PMID- 35724509
OWN - NLM
STAT- MEDLINE
DCOM- 20220908
LR  - 20220908
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 153
DP  - 2022 Sep
TI  - Diet-gut microbiota-epigenetics in metabolic diseases: From mechanisms to 
      therapeutics.
PG  - 113290
LID - S0753-3322(22)00679-5 [pii]
LID - 10.1016/j.biopha.2022.113290 [doi]
AB  - The prevalence of metabolic diseases, including obesity, dyslipidemia, type 2 
      diabetes mellitus (T2DM), and non-alcoholic fatty liver disease (NAFLD), is a 
      severe burden in human society owing to the ensuing high morbidity and mortality. 
      Various factors linked to metabolic disorders, particularly environmental factors 
      (such as diet and gut microbiota) and epigenetic modifications, contribute to the 
      progression of metabolic diseases. Dietary components and habits regulate 
      alterations in gut microbiota; in turn, microbiota-derived metabolites, such as 
      short-chain fatty acids (SCFAs), are influenced by diet. Interestingly, 
      diet-derived microbial metabolites appear to produce substrates and enzymatic 
      regulators for epigenetic modifications (such as DNA methylation, histone 
      modifications, and non-coding RNA expression). Epigenetic changes mediated by 
      microbial metabolites participate in metabolic disorders via alterations in 
      intestinal permeability, immune responses, inflammatory reactions, and insulin 
      resistance. In addition, microbial metabolites can trigger inflammatory immune 
      responses and microbiota dysbiosis by directly binding to G-protein-coupled 
      receptors (GPCRs). Hence, diet-gut microbiota-epigenetics may play a role in 
      metabolic diseases. However, their complex relationships with metabolic diseases 
      remain largely unknown and require further investigation. This review aimed to 
      elaborate on the interactions among diet, gut microbiota, and epigenetics to 
      uncover the mechanisms and therapeutics of metabolic diseases.
CI  - Copyright (c) 2022. Published by Elsevier Masson SAS.
FAU - Li, Dan
AU  - Li D
AD  - Guang'an men Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, 
      China. Electronic address: lidan74188@163.com.
FAU - Li, Yujuan
AU  - Li Y
AD  - Guang'an men Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, 
      China. Electronic address: 1161418096@qq.com.
FAU - Yang, Shengjie
AU  - Yang S
AD  - Guang'an men Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, 
      China. Electronic address: 17862954467@163.com.
FAU - Lu, Jing
AU  - Lu J
AD  - Guang'an men Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, 
      China. Electronic address: 1805541173@qq.com.
FAU - Jin, Xiao
AU  - Jin X
AD  - Guang'an men Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, 
      China. Electronic address: jinxiaojx0320@163.com.
FAU - Wu, Min
AU  - Wu M
AD  - Guang'an men Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, 
      China. Electronic address: wumin19762000@126.com.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220617
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
SB  - IM
MH  - *Diabetes Mellitus, Type 2
MH  - Diet
MH  - Epigenesis, Genetic
MH  - *Gastrointestinal Microbiome/genetics
MH  - Humans
MH  - *Metabolic Diseases/genetics/therapy
OTO - NOTNLM
OT  - Diet
OT  - Epigenetics
OT  - Gut microbiota
OT  - Metabolic diseases
OT  - Microbiota-derived metabolites
EDAT- 2022/06/21 06:00
MHDA- 2022/09/09 06:00
CRDT- 2022/06/20 18:16
PHST- 2022/04/20 00:00 [received]
PHST- 2022/05/26 00:00 [revised]
PHST- 2022/06/09 00:00 [accepted]
PHST- 2022/06/21 06:00 [pubmed]
PHST- 2022/09/09 06:00 [medline]
PHST- 2022/06/20 18:16 [entrez]
AID - S0753-3322(22)00679-5 [pii]
AID - 10.1016/j.biopha.2022.113290 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2022 Sep;153:113290. doi: 10.1016/j.biopha.2022.113290. Epub 
      2022 Jun 17.