Pathophysiology of NAFLD and NASH in Experimental Models: The Role of Food Intake Regulating Peptides

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388963%3A_____%2F20%3A00536858" target="_blank" >RIV/61388963:_____/20:00536858 - isvavai.cz</a>

Alternative codes found

RIV/67985823:_____/20:00535779

Result on the web

<a href="https://doi.org/10.3389/fendo.2020.597583" target="_blank" >https://doi.org/10.3389/fendo.2020.597583</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3389/fendo.2020.597583" target="_blank" >10.3389/fendo.2020.597583</a>

Result language

angličtina

Original language name

Pathophysiology of NAFLD and NASH in Experimental Models: The Role of Food Intake Regulating Peptides

Original language description

Obesity, diabetes, insulin resistance, sedentary lifestyle, and Western diet are the key factors underlying non-alcoholic fatty liver disease (NAFLD), one of the most common liver diseases in developed countries. In many cases, NAFLD further progresses to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and to hepatocellular carcinoma. The hepatic lipotoxicity and non-liver factors, such as adipose tissue inflammation and gastrointestinal imbalances were linked to evolution of NAFLD. Nowadays, the degree of adipose tissue inflammation was shown to directly correlate with the severity of NAFLD. Consumption of higher caloric intake is increasingly emerging as a fuel of metabolic inflammation not only in obesity-related disorders but also NAFLD. However, multiple causes of NAFLD are the reason why the mechanisms of NAFLD progression to NASH are still not well understood. In this review, we explore the role of food intake regulating peptides in NAFLD and NASH mouse models. Leptin, an anorexigenic peptide, is involved in hepatic metabolism, and has an effect on NAFLD experimental models. Glucagon-like peptide-1 (GLP-1), another anorexigenic peptide, and GLP-1 receptor agonists (GLP-1R), represent potential therapeutic agents to prevent NAFLD progression to NASH. On the other hand, the deletion of ghrelin, an orexigenic peptide, prevents age-associated hepatic steatosis in mice. Because of the increasing incidence of NAFLD and NASH worldwide, the selection of appropriate animal models is important to clarify aspects of pathogenesis and progression in this field.

Czech name

—

Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30202 - Endocrinology and metabolism (including diabetes, hormones)

Project

<a href="/en/project/GA18-10591S" target="_blank" >GA18-10591S: Lipidized analogs of prolactin-releasing peptide as potential agents for obesity therapy: search for mechanism of action</a><br>

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2020

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Frontiers in Endocrinology

ISSN

1664-2392

e-ISSN

—

Volume of the periodical

11

Issue of the periodical within the volume

Nov 26

Country of publishing house

CH - SWITZERLAND

Number of pages

19

Pages from-to

597583

UT code for WoS article

000596829300001

EID of the result in the Scopus database

2-s2.0-85097500303