◽  
Author(s):  
Kyoko Takahashi ◽  
Yutaka Sugi ◽  
Kou Nakano ◽  
Tetsuro Kobayakawa ◽  
Yusuke Nakanishi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Epithelial Cells ◽  
Gut Microbiota ◽  
Regulation Of Gene Expression ◽  
Colonic Epithelial Cells

Analysis of Septin 9 gene expression in laser microdissected colonic epithelial cells along the colorectal adenoma-carcinoma sequence

2011 ◽  
Vol 49 (05) ◽  
Author(s):  
A Kalmár ◽  
K Tóth ◽  
S Spisák ◽  
O Galamb ◽  
B Wichmann ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Colorectal Adenoma ◽  
Colonic Epithelial Cells ◽  
Septin 9

scholarly journals The Crohn’s disease associated SNP rs6651252 impacts MYC gene expression in human colonic epithelial cells

PLoS ONE ◽  
2019 ◽  
Vol 14 (2) ◽  
pp. e0212850 ◽  
Author(s):  
Stephen M. Matthews ◽  
Melanie A. Eshelman ◽  
Arthur S. Berg ◽  
Walter A. Koltun ◽  
Gregory S. Yochum
Keyword(s):  
Gene Expression ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Epithelial Cells ◽  
Colonic Epithelial Cells ◽  
Myc Gene

P165 INFLUENCE OF THE GUT MICROBIOTA ON COLONIC HISTONE MODIFICATIONS THROUGH BUTYRATE METABOLISM UNDER HEALTHY AND INFLAMMATORY CONDITIONS

2020 ◽  
Vol 26 (Supplement_1) ◽  
pp. S40-S41
Author(s):  
Peder Lund ◽  
Sarah Smith ◽  
Johayra Simithy ◽  
Lillian Chau ◽  
Elliot Friedman ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Epithelial Cells ◽  
Gut Microbiota ◽  
Histone Acetylation ◽  
Metabolic Pathways ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Isotope Tracing ◽  
Colonic Epithelial Cells ◽  
Germ Free

Abstract Inflammatory bowel disease (IBD) is often associated with a disruption in the composition and activity of the gut microbiota, referred to as dysbiosis. Since the microbiota has the potential to interact with host epithelial cells through small molecules generated from microbial metabolism, knowledge of how inflammation alters the microbial metabolome and how epithelial cells react is important for a better understanding of how IBD develops and persists. Butyrate, a short chain fatty acid produced through fermentation of dietary polysaccharides, has long been known to inhibit histone deacetylases (HDACs), which represent one of the many types of enzymes responsible for the epigenetic control of gene expression through the post-translational modification of histone proteins. We and others have observed that colonic epithelial cells from germ-free mice have reduced levels of acetylation on histone H4, which appears to be distributed throughout the genome based on sequencing analysis. The decreased levels of H4 acetylation may stem from a lack of butyrate, and therefore uninhibited HDAC activity, in germ-free mice. However, since colonic epithelial cells utilize short chain fatty acids as an energy source, an alternative explanation is that the germ-free condition results in less oxidation of butyrate to acetyl-CoA, which is the donor substrate for histone acetylation reactions. Isotope tracing experiments, in which cultured cells were incubated with labeled butyrate, demonstrated that the acetyl groups of histones contained carbon derived from butyrate. We have also performed isotope tracing experiments in mice using labeled inulin, a plant polysaccharide that presumably undergoes fermentation into short chain fatty acids. In this more physiologically relevant model, we detected isotope incorporation into the acetylated histones of colonic epithelial cells at rates of 5–20%, which appears dependent on the microbiota since labeling is sensitive to antibiotic treatment. To identify the metabolic pathways that link inulin to histone acetylation, we are investigating which metabolites become isotopically labeled using untargeted metabolomics. We will apply the same approach to the DSS-induced model of colitis to investigate how inflammation modulates the gut metabolome as well as the metabolic connections between the microbiota and the host. Our studies may uncover metabolic pathways that become dysregulated during inflammation, which may contribute to the pathogenesis of diseases such as IBD.

Induction of heat shock gene expression in colonic epithelial cells after incubation with Escherichia coli or endotoxin

1995 ◽  
Vol 23 (8) ◽  
pp. 1371-1376 ◽  
Author(s):  
Edwin A. Deitch ◽  
Stephen C. Beck ◽  
Nestor C. Cruz ◽  
Antonio De Maio
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Heat Shock ◽  
Epithelial Cells ◽  
Heat Shock Gene ◽  
Colonic Epithelial Cells ◽  
Shock Gene ◽  
Heat Shock Gene Expression

scholarly journals MEK Is a Key Modulator for TLR5-induced Interleukin-8 and MIP3α Gene Expression in Non-transformed Human Colonic Epithelial Cells

2004 ◽  
Vol 279 (24) ◽  
pp. 25179-25188 ◽  
Author(s):  
Sang Hoon Rhee ◽  
Andrew C. Keates ◽  
Mary P. Moyer ◽  
Charalabos Pothoulakis
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Interleukin 8 ◽  
Colonic Epithelial Cells

scholarly journals Regulation of basal promoter activity of the human thiamine pyrophosphate transporter SLC44A4 in human intestinal epithelial cells

2015 ◽  
Vol 308 (9) ◽  
pp. C750-C757 ◽  
Author(s):  
Svetlana M. Nabokina ◽  
Mel Brendan Ramos ◽  
Judith E. Valle ◽  
Hamid M. Said
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Epithelial Cells ◽  
Promoter Activity ◽  
Minimal Promoter ◽  
Thiamine Pyrophosphate ◽  
Luciferase Reporter ◽  
Uptake System ◽  
Colonic Epithelial Cells ◽  
Basal Promoter Activity

Microbiota of the large intestine synthesize considerable amount of vitamin B1 in the form of thiamine pyrophosphate (TPP). There is a specific high-affinity regulated carrier-mediated uptake system for TPP in human colonocytes (product of the SLC44A4 gene). The mechanisms of regulation of SLC44A4 gene expression are currently unknown. In this study, we characterized the SLC44A4 minimal promoter region and identified transcription factors important for basal promoter activity in colonic epithelial cells. The 5′-regulatory region of the SLC44A4 gene (1,022 bp) was cloned and showed promoter activity upon transient transfection into human colonic epithelial NCM460 cells. With the use of a series of 5′- and 3′-deletion luciferase reporter constructs, the minimal genomic region that required basal transcription of the SLC44A4 gene expression was mapped between nucleotides −178 and +88 (using the distal transcriptional start site as +1). Mutational analysis performed on putative cis-regulatory elements established the involvement of ETS/ELF3 [E26 transformation-specific sequence (ETS) proteins], cAMP-responsive element (CRE), and SP1/GC-box sequence motifs in basal SLC44A4 promoter activity. By means of EMSA, binding of ELF3 and CRE-binding protein-1 (CREB-1) transcription factors to the SLC44A4 minimal promoter was shown. Contribution of CREB into SLC44A4 promoter activity was confirmed using NCM460 cells overexpressing CREB. We also found high expression of ELF3 and CREB-1 in colonic (NCM460) compared with noncolonic (ARPE19) cells, suggesting their possible contribution to colon-specific pattern of SLC44A4 expression. This study represents the first characterization of the SLC44A4 promoter and reports the importance of both ELF3 and CREB-1 transcription factors in the maintenance of basal promoter activity in colonic epithelial cells.

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