PMID- 37764646
OWN - NLM
STAT- Publisher
LR  - 20231003
IS  - 2072-6643 (Electronic)
IS  - 2072-6643 (Linking)
VI  - 15
IP  - 18
DP  - 2023 Sep 5
TI  - Theabrownin from Dark Tea Ameliorates Insulin Resistance via Attenuating 
      Oxidative Stress and Modulating IRS-1/PI3K/Akt Pathway in HepG2 Cells.
LID - 10.3390/nu15183862 [doi]
LID - 3862
AB  - Dark tea has great potential in regulating glycolipid metabolism, and theabrownin 
      (TB) is considered to be the characteristic and bioactive constituent of dark 
      tea. This study evaluated the ability of TB1 (fermented for 7 days) and TB2 
      (fermented for 14 days) isolated from dark tea to reverse insulin resistance (IR) 
      in HepG2 cells. The results indicated that TB significantly ameliorated oxidative 
      stress by improving mitochondrial function. In addition, TB improved glycogen 
      synthesis and glucose consumption, and inhibited gluconeogenesis and fatty acid 
      synthesis, by regulating GSK3beta (Glycogen synthase kinase 3beta), G6Pase 
      (Glucose-6-phosphatase), GCK (Glucokinase), PEPCK1 (Phosphoenolpyruvate carboxy 
      kinase 1), SREBP-1C (sterol regulatory element-binding protein 1C), FASN (fatty 
      acid synthase), and ACC (Acetyl-CoA carboxylase). Additionally, the results of 
      Western blot and real-time PCR experiments demonstrated that TB modulated 
      glucolipid metabolism through the IRS-1 (Insulin receptor substrate 1)/PI3K 
      (phosphatidylinositol-3 kinase)/Akt (protein kinase B) signaling pathway. 
      Treatment with the PI3K inhibitor demonstrated a favorable correlation between 
      PI3K activation and TB action on glycolipid metabolism. Notably, we observed that 
      TB2 had a greater effect on improving insulin resistance compared with TB1, 
      which, due to its prolonged fermentation time, increased the degree of oxidative 
      polymerization of TB.
FAU - Liu, Jia
AU  - Liu J
AD  - Department of Food Science and Engineering, Institute of Science and Technology, 
      Jinan University, Guangzhou 510632, China.
FAU - Wang, Xuan
AU  - Wang X
AD  - State Key Laboratory of Quality Research in Chinese Medicine, Macau Institute for 
      Applied Research in Medicine and Health, Macau University of Science and 
      Technology, Taipa 999078, China.
FAU - Zhu, Yuanqin
AU  - Zhu Y
AD  - Department of Food Science and Engineering, Institute of Science and Technology, 
      Jinan University, Guangzhou 510632, China.
FAU - Deng, Huilin
AU  - Deng H
AD  - Department of Food Science and Engineering, Institute of Science and Technology, 
      Jinan University, Guangzhou 510632, China.
FAU - Huang, Xin
AU  - Huang X
AD  - Department of Food Science and Engineering, Institute of Science and Technology, 
      Jinan University, Guangzhou 510632, China.
FAU - Jayavanth, Pallavi
AU  - Jayavanth P
AD  - International School, Jinan University, 601 Huangpu Road, Guangzhou 510632, 
      China.
FAU - Xiao, Ying
AU  - Xiao Y
AD  - Faculty of Medicine, Macau University of Science and Technology, Taipa 999078, 
      China.
FAU - Wu, Jianlin
AU  - Wu J
AD  - State Key Laboratory of Quality Research in Chinese Medicine, Macau Institute for 
      Applied Research in Medicine and Health, Macau University of Science and 
      Technology, Taipa 999078, China.
FAU - Jiao, Rui
AU  - Jiao R
AD  - Department of Food Science and Engineering, Institute of Science and Technology, 
      Jinan University, Guangzhou 510632, China.
LA  - eng
GR  - 32272310/The National Natural Science Foundation of China/
GR  - FDCT 0067/2020/A2/the Science and Technology Development Fund, Macau SAR/
PT  - Journal Article
DEP - 20230905
PL  - Switzerland
TA  - Nutrients
JT  - Nutrients
JID - 101521595
SB  - IM
PMC - PMC10536292
OTO - NOTNLM
OT  - PI3K/Akt pathway
OT  - dark tea
OT  - glucolipid metabolism
OT  - insulin resistance
OT  - theabrownin
COIS- The authors declare that they have no known competing financial interest or 
      personal relationship that could have appeared to influence the work reported in 
      this paper.
EDAT- 2023/09/28 06:42
MHDA- 2023/09/28 06:42
PMCR- 2023/09/05
CRDT- 2023/09/28 01:34
PHST- 2023/08/16 00:00 [received]
PHST- 2023/08/26 00:00 [revised]
PHST- 2023/08/28 00:00 [accepted]
PHST- 2023/09/28 06:42 [medline]
PHST- 2023/09/28 06:42 [pubmed]
PHST- 2023/09/28 01:34 [entrez]
PHST- 2023/09/05 00:00 [pmc-release]
AID - nu15183862 [pii]
AID - nutrients-15-03862 [pii]
AID - 10.3390/nu15183862 [doi]
PST - epublish
SO  - Nutrients. 2023 Sep 5;15(18):3862. doi: 10.3390/nu15183862.