Year: 2020
Type: dissertation
Abstract: In this doctoral dissertation, Wang Y describes the pathophysiology of non-alcoholic steatohepatitis.The content is summarized as follows. PurposeNon-alcoholic steatohepatitis (NASH) is the most common chronic liver disease in adults.Epidemiologic and animal studies implicate overconsumption of dietary sugar, particularly fructose, is suspected to be a critical contributor to the development of NASH.Carbohydrate response element binding protein (ChREBP) is a key transcriptional regulator of de novo lipogenesis (DNL).ChREBP is reported as an important factor in response to fructose-induced hepatic steatosis and hepatitis by regulating both gene expression and secretion of fibrosis growth factor 21 (FGF21).However, mechanisms underlying fructose modulation of ChREBP-FGF21 axis are still unclear.cAMP responsive element binding protein H(CREBH) is a membrane-bound transcription factor which regulates lipid metabolism.CREBH and peroxisome proliferator-activated receptor alpha (PPARa) co-activate hepatic Fgf21 expression and exert effects on energy metabolism through the modulation of plasma FGF21 levels.Previously, the group reported that deficiency of CREBH exacerbates non-alcoholic fatty liver disease (NAFLD) and NASH.Here, the author investigated to define if CREBH affects ChREBP-FGF21 axis in response to hepatic fructose metabolism. Material and methodThe author fed 8-week-old male wild type (WT) mice and CREBH KO (CKO) mice with a high-fructose diet
Author: Wang, Yunong
Language: English
Subfield: Hepatology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W7146253747