4-Octyl Itaconate Supplementation Relieves Soybean Diet-Induced Liver Inflammation and Glycolipid Metabolic Disorders by Activating the Nrf2-Pparγ Pathway in Juvenile Gibel Carp

2021 ◽  
Author(s):  
Lele Fu ◽  
Haokun Liu ◽  
Wanjie Cai ◽  
Dong Han ◽  
Xiaoming Zhu ◽  
...  
Keyword(s):  
Metabolic Disorders ◽  
Gibel Carp ◽  
Liver Inflammation ◽  
Soybean Diet

scholarly journals TAK1: A Molecular Link Between Liver Inflammation, Fibrosis, Steatosis, and Carcinogenesis

2021 ◽  
Vol 9 ◽  
Author(s):  
Weijun Wang ◽  
Wenkang Gao ◽  
Qingjing Zhu ◽  
Afnan Alasbahi ◽  
Ekihiro Seki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Protein Kinase ◽  
Metabolic Disorders ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Underlying Mechanism ◽  
Liver Inflammation ◽  
Engineering Technology ◽  
Functional Roles ◽  
Amp Activated Protein Kinase

Chronic insult and persistent injury can cause liver inflammation, fibrosis, and carcinogenesis; it can also be associated with metabolic disorders. Identification of critical molecules that link the process of inflammation and carcinogenesis will provide prospective therapeutic targets for liver diseases. Rapid advancements in gene engineering technology have allowed the elucidation of the underlying mechanism of transformation, from inflammation and metabolic disorders to carcinogenesis. Transforming growth factor-β-activated kinase 1 (TAK1) is an upstream intracellular protein kinase of nuclear factor kappa-B (NF-κB) and c-Jun N-terminal kinases, which are activated by numerous cytokines, growth factors, and microbial products. In this study, we highlighted the functional roles of TAK1 and its interaction with transforming growth factor-β, WNT, AMP-activated protein kinase, and NF-κB signaling pathways in liver inflammation, steatosis, fibrosis, and carcinogenesis based on previously published articles.

Liver inflammation abrogates T cell mediated tolerance against particulate antigens induced by liver Kupffer cells

2015 ◽  
Vol 53 (01) ◽  
Author(s):  
F Heymann ◽  
J Peusquens ◽  
I Ludwig-Portugall ◽  
M Kohlhepp ◽  
C Ergen ◽  
...  
Keyword(s):  
T Cell ◽  
Kupffer Cells ◽  
Liver Inflammation

Plasminogen Activation in Diabetes Mellitus: Normalization of Blood Sugar Levels Improves Impaired Enzyme Kinetics In Vitro

1985 ◽  
Vol 54 (02) ◽  
pp. 413-414 ◽  
Author(s):  
Margarethe Geiger ◽  
Bernd R Binder
Keyword(s):  
Plasminogen Activator ◽  
Blood Sugar ◽  
Metabolic Disorders ◽  
Normal Values ◽  
Diabetic Patients ◽  
Type I ◽  
Plasminogen Activation ◽  
Lag Period ◽  
Sugar Levels

SummaryWe have demonstrated previously that fibrin enhanced plasmin formation by the vascular plasminogen activator was significantly impaired, when components isolated from the plasma of three uncontrolled diabetic patients (type I) were used to study plasminogen activation in vitro. In the present study it can be demonstrated that functional properties of the vascular plasminogen activators as well as of the plasminogens from the same three diabetic patients are significantly improved after normalization of blood sugar levels and improvement of HbAlc values. Most pronounced the Km of diabetic vascular plasminogen activator in the presence of fibrin returned to normal values, and for diabetic plasminogen the prolonged lag period until maximal plasmin formation occurred was shortened to almost control values. From these data we conclude that the observed abnormalities of in vitro fibrinolysis are not primarily associated with the diabetic disease, but might be secondary to metabolic disorders caused by diabetes.

Clinical, morphological and biochemical signs of polymycotoxicosis in highly productive cows

2020 ◽  
pp. 14-17
Author(s):  
Irina A. Shkuratova ◽  
◽  
Lyudmila I. Drozdova ◽  
Aleksander I. Belousov ◽  
Keyword(s):  
Metabolic Disorders ◽  
Hepatorenal Syndrome ◽  
Morphological Changes ◽  
Clinical Manifestations ◽  
The Body ◽  
Feed Mixture ◽  
Milk Productivity ◽  
Structural Disorders ◽  
Increased Sensitivity ◽  
Penicillium Spp

Mycotoxicological monitoring of forages shows that the problem of mycotoxicosis has been relevant for several decades. Minimal doses of mycotoxins in feed lead to a decrease in milk productivity, increased sensitivity to infectious and non-infectious diseases. When several mycotoxins enter the body simultaneously, a synergistic effect develops, causing a significant increase in toxicity. Feed contaminated with several types of fungi and their toxins is dangerous for dairy cattle. It was found that the feed mixture contained the types of associations of Aspergillus spp. fungi + Fusarium; Aspergillus spp. + Penicillium spp. + Mucor spp; Fusarium + Penicillium; Mucor spp. + Fusarium + Ustilaginales. Pathogenetic features of metabolic and morphological changes in highly productive cows with polymycotoxicosis were studied. Feeding food contaminated with various metabolites of mold fungi leads to the development of signs of chronic toxemia in animals. Clinical manifestations are the development of diarrhea and dehydration, with a decrease in milk productivity. Metabolic disorders feature the development of an inflammatory process, metabolic acidosis, hyperfermentonemia, with an increase in the amount of creatinine and urea in the blood serum. Metabolic signs indicate the development of hepatorenal syndrome due to structural disorders of the liver and kidneys. Histological signs of polymicotoxicosis are intracapillary and hemorrhagic glomerulonephritis, hepatocyte micronecrosis, and proliferation of connective tissue stroma cells, which leads to the development of atrophic cirrhosis in the interstitial and circular phases.

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