ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010
Decreased phospho-Akt signaling in a mouse model of total parenteral nutrition: a potential mechanism for the development of intestinal mucosal atrophy.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Pooled it
- Parenteral Nutrition, Inflammatory Bowel Disease, and Gut Barrier: An Intricate Plot.Nutrients · 2024Review
- Oral Treatment With Ileal Spores Triggers Immunometabolic Shifts in Chicken Gut.Frontiers in veterinary science · 2020Article
- Interdependency of EGF and GLP-2 Signaling in Attenuating Mucosal Atrophy in a Mouse Model of Parenteral Nutrition.Cellular and molecular gastroenterology and hepatology · 2017Article
- Bacterial nutrient foraging in a mouse model of enteral nutrient deprivation: insight into the gut origin of sepsis.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Partial Enteral Nutrition Mitigated Ischemia/Reperfusion-Induced Damage of Rat Small Intestinal Barrier.Nutrients · 2016Article
- Diet-dependent, microbiota-independent regulation of IL-10-producing lamina propria macrophages in the small intestine.Scientific reports · 2016Article
- Tight Junction Ultrastructure Alterations in a Mouse Model of Enteral Nutrient Deprivation.Digestive diseases and sciences · 2016Article
- Homeostasis alteration within small intestinal mucosa after acute enteral refeeding in total parenteral nutrition mouse model.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Loss of ADAM17-Mediated Tumor Necrosis Factor Alpha Signaling in Intestinal Cells Attenuates Mucosal Atrophy in a Mouse Model of Parenteral Nutrition.Molecular and cellular biology · 2015Article
- TPN-associated intestinal epithelial cell atrophy is modulated by TLR4/EGF signaling pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Enteral nutrient deprivation in patients leads to a loss of intestinal epithelial barrier function.Surgery · 2015Article
- Glutamate prevents intestinal atrophy via luminal nutrient sensing in a mouse model of total parenteral nutrition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Distraction-induced intestinal growth: the role of mechanotransduction mechanisms in a mouse model of short bowel syndrome.Tissue engineering. Part A · 2014Article
- ErbB receptors and their growth factor ligands in pediatric intestinal inflammation.Pediatric research · 2014Review
- Colonic enteric nervous system analysis during parenteral nutrition.The Journal of surgical research · 2013Article
- Total parenteral nutrition-associated lamina propria inflammation in mice is mediated by a MyD88-dependent mechanism.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Glycyrrhizin represses total parenteral nutrition-associated acute liver injury in rats by suppressing endoplasmic reticulum stress.International journal of molecular sciences · 2013Article
- Intestinal epithelial cell apoptosis and loss of barrier function in the setting of altered microbiota with enteral nutrient deprivation.Frontiers in cellular and infection microbiology · 2013Review
- Mesenteric neovascularization with distraction-induced intestinal growth: enterogenesis.Pediatric surgery international · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Total parenteral nutrition (TPN) leads to a decline in phosphatidylinositol 3-kinase (PI3K)/phospho-Akt (p-Akt) activity, affecting downstream signaling, reducing epithelial cell (EC) proliferation, and contributing to intestinal mucosal atrophy. We hypothesized that promoting Akt activity would prevent these changes. We used a novel Akt-activating peptide, TCL1 (a head-to-tail dimer of the Akt-binding domain of T-cell lymphoma-1), or an inactive mutant sequence TCL1G conjugated to a transactivator of transcription peptide sequence to promote intracellular uptake. Four groups of mice were studied, enteral nutrition group (control), control mice given a functioning TCL1 (control + TCL1), TPN mice given TCL1G (control peptide, TPN + TCL1G); and TPN mice given TCL1. TPN mice given TCL1G showed a significant decrease in jejunal EC p-Akt (Ser473 and Thr308) abundance, whereas TPN + TCL1 mice showed increased p-Akt (Ser473) abundance. Phosphorylation of beta-catenin and glycogen synthase kinase-3beta (downstream targets of Akt signaling) were also decreased in the TPN + TCL1G group and completely prevented in the TPN + TCL1 group. Use of TCL1 nearly completely prevented the decline in EC proliferation seen in the TPN + TCL1G group, as well as partly returned EC apoptosis levels close to controls. The mammalian target of rapamycin pathway demonstrated a similar reduction in activity in the TPN + TCL1G group that was significantly prevented in the TPN + TCL1 group. These results support a significant loss of PI3K/p-Akt signaling upon replacing enteral nutrition with TPN, and prevention of this loss demonstrates the key importance of PI3K/p-Akt signaling in maintaining gut integrity including EC proliferation and reduction in apoptosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.