scholarly journals Dietary Glucose Increases Glucose Absorption and Lipid Deposition via SGLT1/2 Signaling and Acetylated ChREBP in the Intestine and Isolated Intestinal Epithelial Cells of Yellow Catfish

2020 ◽  
Vol 150 (7) ◽  
pp. 1790-1798 ◽  
Author(s):  
Tao Zhao ◽  
Shui-Bo Yang ◽  
Guang-Hui Chen ◽  
Yi-Huan Xu ◽  
Yi-Chuang Xu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lipid Metabolism ◽  
Epithelial Cells ◽  
Fatty Acid Synthase ◽  
Intestinal Epithelial Cells ◽  
Glucose Absorption ◽  
Lipid Deposition ◽  
Intestinal Epithelial ◽  
Yellow Catfish ◽  
Induced Changes

ABSTRACT Background Dietary carbohydrate affects intestinal glucose absorption and lipid deposition, but the underlying mechanisms are unknown. Objectives We used yellow catfish and their isolated intestinal epithelial cells (IECs) to test the hypothesis that sodium/glucose cotransporters (SGLTs) 1/2 and acetylated carbohydrate response element binding protein (ChREBP) mediated glucose-induced changes in glucose absorption and lipid metabolism. Methods Yellow catfish (mean ± SEM weight: 4.68 ± 0.02 g, 3 mo old, mixed sex) were fed diets containing 250 g carbohydrates/kg from glucose (G, control), corn starch (CS), sucrose (S), potato starch (PS), or dextrin (D) for 10 wk. IECs were isolated from different yellow catfish and incubated for 24 h in a control or glucose (15 mM) solution with or without a 2-h pretreatment with an inhibitor [sotagliflozin (LX-4211) or tubastatin A (TBSA)]. Human embryonic kidney cells (HEK293T cells) were transfected with a Flag-ChREBP plasmid to explore ChREBP acetylation. Triglyceride (TG) and glucose concentrations and enzymatic activities were measured in the intestine and IECs of yellow catfish. They also were subjected to immunofluorescence, immunoprecipitation, qPCR, and immunoblotting. Immunoblotting and immunoprecipitation were performed with HEK293T cells. Results The G group had greater intestine TGs (0.99- to 2.30-fold); activities of glucose 6-phospate dehydrogenase, 6-phosphogluconate dehydrogenase, and isocitrate dehydrogenase (0.12- to 2.10-fold); and expression of lipogenic genes (0.32- to 2.34-fold) than the CS, PS, and D groups. The G group had greater intestine sglt1/2 mRNA and protein expression than the CS, S and D groups (0.35- to 1.12-fold and 0.40- to 4.67-fold, respectively), but lower mRNA amounts of lipolytic genes (48.6%–65.8%) than the CS and PS groups. LX-4211 alleviated the glucose-induced increase in sglt1/2 mRNA (38.2%–47.4%) and SGLT1 protein (48.0%) expression, TGs (29.3%), and lipogenic enzyme activities (27.7%–42.1%) and gene expression (38.0%–55.5%) in the IECs. TBSA promoted the glucose-induced increase in TGs (11.3%), fatty acid synthase activity (32.6%), and lipogenic gene expression (21.6%–34.4%) in the IECs and acetylated ChREBP (10.5%) in HEK293T cells. Conclusions SGLT1/2 signaling and acetylated ChREBP mediated glucose-induced changes in glucose absorption and lipid metabolism in the intestine and IECs of yellow catfish.

scholarly journals Endoplasmic Reticulum Stress–Mediated Autophagy and Apoptosis Alleviate Dietary Fat–Induced Triglyceride Accumulation in the Intestine and in Isolated Intestinal Epithelial Cells of Yellow Catfish

2019 ◽  
Vol 149 (10) ◽  
pp. 1732-1741 ◽  
Author(s):  
Shi-Cheng Ling ◽  
Kun Wu ◽  
Dian-Guang Zhang ◽  
Zhi Luo
Keyword(s):  
Endoplasmic Reticulum ◽  
Lipid Metabolism ◽  
Epithelial Cells ◽  
Er Stress ◽  
Dietary Fat ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Yellow Catfish ◽  
Triglyceride Accumulation ◽  
Induced Changes

ABSTRACTBackgroundThe intestine is the main organ for absorbing dietary fat. High dietary lipid intake leads to fat deposition in the intestine and adversely influences fat absorption and health, but the underlying mechanism is unknown.ObjectivesWe used yellow catfish and their isolated intestinal epithelial cells to test the hypothesis that endoplasmic reticulum (ER) stress, autophagy, and apoptosis mediate fat-induced changes in lipid metabolism.MethodsMale and female yellow catfish (weight: 3.79 ± 0.16 g; age: 3 mo) were fed diets containing lipid at 6.98% (low-fat diet; LFD), 11.3% (middle-fat diet; MFD), or 15.4% (high-fat diet; HFD) (by weight) for 8 wk. Each dietary group had 3 replicates, 30 fish per replicate. Their intestinal epithelial cells were isolated and incubated for 24 h in control solution or various concentrations of fatty acids (FAs) with or without 2-h pretreatment with an inhibitor [3-methyladenine (3-MA), 4-phenyl butyric acid (4-PBA), or Ac-DVED-CHO (AC)]. Triglyceride (TG) contents, genes, and enzymes involved in lipid metabolism, ER stress, autophagy, and apoptosis were determined in intestinal tissue and cells; immunoblotting, BODIPY 493/503 staining, ultrastructural observation, and the detection of autophagic and apoptotic vesicles were performed on intestinal cells.ResultsCompared with the LFD and MFD, the HFD increased intestinal TG content by 120–226%, activities of lipogenic enzymes by 19.0–245%, expression of genes related to lipogenesis (0.77–8.4-fold), lipolysis (0.36–6.0-fold), FA transport proteins (0.79–1.7-fold), ER stress (0.55–7.5-fold), autophagy (0.56–4.2-fold), and apoptosis (0.80–5.2-fold). Using isolated intestinal epithelial cells and inhibitors (4-PBA, 3-MA, and AC), we found that ER stress mediated FA-induced activation of autophagy (11.0–50.1%) and apoptosis (10.4–32.0%), and lipophagy and apoptosis mediated FA-induced lipolysis (3.40–41.6%).ConclusionsAn HFD upregulated lipogenesis, lipolysis, and FA transport, induced ER stress, and activated autophagy and apoptosis. ER stress, autophagy, and apoptosis play important regulatory roles in fat-induced changes in lipid metabolism in the intestine and intestinal epithelial cells of yellow catfish.

scholarly journals CDX2 regulates interleukin‐33 gene expression in intestinal epithelial cells (LS174T)

FEBS Open Bio ◽  
2021 ◽  
Author(s):  
Sylvester Larsen ◽  
Jakob Benedict Seidelin ◽  
Johanne Davidsen ◽  
Katja Dahlgaard ◽  
Claus Henrik Nielsen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Interleukin 33

Burn-Induced Circulating Factor(s) Modulates Gene, Expression in Intestinal Epithelial Cells, IEC-6: A cDNA Microarray Study

2000 ◽  
Vol 21 ◽  
pp. S228
Author(s):  
M. Varedi ◽  
H. M. Lee ◽  
G. H. Greeley ◽  
D. N. Herndon ◽  
E. W. Englander
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Cdna Microarray ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Microarray Study

GENE EXPRESSION IN INTESTINAL EPITHELIAL CELLS, IEC-6, IS ALTERED BY BURN INJURY-INDUCED CIRCULATING FACTORS

Shock ◽  
2001 ◽  
Vol 16 (4) ◽  
pp. 259-263 ◽  
Author(s):  
Maryam Varedi ◽  
Heung-Man Lee ◽  
George H. Greeley ◽  
David N. Herndon ◽  
Ella W. Englander
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Burn Injury ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

Comparison of gene expression and activation of transcription factors in organoid-derived monolayer intestinal epithelial cells and organoids

2021 ◽  
Author(s):  
Yu Takahashi ◽  
Yu Inoue ◽  
Keitaro Kuze ◽  
Shintaro Sato ◽  
Makoto Shimizu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Gene Expression Regulation ◽  
Intestinal Epithelial Cells ◽  
Three Dimensional ◽  
Culture Conditions ◽  
Dependent Manner ◽  
Intestinal Epithelial

Abstract Intestinal organoids better represent in vivo intestinal properties than conventionally used established cell lines in vitro. However, they are maintained in three-dimensional culture conditions that may be accompanied by handling complexities. We characterized the properties of human organoid-derived two-dimensionally cultured intestinal epithelial cells (IECs) compared with those of their parental organoids. We found that the expression of several intestinal markers and functional genes were indistinguishable between monolayer IECs and organoids. We further confirmed that their specific ligands equally activate intestinal ligand-activated transcriptional regulators in a dose-dependent manner. The results suggest that culture conditions do not significantly influence the fundamental properties of monolayer IECs originating from organoids, at least from the perspective of gene expression regulation. This will enable their use as novel biological tools to investigate the physiological functions of the human intestine.

scholarly journals Endotoxin Increases Type II-Phospholipase A2 Gene Expression in Rat Intestinal Epithelial Cells

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 108A-108A
Author(s):  
Michael Amer ◽  
Yu Xiao ◽  
Luba Adler ◽  
Michael S Caplan
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Phospholipase A2 ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Type Ii

Influence of TNF-α on the gene expression profile in src transtormed intestinal epithelial cells

2001 ◽  
Vol 120 (5) ◽  
pp. A300 ◽  
Author(s):  
Naoki Kawai ◽  
Shingo Tsuji ◽  
Masahiko Tsujii ◽  
Masato Komori ◽  
Arata Kimura ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Tnf Α

scholarly journals Alteration in Inflammatory Responses and Cytochrome P450 Expression of Porcine Jejunal Cells by Drinking Water Supplements

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Orsolya Palócz ◽  
Géza Szita ◽  
György Csikó
Keyword(s):  
Gene Expression ◽  
Drinking Water ◽  
Cytochrome P450 ◽  
Epithelial Cells ◽  
Fulvic Acid ◽  
Intestinal Epithelial Cells ◽  
Feed Additives ◽  
Feed Additive ◽  
Mrna Levels ◽  
Intestinal Epithelial

The intestinal epithelium is the first determining barrier to the drugs administered per os. Cytochrome P450 (CYP) enzymes are substantial in the initial step of xenobiotic metabolism; therefore, intestinal CYP enzyme activities could be an important influencing factor of the oral utilization of xenobiotic substances. In this study, the effect of four drinking water supplements on CYP mRNA levels of porcine intestinal epithelial cells was examined. Further goal of the study is to describe the effect of these feed additives on the proinflammatory response of the LPS-treated enterocytes. The nontransformed porcine intestinal epithelial cells (IPEC-J2) were grown on six-well polyester membrane inserts. Cell cultures were treated with LPS (10 μg/ml), β-glucan (5 and 50 μg/ml), sanguinarine-containing additive (5 and 50 μg/ml), drinking water acidifier (0.1 and 1 μl/ml), and fulvic acid (25 and 250 μg/ml) for 1 hour. Cells were washed with culture medium and incubated for additional 1 h before total RNA isolation. IL-6, IL-8, TNF-α, HSP70, CYP1A1, CYP1A2, and CYP3A29 mRNA levels were measured. The LPS treatment upregulated the gene expression of IL-8 and TNF-α. The relative gene expression of IL-6 remained unchanged and TNF-α and HSP70 were downregulated after the treatment with each feed additive. CYP1A1 and CYP1A2 expressions increased after sanguinarine-containing solution, fulvic acid, and drinking water acidifier treatment. None of the treatments changed the gene expression of CYP3A29, responsible for the metabolism of the majority of drug substances used in swine industry. The feed additive substances inhibited the expression of proinflammatory mediators HSP70 and TNF-α; however, β-glucan and fulvic acid elevated the production of the chemokine IL-8 mRNA in endotoxin-treated enterocytes. All acidic supplements increased the expression of CYP1A1 gene; their constituents may serve as a ligand of CYP1A1 nuclear receptors.

Nitric oxide regulates energy metabolism and Bcl-2 expression in intestinal epithelial cells

1998 ◽  
Vol 274 (5) ◽  
pp. G797-G801 ◽  
Author(s):  
Manabu Nishikawa ◽  
Kenta Takeda ◽  
Eisuke F. Sato ◽  
Tetso Kuroki ◽  
Masayasu Inoue
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Prolonged Exposure ◽  
Intestinal Epithelial Cells ◽  
Enteric Bacteria ◽  
Intestinal Lumen ◽  
Intestinal Epithelial ◽  
Mucosal Cells ◽  
Respiration Of Mitochondria ◽  
Induced Changes

Nitric oxide (NO) inhibits the respiration of mitochondria and enteric bacteria, particularly under low O2concentration, and induces apoptosis of various types of cells. To gain insight into the molecular role of NO in the intestine, we examined its effects on the respiration, Ca2+status, and expression of Bcl-2 in cultured intestinal epithelial cells (IEC-6). NO reversibly inhibited the respiration of IEC-6 cells, especially under physiologically low O2concentration. Although NO elevated cytosolic Ca2+as determined by the fura 2 method, the cells were fairly resistant to NO. Kinetic analysis revealed that prolonged exposure to NO elevated the levels of Bcl-2 and suppressed the NO-induced changes in Ca2+status of the cells. Because Bcl-2 possesses antiapoptotic function, toxic NO effects might appear minimally in enterocytes enriched with Bcl-2. Thus NO might effectively exhibit its antibacterial action in anaerobic intestinal lumen without inducing apoptosis of Bcl-2-enriched mucosal cells.

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