Gastroenterology articles within Nature Communications

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  • Article
    | Open Access

    Gut microbial dysbiosis has been implicated in the pathogenesis of inflammatory bowel disease. Here, the authors examine host-microbiota protein interactions that occur in inflammatory bowel disease; they show an upregulation in proteins related to antimicrobial activities, and alterations in intestinal extracellular vesicles that are associated with aberrant microbiota-interactions.

    • Xu Zhang
    • , Shelley A. Deeke
    •  & Daniel Figeys

  • Article
    | Open Access

    Insulin promotes lipogenesis but, on the other hand, insulin resistance is associated with increased lipogenesis in the liver. Here the authors show that Snail1 is upregulated by insulin and inhibits lipogenesis by repressing Fasn expression but insulin-mediated Snail1 upregulation is impaired during obesity and insulin resistance.

    • Yan Liu
    • , Lin Jiang
    •  & Liangyou Rui

  • Article
    | Open Access

    FXR plays an important role in bile acid homeostasis by transcriptionally modulating several enterohepatic genes, including intestinal FGF19, that repress hepatic bile acid synthesis. Here the authors show that postprandial FGF19 regulates FXR transcriptional activity via its action on the tyrosine kinase Src, which phosphorylates FXR.

    • Sangwon Byun
    • , Dong-Hyun Kim
    •  & Jongsook Kim Kemper

  • Article
    | Open Access

    Most of the more than 200 known genetic risk loci for inflammatory bowel disease (IBD) reside in regulatory regions. Here, the authors provide eQTL datasets for six circulating immune cell types and ileal, colonic and rectal biopsies to map regulatory modules and identify potential causative genes for IBD.

    • Yukihide Momozawa
    • , Julia Dmitrieva
    •  & Michel Georges

  • Article
    | Open Access

    Steatosis is characterized by initial accumulation of lipids, followed by inflammation and ultimately fibrosis. Here the authors show that the histone demethylase Plant Homeodomain Finger 2 protects liver form steatosis progression by acting as a co-activator of ChREBP, thus, favouring lipid accumulation without inflammation.

    • Julien Bricambert
    • , Marie-Clotilde Alves-Guerra
    •  & Renaud Dentin

  • Article
    | Open Access

    Many SNPs associated with inflammatory bowel disease are located in non-coding genomic regions. Here, the authors perform CAGE-sequencing on descending colon biopsies of Crohn’s disease and ulcerative colitis patients to map transcription start sites and enhancer activity for analysis of regulatory regions.

    • Mette Boyd
    • , Malte Thodberg
    •  & Albin Sandelin

  • Article
    | Open Access

    Senescence has been suggested as causing biliary cholangiopathies but how this is regulated is unclear. Here, the authors generate a mouse model of biliary senescence by deleting Mdm2 in bile ducts and show that inhibiting TGFβ limits senescence-dependent aggravation of cholangiopathies.

    • Sofia Ferreira-Gonzalez
    • , Wei-Yu Lu
    •  & Stuart J. Forbes

  • Article
    | Open Access

    Gut microbial dysbiosis in infancy is associated with childhood atopy and the development of asthma. Here, the authors show that gut microbiota perturbation is evident in the very earliest stages of postnatal life, continues throughout infancy, and can be partially rescued by Lactobacillus supplementation in high-risk for asthma infants.

    • Juliana Durack
    • , Nikole E. Kimes
    •  & Susan V. Lynch

  • Article
    | Open Access

    Methyl metabolites in the one-carbon cycle, such as phosphatidylcholines and S-adenosylmethionine, play a role in hepatic triglyceride regulation. Here Kim et al. show that AhR and SHP are both involved in the expression of several key enzymes of one-carbon metabolism, with the former regulating them early after feeding and the latter inhibiting AhR at later stages.

    • Young-Chae Kim
    • , Sunmi Seok
    •  & Jongsook Kim Kemper

  • Article
    | Open Access

    How tumor cells control metastatic niche formation is not fully understood. Here, the authors show in a lung metastatic niche, high-metastatic hepatocellular carcinoma cells secrete exosomal miR-1247-3p that leads to activation of β1-integrin-NF-κBsignalling, converting fibroblasts to cancer-associated fibroblasts.

    • Tian Fang
    • , Hongwei Lv
    •  & Hongyang Wang

  • Article
    | Open Access

    Acetaminophen-induced liver injury is one of the most common causes of liver failure and has to be treated within hours of the overdose. Here Barbier-Torres et al. show that targeting MCJ, a mitochondrial negative regulator, even 24 h after the overdose protects liver from acetaminophen-induced damage.

    • Lucía Barbier-Torres
    • , Paula Iruzubieta
    •  & María Luz Martínez-Chantar

  • Article
    | Open Access

    Organ regeneration by transplantation of ESC/iPSC-derived tissues is a promising but still challenging approach. Here Lin et al. show that liver damage caused by a chemical insult induces not only fibrosis but also Lgr5+ cell expansion that can be further promoted by treatment with HGF/R-spondin1.

    • Yuan Lin
    • , Zhe-Ping Fang
    •  & Wei-Jie Zhou

  • Article
    | Open Access

    The transcription factor ERG is key to endothelial lineage specification and vascular homeostasis. Here the authors show that ERG balances TGFβ signalling through the SMAD1 and SMAD3 pathways, protecting the endothelium from endothelial-to-mesenchymal transition and consequent liver fibrosis in mice via a SMAD3-dependent mechanism.

    • Neil P. Dufton
    • , Claire R. Peghaire
    •  & Anna M. Randi

  • Article
    | Open Access

    There is a need for humanised grafts to treat patients with intestinal failure. Here, the authors generate intestinal grafts by recellularizing native intestinal matrix with human induced pluripotent stem cell-derived epithelium and human endothelium, and show nutrient absorption after transplantation in rats.

    • Kentaro Kitano
    • , Dana M. Schwartz
    •  & Harald C. Ott

  • Article
    | Open Access

    Hepatocellular carcinoma is known to harbour numerous genomic and epigenomic aberrations, driving transcriptomic deregulation. Here, the authors integrate genomic, epigenomic, and expression data to reveal three prognostic subtypes, providing insight to the pathobiology of hepatocellular carcinoma.

    • Hyun Goo Woo
    • , Ji-Hye Choi
    •  & Yoon Jun Kim

  • Article
    | Open Access

    Liver mitochondrial metabolism plays an important role for glucose and lipid homeostasis and its alterations contribute to metabolic disorders, including fatty liver and diabetes. Here Perry et al. develop a method for the measurement of hepatic fluxes by using lactate and glucose tracers in combination with NMR spectroscopy.

    • Rachel J. Perry
    • , Liang Peng
    •  & Gerald I. Shulman

  • Article
    | Open Access

    Βeta-cells have recently been shown to be heterogeneous with regard to morphology and function. Here, the authors show that β-cells in zebrafish switch from proliferative to functional states with increasing time since β-cell birth, leading to functional and proliferative heterogeneity.

    • Sumeet Pal Singh
    • , Sharan Janjuha
    •  & Nikolay Ninov

  • Article
    | Open Access

    The accumulation of senescent cells is thought to contribute to the age-associated decline in tissue function. Here, the authors identify HSP90 inhibitors as a new class of senolytic compounds in an in vitro screening and show that administration of a HSP90 inhibitor reduces age-related symptoms in progeroid mice.

    • Heike Fuhrmann-Stroissnigg
    • , Yuan Yuan Ling
    •  & Paul D. Robbins

  • Article
    | Open Access

    Hepcidin controls systemic iron levels by inhibiting intestinal iron absorption and iron recycling. Here, Pasricha et al. demonstrate that the hepcidin-chromatin locus displays HDAC3-mediated reversible epigenetic modifications during both erythropoiesis and iron deficiency.

    • Sant-Rayn Pasricha
    • , Pei Jin Lim
    •  & Hal Drakesmith

  • Article
    | Open Access

    Fatty liver is one of the major features of metabolic syndrome and its development is associated with deregulation of systemic lipid and glucose homeostasis. Here Heidenreich et al. show that retinol saturase is implicated in hepatic lipid metabolism by regulating the activity of the transcription factor ChREBP.

    • Steffi Heidenreich
    • , Nicole Witte
    •  & Michael Schupp

  • Article
    | Open Access

    Efforts to determine the effects of drugs on epithelial barriers could benefit from better in vitro models. Here the authors develop a microfluidic device supporting the growth and function of extracellular matrix-supported intestinal tubules, and evaluate the effect of staurosporine and acetylsalicylic acid on barrier integrity.

    • Sebastiaan J. Trietsch
    • , Elena Naumovska
    •  & Paul Vulto

  • Article
    | Open Access

    Hepatic steatosis development may result from dysregulation of lipid metabolism, which is finely tuned by several transcription factors including the PPAR family. Here Kim et al. show that the nuclear receptor RORα inhibits PPARγ-mediated transcriptional activity by interacting with HDAC3 and competing for the promoters of lipogenic genes.

    • Kyeongkyu Kim
    • , Kyungjin Boo
    •  & Sung Hee Baek

  • Article
    | Open Access

    Lambda interferons (IFNL) are involved in the immune response to viral infection. Here the authors show that zinc can interfere with IFNL signalling, and that in HCV patients the rs12979860 polymorphism regulates blood zinc levels and, subsequently, the hepatic immune response.

    • Scott A. Read
    • , Kate S. O’Connor
    •  & Golo Ahlenstiel

  • Article
    | Open Access

    p53 regulates lipid metabolism and fatty acid oxidation, and its inactivation promotes diet-induced liver steatosis. Here Porteiroet al. show that p53 deficiency leads to compensatory p63 upregulation, which, in turn, triggers endoplasmic reticulum stress through IKKβ activation, fatty acid synthesis and lipid accumulation.

    • Begoña Porteiro
    • , Marcos F. Fondevila
    •  & Ruben Nogueiras

  • Article
    | Open Access

    M cells are intestinal epithelial cells that are specialized to transcytose antigens and bacteria from the intestinal lumen to antigen presenting cells on the other side. Here the authors show that the actin-binding protein Aif1 is highly expressed by intestinal M cells and regulates this transcytosis.

    • Sari Kishikawa
    • , Shintaro Sato
    •  & Hiroshi Kiyono

  • Article
    | Open Access

    Epigenetic perturbations may be an important factor in diseases where both genes and environment play a role. Here, Ventham and colleagues show that DNA methylation changes in inflammatory bowel disease are related to the underlying genotype, and are associated with cell-specific changes to gene expression.

    • N. T. Ventham
    • , N. A. Kennedy
    •  & J. Satsangi

  • Article
    | Open Access

    GCN5 inhibits hepatic gluconeogenesis through acetylation of PGC-1α. Here the authors show that GCN5 also activates hepatic gluconeogenesis by acetylating histone H3K9, and that the affinity of GCN5 for its different substrates is regulated via phosphorylation at S275 by PKA in a CITED2-dependent manner.

    • Mashito Sakai
    • , Tomoko Tujimura-Hayakawa
    •  & Michihiro Matsumoto

  • Article
    | Open Access

    Hepatocytes are highly specialized cells and their fate is determined by their position in the liver as either periportal or perivenous hepatocytes. Here, Pu et al. show through genetic lineage tracing for Mfsd2 that periportal hepatocytes proliferate and reprogram into pericentral hepatocytes during liver regeneration and injury.

    • Wenjuan Pu
    • , Hui Zhang
    •  & Bin Zhou

  • Article
    | Open Access

    Activation of hepatic stellate cells is a critical event in the development of fibrosis, which is driven by TGF-beta and inhibited by IFN-gamma. Here Wu et al. show that the RNA binding protein CUGBP1 is increased by TGF-beta signalling and promotes IFN-gamma mRNA degradation.

    • Xingxin Wu
    • , Xudong Wu
    •  & Qiang Xu

  • Article
    | Open Access

    Mice deficient in the pro-inflammatory cytokine IFNγ have improved glucose tolerance. Here, the authors show that this effect depends on the gut microbeAkkermansia muciniphila, whose abundance increases in the absence IFNγ, and which is known to have beneficial effects on host metabolism.

    • Renee L. Greer
    • , Xiaoxi Dong
    •  & Natalia Shulzhenko

  • Article
    | Open Access

    Type 2 diabetes and obesity are associated with increased hepatic gluconeogenesis and lipogenesis, known as selective insulin resistance. Here Kubota et al. explain selective insulin resistance in the liver with the zonal distribution and selective insulin-mediated regulation of Irs1 and Irs2.

    • Naoto Kubota
    • , Tetsuya Kubota
    •  & Takashi Kadowaki

  • Article
    | Open Access

    RNA-binding proteins (RBP) are an emerging group of post-translational regulators. Here the authors show that the RBP vigilin regulates translation of mRNA encoding for proatherogenic proteins—apoB, apoC-III and fibronectin—representing a potential therapeutic target in cardiovascular diseases.

    • Mehrpouya B. Mobin
    • , Stefanie Gerstberger
    •  & Markus Stoffel

  • Article
    | Open Access

    Chronic Hepatitis C infection is associated with a broad spectrum of liver pathologies, ranging from inflammation to fibrosis and liver cancer. Here Thabet et al. identified a polymorphism in the gene MBOAT7 that is associated with increased hepatic inflammation and higher risk of fibrosis development and progression.

    • Khaled Thabet
    • , Anastasia Asimakopoulos
    •  & Rosanna Santaro

  • Article
    | Open Access

    TRAF2 and NCK-interacting protein kinase (TNIK) is a key regulatory component of the TCF4 and β-catenin transcriptional complex. In this study, the authors identify a TNIK inhibitor that blocks Wnt signalling and Wnt-driven colorectal tumorigenesis in mice.

    • Mari Masuda
    • , Yuko Uno
    •  & Tesshi Yamada

  • Article
    | Open Access

    While hundreds of loci are linked with inflammatory bowel diseases (IBDs), the functional consequences of the associated variants remain unclear. Here, the authors screened in ulcerative colitis (UC) patients’ genomes for protein-truncating variants near IBD loci, and identify a protein truncating variant in RNF186to be protective against UC.

    • Manuel A. Rivas
    • , Daniel Graham
    •  & Mark J. Daly

  • Article
    | Open Access

    Application of carbon nanotubes as drug delivery carriers is stalled by uncertainties over their distribution and toxicity in vivo. Here, the authors use animal models to show that, while the bulk of nanotubes is renally cleared, a fraction can be eliminated through an alternative hepatobiliary pathway.

    • Simone Alidori
    • , Robert L. Bowman
    •  & Michael R. McDevitt

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