scholarly journals Liver Autophagy in Anorexia Nervosa and Acute Liver Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Marouane Kheloufi ◽  
Chantal M. Boulanger ◽  
François Durand ◽  
Pierre-Emmanuel Rautou
Keyword(s):  
Cell Death ◽  
Anorexia Nervosa ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Protective Mechanism ◽  
Liver Insufficiency ◽  
Electron Microscopy Analysis ◽  
Microscopy Analysis ◽  
Rescue Mechanism ◽  
Liver Cell Death

Autophagy, a lysosomal catabolic pathway for long-lived proteins and damaged organelles, is crucial for cell homeostasis, and survival under stressful conditions. During starvation, autophagy is induced in numerous organisms ranging from yeast to mammals, and promotes survival by supplying nutrients and energy. In the early neonatal period, when transplacental nutrients supply is interrupted, starvation-induced autophagy is crucial for neonates’ survival. In adult animals, autophagy provides amino acids and participates in glucose metabolism following starvation. In patients with anorexia nervosa, autophagy appears initially protective, allowing cells to copes with nutrient deprivation. However, when starvation is critically prolonged and when body mass index reaches 13 kg/m2or lower, acute liver insufficiency occurs with features of autophagic cell death, which can be observed by electron microscopy analysis of liver biopsy samples. In acetaminophen overdose, a classic cause of severe liver injury, autophagy is induced as a protective mechanism. Pharmacological enhancement of autophagy protects against acetaminophen-induced necrosis. Autophagy is also activated as a rescue mechanism in response to Efavirenz-induced mitochondrial dysfunction. However, Efavirenz overdose blocks autophagy leading to liver cell death. In conclusion, in acute liver injury, autophagy appears as a protective mechanism that can be however blocked or overwhelmed.

Protective Mechanism of Glycyrrhizin on Acute Liver Injury Induced by Carbon Tetrachloride in Mice

2007 ◽  
Vol 30 (10) ◽  
pp. 1898-1904 ◽  
Author(s):  
Chan-Ho Lee ◽  
Sang-Won Park ◽  
Yeong Shik Kim ◽  
Sam Sik Kang ◽  
Jeong Ah Kim ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Protective Mechanism

scholarly journals Acute liver injury and anorexia nervosa: a case report

2019 ◽  
Vol 13 (2) ◽  
pp. 128-131
Author(s):  
Simona Pascolini ◽  
Michele Cevolani ◽  
Federico Lari ◽  
Luigi Muratori ◽  
Marco Lenzi
Keyword(s):  
Body Weight ◽  
Anorexia Nervosa ◽  
Liver Injury ◽  
Parenteral Nutrition ◽  
Nutritional Assessment ◽  
Acute Liver Injury ◽  
Transaminase Level ◽  
Progressive Increase ◽  
Psychiatric Institute ◽  
History Of

Anorexia nervosa is an eating disorder characterized by restriction of energy intake leading to a significant decrease in body weight. While it is primarily a psychiatric disorder, numerous medical complications can occur. In this article we describe a case of a 25-year-old woman with a 12-year history of severe restrictive anorexia nervosa that was referred to the Emergency Service of our Hospital, transferred from a psychiatric institute, for severe weight loss, dehydration, and progressive increase in transaminases. During the hospital stay she developed an acute liver injury with an increase in transaminase level up to 40× the ULN. Infective and immunological causes of acute hepatitis were excluded. In the suspect of severe starvation acute liver injury, we performed a nutritional assessment and started parenteral nutrition. After 15 days of parenteral nutrition, she gained 2.5 kg of body weight and liver tests were drastically reduced and nearly normal.

scholarly journals Severe Starvation-Induced Hepatocyte Autophagy as a Cause of Acute Liver Injury in Anorexia Nervosa: A Case Report

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
S. Restellini ◽  
L. Spahr ◽  
L. Rubbia Brandt
Keyword(s):  
Anorexia Nervosa ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Clinical Situation ◽  
Severe Malnutrition ◽  
Hepatic Glycogen ◽  
Glycogen Depletion ◽  
Case Presentation ◽  
Common Causes ◽  
Liver Tests

Introduction. Mild elevation of transaminase may be observed in anorexia nervosa, but acute liver injury is uncommon. A complex programmed cell death in response to starvation, called autophagy, has been described in experimental and human studies.Case Presentation. A 24-year-old woman suffering from anorexia nervosa was hospitalized for severe malnutrition. At admission, there were biological signs of acute liver injury but no electrolytic imbalance. After having ruled out the most common causes of liver injury, the patient was carefully refed. As liver tests remained abnormal, liver biopsy was performed. At histology and electron microscopy, numerous signs suggestive of starvation-induced hepatocyte autophagy were found.Discussion. Severe starvation can be associated with acute liver injury that is slowly reversible with careful enteral nutrition. In this clinical situation, profound hepatic glycogen depletion in association with autophagy appears as the leading cause of liver injury.

miR-223 represents a biomarker in acute and chronic liver injury

2017 ◽  
Vol 131 (15) ◽  
pp. 1971-1987 ◽  
Author(s):  
Florian Schueller ◽  
Sanchari Roy ◽  
Sven Heiko Loosen ◽  
Jan Alder ◽  
Christiane Koppe ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Cirrhosis ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Liver Diseases ◽  
Acute Liver Injury ◽  
Chronic Liver ◽  
Published Data ◽  
Duct Ligation

Background: Dysregulation of miRNAs has been described in tissue and serum from patients with acute and chronic liver diseases. However, only little information on the role of miR-223 in the pathophysiology of acute liver failure (ALF) and liver cirrhosis is available. Methods: We analysed cell and tissue specific expression levels as well as serum concentrations of miR-223 in mouse models of acute (hepatic ischaemia and reperfusion, single CCl4 injection) and chronic (repetitive CCl4 injection, bile duct ligation (BDL)) liver diseases. Results were validated in patients and correlated with clinical data. The specific hepatic role of miR-223 was analysed by using miR-223−/− mice in these models. Results: miR-223 expression was significantly dysregulated in livers from mice after induction of acute liver injury and liver fibrosis as well as in liver samples from patients with ALF or liver cirrhosis. In acute and chronic models, hepatic miR-223 up-regulation was restricted to hepatocytes and correlated with degree of liver injury and hepatic cell death. Moreover, elevated miR-223 expression was reflected by significantly higher serum levels of miR-223 during acute liver injury. However, functional in vitro and in vivo experiments revealed no differences in the degree of liver cell death and liver fibrosis as miR-223−/− mice behaved identical with wild-type (wt) mice in all tested models. Conclusion: miR-223 represents a promising diagnostic marker in a panel of serum markers of liver injury. Together with previously published data, our results highlight that the role of miR-223 in the pathophysiology of the liver is complex and needs further analysis.

scholarly journals The protein tyrosine kinase SYK regulates the alternative p38 activation in liver during acute liver inflammation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Bo-Ram Bang ◽  
Kyung Ho Han ◽  
Goo-Young Seo ◽  
Michael Croft ◽  
Young Jun Kang
Keyword(s):  
Cell Death ◽  
Liver Injury ◽  
Host Defense ◽  
Protein Tyrosine Kinase ◽  
Inflammatory Responses ◽  
Acute Liver Injury ◽  
Critical Role ◽  
Liver Inflammation ◽  
Hepatocyte Death

AbstractTwo distinct p38 signaling pathways, classical and alternative, have been identified to regulate inflammatory responses in host defense and disease development. The role of alternative p38 activation in liver inflammation is elusive, while classical p38 signaling in hepatocytes plays a role in regulating the induction of cell death in autoimmune-mediated acute liver injury. In this study, we found that a mutation of alternative p38 in mice augmented the severity of acute liver inflammation. Moreover, TNF-induced hepatocyte death was augmented by a mutation of alternative p38, suggesting that alternative p38 signaling in hepatocytes contributed more significantly to the pathology of acute liver injury. Furthermore, SYK-Vav-1 signaling regulates alternative p38 activation and the downregulation of cell death in hepatocytes. Therefore, it is suggested that alternative p38 signaling in the liver plays a critical role in the induction and subsequent pathological changes of acute liver injury. Collectively, our results imply that p38 signaling in hepatocytes plays a crucial role to prevent excessive liver injury by regulating the induction of cell death and inflammation.

scholarly journals Protective Mechanism of Andrographolide against Carbon Tetrachloride-Induced Acute Liver Injury in Mice

2011 ◽  
Vol 34 (11) ◽  
pp. 1666-1670 ◽  
Author(s):  
Ju-Feng Ye ◽  
Hang Zhu ◽  
Zhi-Feng Zhou ◽  
Ri-Bo Xiong ◽  
Xi-Wen Wang ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Protective Mechanism

scholarly journals The protective mechanism of schisandrin A ind-galactosamine-induced acute liver injury through activation of autophagy

2014 ◽  
Vol 52 (10) ◽  
pp. 1302-1307 ◽  
Author(s):  
Ye Lu ◽  
Wen-Juan Wang ◽  
Yun-Zhen Song ◽  
Zhong-Qin Liang
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Protective Mechanism
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