Inhibition of LXR signaling by SULT2B1b promotes liver regeneration after partial hepatectomy in mouse models of nonalcoholic fatty liver disease

2020 ◽  
Vol 319 (1) ◽  
pp. G87-G96
Author(s):  
Xin Zhang ◽  
Yuyin Xu ◽  
Qianming Bai ◽  
Xiaobo Li ◽  
Jing Han ◽  
...  

This study demonstrates for the first time that hydroxysteroid sulfotransferase 2B1b (SULT2B1b) overexpression promotes the regeneration of fatty liver after partial hepatectomy in mice with nonalcoholic fatty liver disease, while reducing triglyceride accumulation in the regenerative fatty liver. Liver X receptor signaling may be crucial in the SULT2B1b-mediated regeneration of fatty liver. Thus, SULT2B1b may be a potential target for treating hepatic steatosis-related liver regeneration disorders.

2019 ◽  
Vol 3 (8) ◽  
pp. 1036-1049 ◽  
Author(s):  
Ashley Cast ◽  
Meenasri Kumbaji ◽  
Amber D'Souza ◽  
Katherine Rodriguez ◽  
Anita Gupta ◽  
...  

Surgery Today ◽  
2009 ◽  
Vol 39 (7) ◽  
pp. 592-597 ◽  
Author(s):  
Mehmet Ali Uzun ◽  
Neset Koksal ◽  
Huseyin Kadioglu ◽  
Yusuf Gunerhan ◽  
Suat Aktas ◽  
...  

2021 ◽  
Vol 67 (5) ◽  
pp. 58-66
Author(s):  
N. A. Mazerkina ◽  
A. N. Savateev ◽  
S. K. Gorelyshev ◽  
S. A. Mariashev ◽  
S. A. Beregovskaya ◽  
...  

We describe a 15-year girl, who developed panhypopituitarism and diencephalic obesity after surgical excision of craniopharyngioma, followed by nonalcoholic fatty liver disease and cirrhosis 5 years after surgery. Cirrhosis in this case manifested by hypoxia due to hepatopulmonary syndrome, and despite cure of craniopharyngioma by surgery and radiosurgery treatment and adequate hormonal substitution therapy patient died 9 years after surgery. Growth hormone substitutional therapy in patients with hypopituitarism, and steatohepatitis may decrease liver triglyceride accumulation and prevent end-stage liver disease.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A287-A288
Author(s):  
Parveez Ahamed Abdul Azees ◽  
Juan Pablo Palavicini ◽  
Xianlin Han ◽  
Adam Salmon ◽  
Amrita Kamat

Abstract The objective of the proposed study is to investigate the feasibility of the marmoset as an animal model to study age-associated nonalcoholic fatty liver disease (NAFLD). This chronic liver disease includes a spectrum of disorders ranging from increased triglyceride accumulation in the liver or hepatic steatosis to the more severe inflammatory form nonalcoholic steatohepatitis that can lead to cirrhosis and even hepatocellular carcinoma in individuals who do not have a history of alcohol abuse. Aging increases the prevalence of NAFLD and is strongly associated with the progression and severity of this disease. End-stage hepatic failure and liver cancer resulting from advanced NAFLD are leading indications for liver transplantation enhancing the burden on our healthcare systems. Accumulating clinical evidence also suggests that patients with NAFLD have a higher prevalence of cardiovascular disease. Pathogenetic mechanisms involved in the development and progression of NAFLD are poorly understood and as such, there is a lack of effective therapies. The common marmoset is a relatively short-lived non-human primate that recapitulates many of the physiological changes that occur in human aging. We hypothesized an age-associated increase in hepatic steatosis and alterations in serum lipid profile in the marmoset model. An increase in triglyceride levels and oil red o staining in liver tissues of old marmosets compared to young animals was observed suggesting an age-associated increase in hepatic steatosis in marmosets as observed in humans. Lipidomic studies were also performed using blood samples from male and female marmosets to investigate age-associated changes in specific lipid species, which are characteristic of aberrant lipid metabolism. Analysis of the results revealed significant decreases in several phosphatidylethanolamine, phosphatidylcholine, and sphingomyelin species in the plasma of old marmosets compared to young marmosets. We are now performing studies to determine whether the observed changes in different lipid species could influence the development of cardiovascular disease and provide new insights underlying the mechanisms of NAFLD development with aging.


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