scholarly journals Aging-associated impairment in metabolic compensation by subcutaneous adipose tissue promotes diet-induced fatty liver disease in mice

2019 ◽  
Vol Volume 12 ◽  
pp. 1473-1492 ◽  
Author(s):  
Hiroyoshi Taketani ◽  
Taichiro Nishikawa ◽  
Hisakazu Nakajima ◽  
Kazuki Kodo ◽  
Satoru Sugimoto ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Liver Disease ◽  
Fatty Liver ◽  
Subcutaneous Adipose Tissue ◽  
Fatty Liver Disease ◽  
Metabolic Compensation ◽  
Subcutaneous Adipose

scholarly journals High-fructose feeding does not induce steatosis or non-alcoholic fatty liver disease in pigs

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nikolaj H. Schmidt ◽  
Pia Svendsen ◽  
Julián Albarrán-Juárez ◽  
Søren K. Moestrup ◽  
Jacob Fog Bentzon
Keyword(s):  
Adipose Tissue ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Histopathological Examination ◽  
De Novo Lipogenesis ◽  
Large Animal ◽  
Alcoholic Fatty Liver ◽  
High Fructose ◽  
Alcoholic Fatty Liver Disease

AbstractNon-alcoholic fatty liver disease (NAFLD) is an increasingly prevalent condition that has been linked to high-fructose corn syrup consumption with induction of hepatic de novo lipogenesis (DNL) as the suggested central mechanism. Feeding diets very high in fructose (> 60%) rapidly induce several features of NAFLD in rodents, but similar diets have not yet been applied in larger animals, such as pigs. With the aim to develop a large animal NAFLD model, we analysed the effects of feeding a high-fructose (HF, 60% w/w) diet for four weeks to castrated male Danish Landrace-York-Duroc pigs. HF feeding upregulated expression of hepatic DNL proteins, but levels were low compared with adipose tissue. No steatosis or hepatocellular ballooning was seen on histopathological examination, and plasma levels of transaminases were similar between groups. Inflammatory infiltrates and the amount of connective tissue was slightly elevated in liver sections from fructose-fed pigs, which was corroborated by up-regulation of macrophage marker expression in liver homogenates. Supported by RNA-profiling, quantitative protein analysis, histopathological examination, and biochemistry, our data suggest that pigs, contrary to rodents and humans, are protected against fructose-induced steatosis by relying on adipose tissue rather than liver for DNL.

737 Circulating and adipose tissue expression of visfatin in non-alcoholic fatty liver disease

2006 ◽  
Vol 44 ◽  
pp. S263-S264
Author(s):  
G. Soardol ◽  
C. Pagano ◽  
D. Donnini ◽  
C. Pilone ◽  
L. Domenis ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Tissue Expression ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

scholarly journals The Atypical Cannabinoid Abn-CBD Reduces Inflammation and Protects Liver, Pancreas, and Adipose Tissue in a Mouse Model of Prediabetes and Non-alcoholic Fatty Liver Disease

2020 ◽  
Vol 11 ◽  
Author(s):  
Silvana Y. Romero-Zerbo ◽  
María García-Fernández ◽  
Vanesa Espinosa-Jiménez ◽  
Macarena Pozo-Morales ◽  
Alejandro Escamilla-Sánchez ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Liver Disease ◽  
Mouse Model ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

scholarly journals Macrophages as Key Players during Adipose Tissue–Liver Crosstalk in Nonalcoholic Fatty Liver Disease

2019 ◽  
Vol 39 (03) ◽  
pp. 291-300 ◽  
Author(s):  
Hannelie Korf ◽  
Markus Boesch ◽  
Lore Meelberghs ◽  
Schalk van der Merwe
Keyword(s):  
Adipose Tissue ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Disease Progression ◽  
Fatty Liver Disease ◽  
Metabolic Profile ◽  
Cell Activation ◽  
Immune Cell ◽  
Nonalcoholic Fatty Liver

AbstractNonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in Western countries that could lead to serious health problems including liver failure, cancer, or death. The term NAFLD includes a spectrum of disease states with histological features ranging from simple steatosis to nonalcoholic steatohepatitis (NASH). A key aspect within this research field is the identification of pathogenic factors that trigger inflammation, thus fueling the transition from nonalcoholic fatty liver to NASH. These inflammatory triggers may originate from within the liver as a result of innate immune cell activation and/or hepatocyte injury. Additionally, they may originate from other sites such as adipose tissue or the intestinal tract. In the current review, the authors will primarily focus on events within adipose tissue which may be of importance in triggering the disease progression. They specifically focus on the role of adipose tissue macrophages during NAFLD pathogenesis and how microenvironmental factors may shape their metabolic profile. They further dissect how redirecting the macrophage's metabolic profile alters their immunological functions. Finally, they discuss the opportunities and challenges of targeting macrophages to interfere in disease progression.

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