scholarly journals Metabolic and hepatic effects of liraglutide, obeticholic acid and elafibranor in diet-induced obese mouse models of biopsy-confirmed nonalcoholic steatohepatitis

2018 ◽  
Vol 24 (2) ◽  
pp. 179-194 ◽  
Author(s):  
Kirstine S Tølbøl ◽  
Maria NB Kristiansen ◽  
Henrik H Hansen ◽  
Sanne S Veidal ◽  
Kristoffer TG Rigbolt ◽  
...  
Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2020-P
Author(s):  
BRANDON B. BOLAND ◽  
HENRIK H. HANSEN ◽  
MICHELLE BOLAND ◽  
DENISE ORÓ ◽  
KIRSTINE SLOTH TØLBØL ◽  
...  

2021 ◽  
Vol 22 (7) ◽  
pp. 3407
Author(s):  
Chung-Ze Wu ◽  
Li-Chien Chang ◽  
Chao-Wen Cheng ◽  
Te-Chao Fang ◽  
Yuh-Feng Lin ◽  
...  

In recent decades, the obesity epidemic has resulted in morbidity and mortality rates increasing globally. In this study, using obese mouse models, we investigated the relationship among urokinase plasminogen activator (uPA), metabolic disorders, glomerular filtration rate, and adipose tissues. Two groups, each comprised of C57BL/6J and BALB/c male mice, were fed a chow diet (CD) and a high fat diet (HFD), respectively. Within the two HFD groups, half of each group were euthanized at 8 weeks (W8) or 16 weeks (W16). Blood, urine and adipose tissues were collected and harvested for evaluation of the effects of obesity. In both mouse models, triglyceride with insulin resistance and body weight increased with duration when fed a HFD in comparison to those in the groups on a CD. In both C57BL/6J and BALB/c HFD mice, levels of serum uPA initially increased significantly in the W8 group, and then the increment decreased in the W16 group. The glomerular filtration rate declined in both HFD groups. The expression of uPA significantly decreased in brown adipose tissue (BAT), but not in white adipose tissue, when compared with that in the CD group. The results suggest a decline in the expression of uPA in BAT in obese m models as the serum uPA increases. There is possibly an association with BAT fibrosis and dysfunction, which may need further study.


2019 ◽  
Vol 39 (11) ◽  
pp. 2082-2093 ◽  
Author(s):  
Paul J. Pockros ◽  
Michael Fuchs ◽  
Bradley Freilich ◽  
Eugene Schiff ◽  
Anita Kohli ◽  
...  

2020 ◽  
Vol 319 (2) ◽  
pp. G197-G211
Author(s):  
Vanessa Pataia ◽  
Saraid McIlvride ◽  
Georgia Papacleovoulou ◽  
Caroline Ovadia ◽  
Julie A. K. McDonald ◽  
...  

We used a mouse model of gestational hypercholanemia to investigate the use of obeticholic acid (OCA), a potent FXR agonist, as a treatment for the hypercholanemia of intrahepatic cholestasis of pregnancy (ICP). The results demonstrate that OCA can improve the fetal bile acid profile. This is relevant not only to women with ICP but also for women who become pregnant while receiving OCA treatment for other conditions such as primary biliary cholangitis and nonalcoholic steatohepatitis.


2016 ◽  
Vol 6 (2) ◽  
pp. 185-200 ◽  
Author(s):  
Ans Jacobs ◽  
Anne‐Sophie Warda ◽  
Jef Verbeek ◽  
David Cassiman ◽  
Pieter Spincemaille

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Andreas Kroh ◽  
Vanina Ivanova ◽  
Hannah Drescher ◽  
Julia Andruszkow ◽  
Thomas Longerich ◽  
...  

A variety of dietary nonalcoholic steatohepatitis (NASH) mouse models are available, and choosing the appropriate mouse model is one of the most important steps in the design of NASH studies. In addition to the histopathological and metabolic findings of NASH, a sufficient mouse model should guarantee a robust clinical status and good animal welfare. Three different NASH diets, a high-fat diet (HFD60), a western diet (WD), and a cafeteria diet (CAFD), were fed for 12 or 16 weeks. Metabolic assessment was conducted at baseline and before scheduled sacrifice, and liver inflammation was analyzed via fluorescence-associated cell sorting and histopathological examination. Clinical health conditions were scored weekly to assess the impact on animal welfare. The HFD60 and WD were identified as suitable NASH mouse models without a significant strain on animal welfare. Furthermore, the progression of inflammation and liver fibrosis was associated with a decreased proportion of CD3+ NK1.1+ cells. The WD represents a model of advanced-stage NASH, and the HFD60 is a strong model of nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome. However, the CAFD should not be considered a NASH model.


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