PMID- 36017311
OWN - NLM
STAT- MEDLINE
DCOM- 20220829
LR  - 20220829
IS  - 1664-2392 (Print)
IS  - 1664-2392 (Electronic)
IS  - 1664-2392 (Linking)
VI  - 13
DP  - 2022
TI  - Perturbation on gut microbiota impedes the onset of obesity in high fat 
      diet-induced mice.
PG  - 795371
LID - 10.3389/fendo.2022.795371 [doi]
LID - 795371
AB  - High-calorie intake has become one of the most common causes of dietary obesity, 
      which eventually develops into type 2 diabetes mellitus (T2DM). Microbiota, along 
      with the length of the gastrointestinal tract, is related to metabolic disorders, 
      but its shifts and following impact on metabolic disorders due to external 
      perturbation are still unclear. To evaluate shifts of microbiota from the 
      proximal to the distal intestine and their impact on metabolic disorders, we 
      profiled jejunal and colonic microbiota with the perturbation using high salt 
      (HS) and antibiotic-induced microbiota depletion (AIMD) in diet-induced obesity 
      (DIO) mice and analyzed the association with parameters of both obesity and blood 
      glucose. After ten weeks of feeding DIO mice with HS intake and AIMD, they failed 
      to develop obesity. The DIO mice with HS intake had T2DM symptoms, whereas the 
      AIMD DIO mice showed no significant difference in blood glucose parameters. We 
      observed that the jejunal and colonic microbiota had shifted due to settled 
      perturbation, and jejunal microbiota within a group were more dispersed than 
      colonic microbiota. After further analyzing jejunal microbiota using quantified 
      amplicon sequencing, we found that the absolute abundance of Colidextribacter (R 
      = 0.695, p = 0.001) and Faecalibaculum (R = 0.631, p = 0.005) in the jejunum was 
      positively correlated with the changes in BW and FBG levels. The predicted 
      pathway of glucose and metabolism of other substances significantly changed 
      between groups (p <0.05). We demonstrated that the onset of obesity and T2DM in 
      DIO mice is impeded when the gut microbiota is perturbed; thus, this pathogenesis 
      depends on the gut microbiota.
CI  - Copyright (c) 2022 Yu, Yu, Kerem and Ren.
FAU - Yu, Zhongjia
AU  - Yu Z
AD  - Center for Energy Metabolism and Reproduction, Shenzhen Institute of Advanced 
      Technology, Chinese Academy of Sciences, Shenzhen, China.
FAU - Yu, Xiang-Fang
AU  - Yu XF
AD  - Center for Energy Metabolism and Reproduction, Shenzhen Institute of Advanced 
      Technology, Chinese Academy of Sciences, Shenzhen, China.
AD  - Shenzhen College of Advanced Technology, University of Chinese Academy of 
      Sciences, Shenzhen, China.
FAU - Kerem, Goher
AU  - Kerem G
AD  - Xinjiang Key Laboratory of Special Species Conservation and Regulatory Biology, 
      College of Life Science, Xinjiang Normal University, Urumqi, China.
FAU - Ren, Pei-Gen
AU  - Ren PG
AD  - Center for Energy Metabolism and Reproduction, Shenzhen Institute of Advanced 
      Technology, Chinese Academy of Sciences, Shenzhen, China.
AD  - Shenzhen College of Advanced Technology, University of Chinese Academy of 
      Sciences, Shenzhen, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220809
PL  - Switzerland
TA  - Front Endocrinol (Lausanne)
JT  - Frontiers in endocrinology
JID - 101555782
RN  - 0 (Blood Glucose)
SB  - IM
MH  - Animals
MH  - Blood Glucose
MH  - *Diabetes Mellitus, Type 2/complications
MH  - Diet, High-Fat/adverse effects
MH  - *Gastrointestinal Microbiome
MH  - *Metabolic Diseases/complications
MH  - Mice
MH  - Mice, Obese
MH  - Obesity/etiology/metabolism
PMC - PMC9395671
OTO - NOTNLM
OT  - T2DM
OT  - bioinformatic pipelines
OT  - jejunal microbiota
OT  - obesity
OT  - perturbation
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2022/08/27 06:00
MHDA- 2022/08/30 06:00
PMCR- 2022/01/01
CRDT- 2022/08/26 02:30
PHST- 2021/10/15 00:00 [received]
PHST- 2022/07/15 00:00 [accepted]
PHST- 2022/08/26 02:30 [entrez]
PHST- 2022/08/27 06:00 [pubmed]
PHST- 2022/08/30 06:00 [medline]
PHST- 2022/01/01 00:00 [pmc-release]
AID - 10.3389/fendo.2022.795371 [doi]
PST - epublish
SO  - Front Endocrinol (Lausanne). 2022 Aug 9;13:795371. doi: 
      10.3389/fendo.2022.795371. eCollection 2022.