Molecular Mechanisms Of Portal Vein Tolerance
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Overview: How Is Alcohol Metabolized by the Body?
ach and bowels and from the portal vein, which leads to the liver. From there it is carried to the liver, where it is exposed to enzymes and metabolized. The rate of the rise of BAC is influ enced by how quickly alcohol is emp-tied from the stomach and the extent of metabolism during this first pass through the stomach and liver (i.e.,
Quantitative T2 changes and susceptibility weighted magnetic
subcardinal vein and portal vein etc., were visualized on GD12. immune tolerance, and the maintenance of pregnancy 3-9]. the molecular mechanisms of placental
Mechanisms controlling hormone secretion in human gut and its
the hepatic portal vein ( Vahl et al. 2007). CCK suppresses hepatic glucose output in rodents by acting on CCK-A receptors on intestinal vagal afferents projecting to the nuclear solitary tract (NTS), a signalling pathway that is perturbed by diet-induced obesity (Cheung et al. 2009). However, whether such mechanism exist in
Inflammatory Pathways in Liver Homeostasis and Liver Injury
gastrointestinal tract via the portal vein (Fig. 1). Circulating blood cells, e.g., from the innate or adaptive immune system, are pressed through a network of sinusoids allowing contact to a variety of intrahepatic cell popula-tions, such as parenchymal liver cells (hepatocytes), endothelial cells, liver-resident macrophage (Kupffer cell)
Cell Metabolism Previews - COnnecting REpositories
the molecular mechanisms underpinning its immediate metabolic beneﬁts remain unclear. New work in this issue (Troy et al., 2008) suggests intestinal glucose production sensed by afferent nerve ﬁbers surrounding the portal vein may be key. Got a sweet tooth? If so, it s not usually considered a good thing at least for your metabolic health.
Role of Docosahexaenoic Acid Treatment in Improving Liver
coupled receptor (GPR)120. Our aim was to investigate in pediatric NAFLD the mechanisms underlying the effects of DHA administration on histo-pathological aspects, GPR120 expression, hepatic progenitor cell activation and macrophage pool. Patients and Methods:20 children with untreated NAFLD were included. Children were treated with DHA for 18
In This Issue of Diabetes
Kuhre et al. Molecular mechanisms of The tolerance that was induced by PD-L1 was explained by a Scale bar, 50 µm. PV, portal vein. Diabetes Volume 64
Normal kinetics of intestinal glucose absorption in the
indicated times from tail vein blood and by using a glucose meter (Glucotrend, Roche Molecular Biochemicals). Isolated, Nonrecirculating, Joint Perfusion of Small Bowel and Liver of Mice. This perfusion system is an isolated, single path, vascular perfusion with an erythrocyte-free perfusion medium via the
Research Paper Molecular signatures of liver dysfunction are
drainage of the portal vein, the direct venous outflow from the intestine, into the liver . In addition, it is a central metabolic organ. Beyond its synthetic capacity for secreted proteins and nutrition, including key proteins within the acute stress response, substances produced by the liver are absorbed by the gut and
back to the liver via portal vein and bind to the fibroblast growth factor receptor 4 (FGFR4) of hepatocytes. Upon activation of FGFR4, c-Jun NH(2)-terminal kinase (JNK) signaling pathway in turn suppresses CYP7A1 gene expression to reduce bile acid synthesis in the liver (Fig. 3).18-21 4.Physiological roles of FXR in the hepatic
Understanding, predicting and achieving liver transplant
balance between tolerance and immunity in the liver 34 36. Conserved molecular mechanisms, which include the detection of danger signals (also known as alarmins, such as ATP and high- mobility group box 1 (HMGB1)), Toll-like receptor (TLR) signalling and inflammasome activation, act as triggers of hepatic inflammatory responses.
Role of Toll-like receptors in immune activation and
of cells induce inﬂammation and tolerance and how these cells work together to maintain immunological balance. The innate immune system is thought to play a major role in maintaining homeostasis in the liver. Gut-derived bacterial products enter the liver through the portal vein. However, liver inﬂammation usu-
Gut-origin sepsis in the critically ill patient
The researchers inserted portal vein catheters for sequen-tial blood sampling in trauma patients and performed con-secutive blood cultures and endotoxin measurements. Even though 30% of patients developed MODS, only 2% of portal venous blood cultures turned out positive, while none of the patients had portal or systemic endotoxemia. The find-
Presentation of hepatocellular antigens
The liver is anorgan inwhichantigen-specific T-cell responsesmanifestabias towardimmune tolerance. This is clearly seen in the rejection of allogeneic liver transplants, and multiple other phenomena suggest that this effect is more general. These include tolerance toward antigens introduced via the portal vein, immune failure to several
Pyruvate Dehydrogenase Kinase 4: A Key Mediator for Metabolic
Specific molecular mechanisms that control liver regeneration have been extensively studied in a rodent model of partial hepatectomy, e.g., as detailed by Huang and Rudnick.(4) Several humoral factors and their intracellular targets were identified as key players in liver regeneration, such as cytokines (e.g.,
aug phys FINAL - Physiology
are regulated by glucose through mechanisms requiring either the K ATP channel sub-units Kir6.2 and Sur1 or the Na+/glucose cotransporter SGLT3, which is a glucose-sens-ing rather than -transporting molecule. 3: entry of glucose into the hepatoportal vein activates a glucose sensor that is linked to vagal afferent nerves projecting to the brain
Development and functional consequences of LPS tolerance in
Brieﬂy, after portal-vein perfusion with Ca -deprived buffer 1 Correspondence: Institute of Molecular Medicine and Experimental Im- munology, University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany.
University of Groningen Molecular and biochemical mechanisms
around the hepatic artery and portal vein and connected to a dual channel ultrasonic transit-time volume flow meter (T206, Transonic). Blood flow was measured continuously during the first 3 hours after reperfusion and twice daily thereafter. In addition, patency of the vascular anastomoses was macroscopically inspected during necropsy.
review article Diabetes, Obesity and Metabolism
the portal vein [12 14]. To explain the regulation of HGP by insulin action at a remote site, several proposed mechanisms (summarized in Figure 1) have been advanced: (i) suppression of glucagon secretion from the pancreatic α-cell [15 17], (ii) reduced availability of circulating gluconeogenic precursors
Toll-Like Receptor Signaling in the Liver
carried through portal vein blood and are considered to play a major role in the clearance of systemic bacterial infection.8 11 Despite the constant exposure to low levels of gut-derived bacteria and bacterial products, there are no signs of ongoing inﬂammation in the normal liver. This lacking response is to some extent explained by very
Hepatic Immune Regulation and Its Involvement in Viral
degradation products, via the portal vein and arterial blood supply fuel large amounts of blood continuously to the liver. The extensive liver sinusoidal meshwork increases the overall vessel diameter in the liver, leading to a slow blood ﬂow that allows interaction of circulating immune cells with
Oral Supplementation of Sodium Butyrate Attenuates the
Mar 30, 2020 glucose tolerance test (GTT) as detailed previously . After 13 weeks, mice were anesthetized through the intraperitoneal injection of 100 mg ketamine + 16 mg xylazine/kg bw. Blood from the portal vein was collected just prior to sacrifice. Liver and intestinal tissue were fixed in neutral-buffered formalin or snap frozen in liquid nitrogen.
Wilson's disease and other neurological copper disorders
molecular mechanisms of the diﬀ erent copper transport diseases are summarised in ﬁ gure 1. M utations resulting in completely absent or non-functional ATP7B protein activity are associated with early-onset, typically hepatic, severe Wilson s disease; these mutations are comparatively
Xenobiotics and autoimmunity: does acetaminophen cause
Molecular mimicry: a theoretical mechanism by which the immune system self-antigens that are structurally similar toforeign antigens; it is due the crossactivation of immunological response. Portal tracts: collections of branches of the portal vein, hepatic artery, and the biliary ducts bound together in perivascular connective tissues
Mechanism of T Cell Tolerance Induction by Murine Hepatic
to donor cells through the portal vein of recipient animals increased their acceptance of solid tissue allografts2,3; and (4) preexposure of soluble antigens via the portal vein leads to systemic immune tolerance.4,5 The mechanism of liver-induced systemic immune tolerance is not well un-derstood, although several hypotheses, including T cell
Effect of portal glucose sensing on incretin hormone
glucose (29, 30) and GLP-1 (25) into the portal vein. In addition, portal vein glucose and GLP-1 sensors have been shown to interact (1, 4, 15, 17, 38). Thus, one aim of the present study was to determine whether incretin hormone secretion is inﬂuenced by the activation of portal vein glucose sensors.
Intensive insulin treatment induces insulin resistance
Intravenous insulin tolerance test Tail blood samples were collected in ad libitum fed animals before (0 min) and 4, 8, 12, and 16 min after i.v. injection of regular insulin (0.75 U/kg BW). The constant rate for blood glucose disappearance during insulin tolerance test (kITT) was calculated based on the linear regression of the Neperian
Macrophages and Dendritic Cells Emerge in the Liver during
The liver is a physiological site of immune tolerance, the breakdown of which induces immunity. Liver antigen-presenting cells may be involved in both immune tolerance and activation. Although inflammatory diseases of the liver are frequently associated with inflammatory bowel diseases, the underlying immunological mechanisms remain to be
Chronic infusion of angiogenesis-(1-7) improves insulin
Glucose tolerance test. After a 6 h fast, the rats were anaesthetized and after the collection of an unchallenged sample (time 0), a solution of 50% glucose (2.0 g/kg body weight) was administered into the peritoneal cavity. During the test blood was collected from the tail vein 15, 30, 60, 90 and 120 min after glucose administration. All blood
2008 Ⅰ. 英文論文 - 近畿大学病院
Kudo M＊, Chiba T, Wakatsuki Y: Molecular mechanisms of portal vein tolerance. Hepatol Res 38: 441-449, 2008. 7. 20. 08 Chung H, Kudo M＊, Takahashi S, Hagiwara S, Sakaguchi Y, Inoue T, Minami Y, Ueshima K, Fukunaga T, Matsunaga T: Comparison of three current staging systems
Basic Allergy and inﬂammation Research Article cells regulate
the portal vein pathway or lymphatic pathway also contribute to the development of immune tolerance against oral Ags. The liver is a possible site of oral tolerance induction. Parenchymal and non-parenchymal cells in the liver have immunomodulatory activ-ities involved in oral tolerance, infection, inﬂammation, cancer, or transplantation [5, 6].
Gut microbiota and liver diseases
the portal vein, and the liver-gut axis is important to understand the pathophysiology of several liver diseases, especially non-alcoholic fatty liver disease and hepatic encephalopathy. Moreover, gut microbiota play a significant role in the development of alcoholic liver disease and hepatocarcinogenesis. Based on these EDITORIAL
Expression of toll-like receptors in hepatic cirrhosis and
(LPS) translocated from the gut into the portal vein, while maintaining its unique capacity to induce immune tolerance. It has been suggested that various TLRs can be widely expressed on hepatocytes, Kupffer cells, sinusoidal endothelial cells, and hepatic stellate cells (HSCs),
Tumor microenviroment and hepatocellular carcinoma metastasis
May 06, 2019 the underlying mechanisms for the maintenance and the dynamic manipulation of inﬂammable microenviroment during tumor pro-gression and metastasis. In this review, we mainly summarize the current understanding of each component of the tumor microenvironment and their roles in the invasion and metastasis of HCC. doi:10.1111/jgh.12091 bs bs banner
Role of Gut Microbiota in Hepatocarcinogenesis
through the portal vein, it is the ﬁrst organ to be exposed to gut-derived toxic factors, including bacteria, damage-associated metabolites, i.e., damage-associated molecular patterns (DAMPs), and bacterial products (i.e., pathogen-associated molecular patterns (PAMPs) [8,9]. Alteration of the intestinal
Section 2: Biphasic Insulin Release: Pools and Signal Modulation
studies where blood could be sampled from the portal vein (1 3), the time lag from the rise of the glucose concentra-tion to the peak insulin response was as short as 60 to 120 s; even in a peripheral vein, the peak response is From the Department of Endocrinology and Metabolism, Hebrew University, Hadassah Medical Center, Jerusalem, Israel.
Antigen-presenting cell function in the tolerogenic liver
the portal venous blood such as lipopolysaccharide (LPS) from Gram-negative bacteria in the gut that potently stimulate antigen-presenting cells (APCs). The tolerogenic properties of the liver are exempli-fied by its roles in oral tolerance and portal venous tolerance, the persistence of microbial infections and
Microbiota-Generated Metabolites Promote Metabolic Benefits
glucose released by IGN is detected by a portal vein glucose sensor that transmits its signal to the brain by the peripheral nervous system to promote beneﬁcial effects on food intake and glucose metabolism (Delaere et al., 2012). This chain of events is of particular relevance with protein-enriched diets
In-vivo and in-vitro screening of medicinal plants for their
anaesthetized with ether and killed by bleeding through the portal vein. The pleural exudate was collected and the pleural cavity was washed with 1.0-ml saline containing heparin (10 IU/ml).The number of migrating leukocytes in the exudate was determined with a Neubauer chamber. Results were expressed as mean
Targeting the TGF‐β1 Pathway to Prevent Normal Tissue Injury
standing of the molecular mechanisms underlying the development of normal tissue injury after cancer ther-apy. In many cases, these injuries are characterized at the histologic level by loss of parenchymal cells, exces-sive fibrosis, and tissue atrophy. Among the many cyto-kines involved in this process, transforming growth