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American Journal of Physiology. Gastrointestinal and Liver Physiology

Xiumei Che, Ki Cheong Park, Soo Jung Park, You Hyun Kang, Hyun A Jin, Joo Wan Kim, Dong Hyuk Seo, Dae Kyu Kim, Tae Il Kim, Won Ho Kim, Seung Won Kim, Jae Hee Cheon
Triggering receptor expressed on myeloid cells 1 (TREM-1)-expressing intestinal macrophages are significantly increased in the colons of patients with inflammatory bowel disease (IBD). We focused here on the effects of guggulsterone on macrophage modulation in colitis as a potential therapeutic molecule in human IBD and explore the underlying mechanisms. Gene expression in macrophages was examined and wound healing assay using HT-29 cells was performed. Colitis in wild type and IL-10-, TLR4-, and MyD88-deficient mice was induced via the administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) into the colon...
March 15, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Kurt A Zimmerman, Cheng Jack Song, Nancy Gonzalez-Mize, Zhang Li, Bradley K Yoder
Hepatorenal fibrocystic disease (HRFCD) is characterized by cysts in the kidney and liver with associated fibrosis and is the result of defects in proteins required for cilia function or assembly. Previous reports indicate that macrophages, mainly M2-like macrophages, contribute to HRFCD, although the origin (yolk-sac derived resident macrophages vs bone-marrow derived infiltrating macrophages) and contribution of these cells to the observed phenotypes is unknown. Herein, we utilize a congenital model of cilia dysfunction (IFT88Orpk ) to study the importance of macrophages in HRFCD...
March 15, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Christopher J Halbrook, Marina Pasca di Magliano, Costas A Lyssiotis
In the event of an injury, normal tissues exit quiescent homeostasis and rapidly engage a complex stromal and immune program. These tissue repair responses are hijacked and become dysregulated in carcinogenesis to form a growth supportive tumor microenvironment. In pancreatic ductal adenocarcinoma (PDA), which remains one of the deadliest major cancers, the microenvironment is a key driver of tumor maintenance that impedes many avenues of therapy. In this review, we outline recent efforts made to uncover the microenvironmental crosstalk mechanisms which support pancreatic cancer cells, and detail the strategies which have been undertaken to help overcome these barriers...
March 15, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Alice Miriam Kitay, Marie-Therese Schneebacher, Anne Schmitt, Katharina Heschl, Sascha Kopic, Tariq I Alfadda, Abrar Alsaihati, Alexander Link, John P Geibel
The H+ ,K+ -ATPase was identified as the primary proton secretory pathway in the gastric parietal cell and is the pharmacological target of agents suppressing acid secretion. Recently, we identified a second acid secretory protein expressed in the parietal cell; the vacuolar H+ -ATPase (V-type ATPase). The aim of the present study was to further characterize the H+ -ATPase activation by modulations in extracellular calcium via the calcium sensing receptor (CaSR). Isolated gastric glands were loaded with the pH indicator dye BCECF [2', 7'-bis-(2- carboxyethyl)-5-(and-6)-carboxyfluorescein, acetoxymethyl ester to measure intracellular pH...
March 8, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Camille Pochard, Sabrina Coquenlorge, Marie Freyssinet, Philippe Naveilhan, Arnaud Bourreille, Michel Neunlist, Malvyne Rolli-Derkinderen
Gone are the days when enteric glial cells (EGC) were considered merely as satellites of enteric neurons. Like their brain counterpart astrocytes, EGC express an impressive number of receptors for neurotransmitters and intercellular messengers, thereby contributing to neuroprotection and to the regulation of neuronal activity. EGC also produce different soluble factors that regulate neighboring cells among which are intestinal epithelial cells. A better understanding of EGC response to an inflammatory environment, often referred to as enteric glial reactivity, could help define the physiological role of EGC and the importance of this reactivity in maintaining gut functions...
March 8, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Lauren Weaver, Abdul-Rizaq Ali Hamoud, David E Stec, Terry D Hinds
The buildup of fat in the liver (hepatic steatosis) is the first step in a series of incidents that may drive hepatic disease. Obesity is the leading cause of nonalcoholic fatty liver disease (NAFLD) in which hepatic steatosis progresses to liver disease. Chronic alcohol exposure also induces fat accumulation in the liver and shares numerous similarities to obesity-induced NAFLD. Regardless, if hepatic steatosis is due to obesity or long-term alcohol use, it still may lead to hepatic fibrosis, cirrhosis, or possibly hepatocellular carcinoma...
March 1, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Charlotte Bayer Christiansen, Maria Buur Nordskov Gabe, Berit Svendsen, Lars Ove Dragsted, Mette Marie Rosenkilde, Jens J Holst
The colonic epithelium harbors a large number of endocrine cells, but little is known about the endocrine functions of the colon. However, the high density of GLP-1 and PYY secreting L-cells is of great interest because of the potential anti-diabetic and anti-obesity effects of GLP-1 and PYY. Short chain fatty acids (SCFAs) produced by local bacterial fermentation are suggested to activate the colonic free fatty acid receptors FFAR2 (GPR43) and FFAR3 (GPR41), stimulating the colonic L-cells. We used the isolated perfused rat colon as a model of colonic endocrine secretion and studied the effects of the predominant SCFAs formed: acetate, propionate and butyrate...
March 1, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Matheus de Castro Fonseca, Andressa França, Rodrigo Machado Florentino, Roberta Cristelli Fonseca, Antônio Carlos Melo, Paula Teixeira Vieira Vidigal, André G Oliveira, Laurent Dubuquoy, Michael H Nathanson, M Fátima Leite
Hepatocyte proliferation during liver regeneration is a well-coordinated process regulated by the activation of several growth factor receptors, including the insulin receptor (IR). The IR can be localized in part to cholesterol-enriched membrane microdomains, but the role of such domains in insulin-mediated events in hepatocytes is not known. We investigated whether partitioning of IRs into cholesterol-enriched membrane rafts is important for the mitogenic effects of insulin in the hepatic cells. IR and lipid rafts were labeled in HepG2 cells and primary rat hepatocytes...
February 22, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Michael Camilleri
This is an editorial summarizing recent new developments in visceral analgesics. This promising field is important as a new approach to address abdominal pain with peripheral visceral analgesics is considered a key approach to addressing the current opioid crisis. Some of the novel compounds address peripheral pain mechanisms through modulation of opioid receptors through biased ligands, nociceptin/orphanin FQ opioid peptide (NOP) receptor or dual action on NOP and μ-opioid receptor, buprenorphine and morphiceptin analogs...
February 22, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Pauline Brige, Geraldine Hery, Anais Palen, Théophile Guilbaud, Christophe Buffat, Anais Moyon, Jean Hardwigsen, Eric Guedj, Benjamin Guillet, Vincent Vidal, Guillaume Gorincour, Sophie Chopinet, Emilie Gregoire
In order to reduce the morbidity and mortality risk for the donor in living donor liver transplantation (LDLT), we previously identified 20% left portal vein (LPV) stenosis as the effective preconditioning to induce cell proliferation in the contralateral lobe without the downstream ipsilateral atrophy. We report, here, the pathways involved in the first hours after the preconditioning and investigate the changes in liver volume and function. Fourteen pigs entered this study. Five of them were used to study the genetic, cellular and molecular mechanisms set up in the early hours after the establishment of our preconditioning...
February 22, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Patrick Tso, Mustafa Vurma, Chih-Wei Ko, Dana M Lee, Stephen DeMichele
Breastmilk lutein is better absorbed by infants than lutein delivered in infant formula. Therefore, we wish to better understand the possible absorption differences of lutein in breast milk versus infant formula by determining its bioavailability after gastric administration and whether the intestinal absorption of lutein can be improved by using new delivery vehicles. STUDY ONE compared the intestinal uptake, and the lymphatic and portal transport of lutein in conscious lymph fistula rats. Four groups of lymph and portal vein cannulated rats (n = 8-10/group) were randomized to receive via the gastric tube increasing doses (10,20,40,or 80mg/kg) of 20% lutein in safflower oil (SO) suspension to assess whether there was a saturable level of lutein that can be absorbed and transported in lymph...
February 22, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Zhao Lei, Meihong Deng, Zhongjie Yi, Qian Sun, Richard A Shapiro, Hongbo Xu, Tunliang Li, Patricia A Loughran, John E Griepentrog, Hai Huang, Melanie J Scott, Feizhou Huang, Timothy R Billiar
Liver ischemia/reperfusion (I/R) injury occurs through induction of oxidative stress and release of damage-associated molecular patterns (DAMPs), including cytosolic DNA released from dysfunctional mitochondria or from the nucleus. Cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS) is a cytosolic DNA sensor known to trigger stimulator of interferon genes (STING) and downstream type1 interferon (IFN-I) pathways, which are pivotal innate immune system responses to pathogen. However, little is known about the role of cGAS/STING in liver I/R injury...
February 15, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Aleix Gavaldà-Navarro, Jose J Pastor, Alessandro Mereu, Francesc Villarroya, Ignacio R Ipharraguerre
Fibroblast growth factor-19 (FGF19) is an emerging endocrine factor involved in the regulation of bile acid homeostasis and energy metabolism in rodents and humans. In pigs, however, the FGF19 system remains largely unexplored. This study was designed to investigate the developmental regulation of the FGF19 system in domestic pigs. Samples of intestinal sections, liver, and plasma were collected from 24 pigs (n = 6) at four developmental stages (birth, pre-weaning, post-weaning, and adulthood). In the intestine, expression of the farnesoid X receptor (FXR) and FGF19 showed a congruent time- and region-dependent regulation, beginning soon after birth to achieve maximal expression in ileum during adulthood...
February 15, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Seiichi Yakabi, Lixin Wang, Hiroshi Karasawa, Pu-Qing Yuan, K Koike, Koji Yakabi, Yvette F Tache
We investigated whether vasoactive intestinal peptide (VIP) and/or prostaglandins contribute to peripheral corticotropin-releasing factor (CRF)-induced CRF1 receptor mediated stimulation of colonic motor function and diarrhea in rats. The VIP antagonist, [4Cl-D-Phe 6 , Leu 17 ]VIP injected intraperitoneally (ip) completely prevented CRF (10 µg/kg, ip)-induced fecal output and diarrhea occurring within the first hour post injection whereas pretreatment with the prostaglandin synthesis inhibitor, indomethacin had no effect...
February 8, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Melina Miia Malinen, Izna Ali, Jacqueline Bezençon, James John Beaudoin, Kim L R Brouwer
The heteromeric steroid transporter, organic solute transporter alpha/beta (OSTα/β; SLC51), was discovered over a decade ago, but its physiological significance in the liver is still uncertain. A major challenge has been the lack of suitable models expressing OSTα/β. Based on observations first reported herein that hepatic OSTα/β is upregulated in nonalcoholic steatohepatitis (NASH), the aim of this research was to develop an in vitro model to evaluate OSTα/β function and interaction with drugs and bile acids...
February 8, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Richard Parker, Christopher J Weston, Zhenhua Miao, Christopher Corbett, Matthew Armstrong, Linda Ertl, Karen Ebsworth, Matthew Walters, Trageen Baumart, Dale Newland, Jeff McMahon, Penglie Zhang, Rajinder Singh, James Campbell, Philip N Newsome, Israel Charo, Thomas Schall, David H Adams
Non-alcoholic fatty liver disease (NAFLD) is a common disease, closely associated with obesity and insulin resistance. We investigated the presence of a subset of myeloid cells associated with metabolic disturbance in the liver of patients with NAFLD and a murine model of obesity-induced liver disease. Gene and protein expression in liver and serum was investigated with rt-PCR or ELISA and correlated to clinical disease. Liver-infiltrating immune cells were isolated from normal or diseased human liver for flow cytometric analysis...
February 8, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Tea Soini, Marjut Pihlajoki, Noora Andersson, Jouko Lohi, Kari A Huppert, David A Rudnick, Stacey S Huppert, David B Wilson, Mikko P Pakarinen, Markku Heikinheimo
Biliary atresia (BA), a neonatal liver disease, is characterized by obstruction of extrahepatic bile ducts with subsequent cholestasis, inflammation, and progressive liver fibrosis. To gain insights into the pathophysiology of BA, we focused attention on GATA6, a transcription factor implicated in biliary development. Early in fetal development GATA6 expression is evident in cholangiocytes and hepatocytes, but by late gestation it is extinguished in hepatocytes. Utilizing a unique set of BA liver samples collected before and after successful portoenterostomy (PE), we found that GATA6 expression is markedly upregulated in hepatocytes of patients with BA compared to healthy and cholestatic disease controls...
February 1, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Courtney Clyburn, R Alberto Travagli, Kirsteen N Browning
Obesity is associated with dysregulation of vagal neurocircuits controlling gastric functions, including food intake and energy balance. In the short term, however, caloric intake is regulated homeostatically, although the precise mechanisms responsible are unknown. The present study examined the effects of acute high fat diet (HFD) on glutamatergic neurotransmission within central vagal neurocircuits and its effects on gastric motility. Sprague-Dawley rats were fed a control or HFD diet (14% or 60% kcal from fat, respectively) for 3-5 days...
January 25, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Laura Tedesco, Giovanni Corsetti, Chiara Ruocco, Maurizio Ragni, Fabio Rossi, Michele O Carruba, Alessandra Valerio, Enzo Nisoli
Chronic alcohol consumption promotes mitochondrial dysfunction, oxidative stress, defective protein metabolism, and fat accumulation in hepatocytes (liver steatosis). Inadequate amino-acid metabolism is worsened by protein malnutrition, frequently present in alcohol-consuming patients, with reduced circulating branched-chain amino acids (BCAAs). Here we asked whether dietary supplementation with a specific amino-acid mixture, enriched in BCAAs (BCAAem) and able to promote mitochondrial function in muscle of middle-aged rodents, would prevent mitochondrial dysfunction and liver steatosis in Wistar rats fed on a Lieber-DeCarli ethanol (EtOH)-containing liquid diet...
January 25, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Hiroto Kinoshita, Yoku Hayakawa, Zhengchuan Niu, Mitsuru Konishi, Masahiro Hata, Mayo Tsuboi, Yuki Hayata, Yohko Hikiba, Sozaburo Ihara, Hayato Nakagawa, Yoshihiro Hirata, Timothy C Wang, K Koike
During human gastric carcinogenesis, intestinal metaplasia (IM) is frequently seen in the atrophic stomach. In mice, a distinct type of metaplasia known as spasmolytic polypeptide-expressing metaplasia (SPEM) is found in several inflammatory and genetically engineered models. Given the diversity of long- and short-term models of mouse SPEM, it remains unclear whether all models have a shared or distinct molecular mechanism. The origin of SPEM in mice is currently under debate. It is postulated that stem or progenitor cells acquire genetic alterations that then supply metaplastic cell clones, while the possibility of transdifferentiation or dedifferentiation from mature gastric chief cells has also been suggested...
January 18, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
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