PMID- 36229811
OWN - NLM
STAT- MEDLINE
DCOM- 20221017
LR  - 20221017
IS  - 2662-7671 (Electronic)
IS  - 2662-7671 (Linking)
VI  - 22
IP  - 1
DP  - 2022 Oct 13
TI  - Cistanche tubulosa phenylethanoid glycosides suppressed adipogenesis 
      in 3T3-L1 adipocytes and improved obesity and insulin resistance in high-fat diet 
      induced obese mice.
PG  - 270
LID - 10.1186/s12906-022-03743-6 [doi]
LID - 270
AB  - BACKGROUND: Cistanche tubulosa is an editable and medicinal traditional Chinese 
      herb and phenylethanoid glycosides are its major components, which have shown 
      various beneficial effects such as anti-tumor, anti-oxidant and neuroprotective 
      activities. However, the anti-obesity effect of C. tubulosa phenylethanoid 
      glycosides (CTPG) and their regulatory effect on gut microbiota are still 
      unclear. In the present study, we investigated its anti-obesity effect and 
      regulatory effect on gut microbiota by 3T3-L1 cell model and obesity mouse model. 
      METHODS: 3T3-L1 adipocytes were used to evaluate CTPG effects on adipogenesis and 
      lipids accumulation. Insulin resistant 3T3-L1 cells were induced and used to 
      measure CTPG effects on glucose consumption and insulin sensitivity. High-fat 
      diet (HFD)-induced C57BL/6 obese mice were used to investigate CTPG effects on 
      fat deposition, glucose and lipid metabolism, insulin resistance and intestinal 
      microorganism. RESULTS: In vitro data showed that CTPG significantly decreased 
      the triglyceride (TG) and non-esterified fatty acid (NEFA) contents of the 
      differentiated 3T3-L1 adipocytes in a concentration-dependent manner without 
      cytotoxicity, and high concentration (100 microg/ml) of CTPG treatment dramatically 
      suppressed the level of monocyte chemoattractant protein-1 (MCP-1) in 3T3-L1 
      mature adipocytes. Meanwhile, CTPG increased glucose consumption and decreased 
      NEFA level in insulin resistant 3T3-L1 cells. We further found that CTPG 
      protected mice from the development of obesity by inhibiting the expansion of 
      adipose tissue and adipocyte hypertrophy, and improved hepatic steatosis by 
      activating AMPKalpha to reduce hepatic fat accumulation. CTPG ameliorated HFD-induced 
      hyperinsulinemia, hyperglycemia, inflammation and insulin resistance by 
      activating IRS1/Akt/GLUT4 insulin signaling pathway in white adipose tissue. 
      Moreover, gut microbiota structure and metabolic functions in HFD-induced obese 
      mice was changed by CTPG, especially short chain fatty acids-producing bacteria 
      including Blautia, Roseburia, Butyrivibrio and Bacteriodes were significantly 
      increased by CTPG treatment. CONCLUSIONS: CTPG effectively suppressed 
      adipogenesis and lipid accumulation in 3T3-L1 adipocytes and ameliorated 
      HFD-induced obesity and insulin resistance through activating AMPKalpha and 
      IRS1/AKT/GLUT4 signaling pathway and regulating the composition and metabolic 
      functions of gut microbiota.
CI  - (c) 2022. The Author(s).
FAU - Abudujilile, Dilinazi
AU  - Abudujilile D
AD  - Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College 
      of Life Science and Technology, Xinjiang University, Urumqi, 830017, China.
FAU - Wang, Weilan
AU  - Wang W
AD  - Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College 
      of Life Science and Technology, Xinjiang University, Urumqi, 830017, China.
FAU - Aimaier, Alimu
AU  - Aimaier A
AD  - Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College 
      of Life Science and Technology, Xinjiang University, Urumqi, 830017, China.
FAU - Chang, Lili
AU  - Chang L
AD  - Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College 
      of Life Science and Technology, Xinjiang University, Urumqi, 830017, China.
FAU - Dong, Yuliang
AU  - Dong Y
AD  - Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College 
      of Life Science and Technology, Xinjiang University, Urumqi, 830017, China.
FAU - Wang, Yiye
AU  - Wang Y
AD  - Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College 
      of Life Science and Technology, Xinjiang University, Urumqi, 830017, China.
FAU - Fan, Xu
AU  - Fan X
AD  - Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College 
      of Life Science and Technology, Xinjiang University, Urumqi, 830017, China.
FAU - Ma, Yu
AU  - Ma Y
AD  - Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College 
      of Life Science and Technology, Xinjiang University, Urumqi, 830017, China.
FAU - Wang, Yongli
AU  - Wang Y
AD  - Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College 
      of Life Science and Technology, Xinjiang University, Urumqi, 830017, China.
FAU - Ziyayiding, Dilinigeer
AU  - Ziyayiding D
AD  - Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College 
      of Life Science and Technology, Xinjiang University, Urumqi, 830017, China.
FAU - Ma, Yuan
AU  - Ma Y
AD  - College of Resource and Environment Sciences, Xinjiang University, Urumqi, 
      830017, China.
FAU - Lv, Jie
AU  - Lv J
AD  - Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College 
      of Life Science and Technology, Xinjiang University, Urumqi, 830017, China. 
      ljyxju@xju.edu.cn.
FAU - Li, Jinyao
AU  - Li J
AD  - Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College 
      of Life Science and Technology, Xinjiang University, Urumqi, 830017, China. 
      lvjie@xju.edu.cn.
LA  - eng
GR  - 2021D04019/the Open Project Fund of Key Laboratory of Xinjiang Uygur Autonomous 
      Region/
GR  - 202004610/Natural Science Youth Foundation of Xinjiang Uygur Autonomous Region/
GR  - BS180222/Doctoral Start-up Foundation of Xinjiang University/
PT  - Journal Article
DEP - 20221013
PL  - England
TA  - BMC Complement Med Ther
JT  - BMC complementary medicine and therapies
JID - 101761232
RN  - 0 (Antioxidants)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Fatty Acids, Nonesterified)
RN  - 0 (Glycosides)
RN  - 0 (Insulins)
RN  - 0 (Triglycerides)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adipocytes
MH  - Adipogenesis
MH  - Animals
MH  - Antioxidants/pharmacology
MH  - Chemokine CCL2
MH  - *Cistanche/metabolism
MH  - Diet, High-Fat
MH  - Fatty Acids, Nonesterified/metabolism/pharmacology
MH  - Glucose/metabolism
MH  - Glycosides/metabolism/pharmacology
MH  - *Insulin Resistance
MH  - *Insulins/metabolism/pharmacology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Obese
MH  - Obesity/drug therapy
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Triglycerides/metabolism
PMC - PMC9564091
OTO - NOTNLM
OT  - Adipocyte
OT  - Cistanche tubulosa phenylethanoid glycosides
OT  - Gut microbiota
OT  - Insulin resistance
OT  - Obesity
COIS- The authors declare no conflict of interest.
EDAT- 2022/10/14 06:00
MHDA- 2022/10/18 06:00
PMCR- 2022/10/13
CRDT- 2022/10/13 23:41
PHST- 2022/05/14 00:00 [received]
PHST- 2022/09/23 00:00 [accepted]
PHST- 2022/10/13 23:41 [entrez]
PHST- 2022/10/14 06:00 [pubmed]
PHST- 2022/10/18 06:00 [medline]
PHST- 2022/10/13 00:00 [pmc-release]
AID - 10.1186/s12906-022-03743-6 [pii]
AID - 3743 [pii]
AID - 10.1186/s12906-022-03743-6 [doi]
PST - epublish
SO  - BMC Complement Med Ther. 2022 Oct 13;22(1):270. doi: 10.1186/s12906-022-03743-6.