Search results for "Hyperammonemia"

Selective regional distribution of tubulin induced in cerebrum by hyperammonemia

1989

Ingestion of ammonium induces hyperammonemia which increases tubulin content in cerebrum but not in cerebellum. We have dissected 11 discrete areas of cerebrum and quantified the tubulin content in control and hyperammonemic rats. An heterogeneity in the induction of tubulin is shown. The areas more affected are ventral hippocampus, dorsal hippocampus, hypothalamus, septum, reticular formation and frontal cortex, in which tubulin content increased by 63%, 27%, 32%, 48%, 45%, and 25%, respectively, after two months of feeding the ammonium diet.

Minimal hepatic encephalopathy is associated with expansion and activation of CD4+CD28−, Th22 and Tfh and B lymphocytes

2017

AbstractPeripheral inflammation acts synergistically with hyperammonemia in inducing neurological alterations in cirrhotic patients with minimal hepatic encephalopathy (MHE). We hypothesized that appearance of MHE would be associated to some specific qualitative change in peripheral inflammation. The aim of this work was to characterize the changes in peripheral inflammation associated to appearance of MHE. We analyzed it by immunophenotyping and cytokine profile analysis, in cirrhotic patients without or with MHE and controls. The main alterations associated specifically with MHE are: 1) increased activation of all subtypes of CD4+ T-lymphocytes, with the increased expression of CD69; 2) i…

Hyperammonemic encephalopathy after urinary diversion. Diet therapy

2016

Urea cycle dysregulation in non-alcoholic fatty liver disease.

2018

Background & Aims: In non-alcoholic steatohepatitis (NASH), the function of urea cycle enzymes (UCEs) may be affected, resulting in hyperammonemia and the risk of disease progression. We aimed to determine whether the expression and function of UCEs are altered in an animal model of NASH and in patients with non-alcoholic fatty liver disease (NAFLD), and whether this process is reversible. Methods: Rats were first fed a high-fat, high-cholesterol diet for 10 months to induce NASH, before being switched onto a normal chow diet to recover. In humans, we obtained liver biopsies from 20 patients with steatosis and 15 with NASH. Primary rat hepatocytes were isolated and cultured with free fatty …

Alteraciones de la neurotransmisión en hipocampo de ratas hiperamonémicas. papel de la neuroinflamación. modulación por GMPc extracelular

2021

La Encefalopatía Hepática (EH) es un síndrome neuropsiquiátrico complejo producido por un fallo hepático. Cuando el hígado falla se producen hiperamonemia (HA) e inflamación que actúan sinérgicamente produciendo neuroinflamación, lo que da lugar a alteraciones en la neurotransmisión y alteraciones cognitivas y motoras. Estudios anteriores del grupo han demostrado que el aumento de los niveles de GMPc extracelular disminuye la neuroinflamación y revierte las alteraciones cognitivas y motoras observadas en ratas hiperamonémicas. Sin embargo, los mecanismos responsables se desconocían. En la presente tesis doctoral hemos demostrado que la hiperamonemia crónica reduce la respuesta de los recept…

A single transient episode of hyperammonemia induces long-lasting alterations in protein kinase A.

2007

A single transient episode of hyperammonemia induces long-lasting alterations in protein kinase A. Am J Physiol Gastrointest Liver Physiol 292: G305-G314,2007; doi:10.1152/ajpgi.00100.2006.-Hepatic encephalopathy in patients with liver disease is associated with poor prognosis. This could be due to the induction by the transient episode of hepatic encephalopathy of long-lasting alterations making patients more susceptible. We show that a single transient episode of hyperammonemia induces long-lasting alterations in signal transduction. The content of the regulatory subunit of the protein kinase dependent on cAMP (PKA-RI) is increased in erythrocytes from cirrhotic patients. This increase is…

Extracellular Vesicles from Hyperammonemic Rats Induce Neuroinflammation and Motor Incoordination in Control Rats.

2020

Minimal hepatic encephalopathy is associated with changes in the peripheral immune system which are transferred to the brain, leading to neuroinflammation and thus to cognitive and motor impairment. Mechanisms by which changes in the immune system induce cerebral alterations remain unclear. Extracellular vesicles (EVs) seem to play a role in this process in certain pathologies. The aim of this work was to assess whether EVs play a role in the induction of neuroinflammation in cerebellum and motor incoordination by chronic hyperammonemia. We characterized the differences in protein cargo of EVs from plasma of hyperammonemic and control rats by proteomics and Western blot. We assessed whether…

Chronic exposure to ammonia induces isoform-selective alterations in the intracellular distribution and NMDA receptor-mediated translocation of prote…

2004

Hyperammonemia is responsible for most neurological alterations in patients with hepatic encephalopathy by mechanisms that remain unclear. Hyperammonemia alters phosphorylation of neuronal protein kinase C (PKC) substrates and impairs NMDA receptor-associated signal transduction. The aim of this work was to analyse the effects of hyperammonemia on the amount and intracellular distribution of PKC isoforms and on translocation of each isoform induced by NMDA receptor activation in cerebellar neurons. Chronic hyperammonemia alters differentially the intracellular distribution of PKC isoforms. The amount of all isoforms (except PKC zeta) was reduced (17-50%) in the particulate fraction. The con…

Differential role of interleukin-1β in neuroinflammation-induced impairment of spatial and nonspatial memory in hyperammonemic rats.

2019

Activated microglia and increased brain IL-1β play a main role in cognitive impairment in much pathology. We studied the role of IL-1β in neuroinflammation-induced impairment of the following different types of learning and memory: novel object recognition (NOR), novel object location (NOL), spatial learning, reference memory (RM), and working memory (WM). All these processes are impaired in hyperammonemic rats. We assessed which of these types of learning and memory are restored by blocking the IL-1 receptor in vivo in hyperammonemic rats and the possible mechanisms involved. Blocking the IL-1 receptor reversed microglial activation in the hippocampus, perirhinal cortex, and prefrontal cor…

Hyperammonemia alters the mismatch negativity in the auditory evoked potential by altering functional connectivity and neurotransmission

2020

Minimal hepatic encephalopathy (MHE) is a neuropsychiatric syndrome produced by central nervous system dysfunction subsequent to liver disease. Hyperammonemia and inflammation act synergistically to alter neurotransmission, leading to the cognitive and motor alterations in MHE, which are reproduced in rat models of chronic hyperammonemia. Patients with MHE show altered functional connectivity in different neural networks and a reduced response in the cognitive potential mismatch negativity (MMN), which correlates with attention deficits. The mechanisms by which MMN is altered in MHE remain unknown. The objectives of this work are as follows: To assess if rats with chronic hyperammonemia rep…