TY - JOUR
T1 - Diet-induced gut dysbiosis and inflammation
T2 - Key drivers of obesity-driven NASH
AU - Kang, Gideon G.
AU - Trevaskis, Natalie L.
AU - Murphy, Andrew J.
AU - Febbraio, Mark A.
N1 - Funding Information:
MAF is supported by an Investigator Grant (APP1194141) from the National Health and Medical Research Council of Australia. Conceptualization, MAF; Literature search and writing – original draft, G.G.K; Writing – review and editing, MAF, NLT, AJM, and GGK; Funding acquisition, MAF; Supervision, MAF, AJM, and NLT. All authors have read and approved the final version of the manuscript. MAF is a shareholder and consultant with N-Gene Research Laboratories Inc. and founder and shareholder of Celesta Therapeutics.
Funding Information:
MAF is supported by an Investigator Grant (APP1194141) from the National Health and Medical Research Council of Australia.
Publisher Copyright:
© 2023
PY - 2023/1/20
Y1 - 2023/1/20
N2 - Sucrose, the primary circulating sugar in plants, contains equal amounts of fructose and glucose. The latter is the predominant circulating sugar in animals and thus the primary fuel source for various tissue and cell types in the body. Chronic excessive energy intake has, however, emerged as a major driver of obesity and associated pathologies including nonalcoholic fatty liver diseases (NAFLD) and the more severe nonalcoholic steatohepatitis (NASH). Consumption of a high-caloric, western-style diet induces gut dysbiosis and inflammation resulting in leaky gut. Translocation of gut-derived bacterial content promotes hepatic inflammation and ER stress, and when either or both of these are combined with steatosis, it can cause NASH. Here, we review the metabolic links between diet-induced changes in the gut and NASH. Furthermore, therapeutic interventions for the treatment of obesity and liver metabolic diseases are also discussed with a focus on restoring the gut-liver axis.
AB - Sucrose, the primary circulating sugar in plants, contains equal amounts of fructose and glucose. The latter is the predominant circulating sugar in animals and thus the primary fuel source for various tissue and cell types in the body. Chronic excessive energy intake has, however, emerged as a major driver of obesity and associated pathologies including nonalcoholic fatty liver diseases (NAFLD) and the more severe nonalcoholic steatohepatitis (NASH). Consumption of a high-caloric, western-style diet induces gut dysbiosis and inflammation resulting in leaky gut. Translocation of gut-derived bacterial content promotes hepatic inflammation and ER stress, and when either or both of these are combined with steatosis, it can cause NASH. Here, we review the metabolic links between diet-induced changes in the gut and NASH. Furthermore, therapeutic interventions for the treatment of obesity and liver metabolic diseases are also discussed with a focus on restoring the gut-liver axis.
KW - Biological sciences
KW - Hepatology
KW - Human metabolism
KW - Immunology
KW - Physiology
UR - http://www.scopus.com/inward/record.url?scp=85147112659&partnerID=8YFLogxK
U2 - 10.1016/j.isci.2022.105905
DO - 10.1016/j.isci.2022.105905
M3 - Review Article
AN - SCOPUS:85147112659
SN - 2589-0042
VL - 26
JO - iScience
JF - iScience
IS - 1
M1 - 105905
ER -