Punicalagin inhibits hepatic lipid deposition in obese mice via AMPK/ACC pathway.
10.19540/j.cnki.cjcmm.20221114.702
- Author:
Re-Na JIENSI
1
;
Zhan-Ying CHANG
2
;
Ruo-Hui NIU
3
;
Xiao-Li GAO
4
Author Information
1. School of Pharmacy, Xinjiang Medical University Urumuqi 830011, China.
2. 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.
3. Korla Hospital of the Second Division of Xinjiang Production and Construction Corps Korla 841000, China.
4. 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.
- Publication Type:Journal Article
- Keywords:
AMPK/ACC signaling pathway;
hepatic lipid deposition;
lipid metabolism;
obesity;
punicalagin
- MeSH:
Rats;
Mice;
Animals;
Mice, Obese;
AMP-Activated Protein Kinases/metabolism*;
PPAR gamma/metabolism*;
Mice, Inbred C57BL;
Liver/metabolism*;
Obesity/genetics*;
Body Weight;
Lipid Metabolism;
Diet, High-Fat/adverse effects*;
Lipids;
Cholesterol
- From:
China Journal of Chinese Materia Medica
2023;48(7):1751-1759
- CountryChina
- Language:Chinese
-
Abstract:
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 γ(PPARγ) and C/EBPα 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 PPARγ and C/EBPα and the protein expression level of ACC were increased, while the mRNA and protein expression levels of CPT-1α(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.
