PMID- 37282949
OWN - NLM
STAT- MEDLINE
DCOM- 20230608
LR  - 20230608
IS  - 1001-5302 (Print)
IS  - 1001-5302 (Linking)
VI  - 48
IP  - 7
DP  - 2023 Apr
TI  - [Punicalagin inhibits hepatic lipid deposition in obese mice via AMPK/ACC 
      pathway].
PG  - 1751-1759
LID - 10.19540/j.cnki.cjcmm.20221114.702 [doi]
AB  - Hepatic lipid deposition is one of the basic manifestations of obesity, and 
      nowadays pharmacological treatment is the most important tool. Punicalagin(PU), a 
      polyphenol derived from pomegranate peel, is a potential anti-obesity substance. 
      In this study, 60 C57BL/6J mice were randomly divided into a normal group and a 
      model group. After establishing a model of simple obesity with a high-fat diet 
      for 12 weeks, the successfully established rat models of obesity were then 
      regrouped into a model group, an orlistat group, a PU low-dose group, a PU 
      medium-dose group, and a PU high-dose group. The normal group was kept on routine 
      diet and other groups continued to feed the high-fat diet. The body weight and 
      food intake were measured and recorded weekly. After 8 weeks, the levels of the 
      four lipids in the serum of each group of mice were determined by an automatic 
      biochemical instrument. Oral glucose tole-rance and intraperitoneal insulin 
      sensitivity were tested. Hemoxylin-eosin(HE) staining was applied to observe the 
      hepatic and adipose tissues. The mRNA expression levels of peroxisome 
      proliferators-activated receptor gamma(PPARgamma) and C/EBPalpha were determined by real-time 
      quantitative polymerase chain reaction(Q-PCR), and the mRNA and protein 
      expression levels of adenosine 5'-monophosphate-activated protein kinase(AMPK), 
      anterior cingulate cortex(ACC), and carnitine palmitoyltransferase 1A(CPT1A) were 
      determined by Western blot. Finally, the body mass, Lee's index, serum total 
      glyceride(TG), serum total cholesterol(TC), and low-density lipoprotein 
      cholesterol(LDL-C) levels were significantly higher and high-density lipoprotein 
      cholesterol(HDL-C) levels were significantly lower in the model group as compared 
      with the normal group. The fat deposition in the liver was significantly 
      increased. The mRNA expression levels of hepatic PPARgamma and C/EBPalpha and the protein 
      expression level of ACC were increased, while the mRNA and protein expression 
      levels of CPT-1alpha(CPT1A) and AMPK were decreased. After PU treatment, the above 
      indexes of obese mice were reversed. In conclusion, PU can decrease the body 
      weight of obese mice and control their food intake. It also plays a role in the 
      regulation of lipid metabolism and glycometabolism metabolism, which can 
      significantly improve hepatic fat deposition. Mechanistically, PU may regulate 
      liver lipid deposition in obese mice by down-regulating lipid synthesis and 
      up-regulating lipolysis through activation of the AMPK/ACC pathway.
FAU - Jiensi, Re-Na
AU  - Jiensi RN
AD  - School of Pharmacy, Xinjiang Medical University Urumuqi 830011, China.
FAU - Chang, Zhan-Ying
AU  - Chang ZY
AD  - School of Pharmacy, Xinjiang Medical University Urumuqi 830011, China State Key 
      Laboratory of Pathogenesis,Prevention and Treatment of High Incidence Diseases in 
      Central Asia Urumuqi 830011, China.
FAU - Niu, Ruo-Hui
AU  - Niu RH
AD  - Korla Hospital of the Second Division of Xinjiang Production and Construction 
      Corps Korla 841000, China.
FAU - Gao, Xiao-Li
AU  - Gao XL
AD  - School of Pharmacy, Xinjiang Medical University Urumuqi 830011, China Key 
      Laboratory of Active Components of Xinjiang Natural Medicine and Drug Release 
      Technology Urumuqi 830011, China.
LA  - chi
PT  - English Abstract
PT  - Journal Article
PL  - China
TA  - Zhongguo Zhong Yao Za Zhi
JT  - Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese 
      materia medica
JID - 8913656
RN  - 65995-63-3 (punicalagin)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - 0 (PPAR gamma)
RN  - 0 (Lipids)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Rats
MH  - Mice
MH  - Animals
MH  - Mice, Obese
MH  - *AMP-Activated Protein Kinases/genetics/metabolism
MH  - *PPAR gamma/genetics/metabolism
MH  - Mice, Inbred C57BL
MH  - Liver/metabolism
MH  - Obesity/drug therapy/genetics
MH  - Body Weight
MH  - Lipid Metabolism
MH  - Diet, High-Fat/adverse effects
MH  - Lipids
MH  - Cholesterol
OTO - NOTNLM
OT  - AMPK/ACC signaling pathway
OT  - hepatic lipid deposition
OT  - lipid metabolism
OT  - obesity
OT  - punicalagin
EDAT- 2023/06/07 06:42
MHDA- 2023/06/08 06:42
CRDT- 2023/06/07 04:14
PHST- 2023/06/08 06:42 [medline]
PHST- 2023/06/07 06:42 [pubmed]
PHST- 2023/06/07 04:14 [entrez]
AID - 10.19540/j.cnki.cjcmm.20221114.702 [doi]
PST - ppublish
SO  - Zhongguo Zhong Yao Za Zhi. 2023 Apr;48(7):1751-1759. doi: 
      10.19540/j.cnki.cjcmm.20221114.702.