(
Humans
Hep G2 Cells
PPAR alpha
/ metabolism
AMP-Activated Protein Kinases
/ metabolism
Fatty Acids, Nonesterified
/ metabolism
Fatty Liver
/ drug therapy
Lipid Metabolism
/ drug effects
Signal Transduction
/ drug effects
Triglycerides
/ metabolism
Isoflavones
/ pharmacology
Sterol Regulatory Element Binding Protein 1
/ metabolism
Acetyl-CoA Carboxylase
/ metabolism
Carnitine O-Palmitoyltransferase
/ metabolism
AMPK
HMC
HepG2
PPARα
hepatic steatosis
Journal
Nutrients
ISSN: 2072-6643
Titre abrégé: Nutrients
Pays: Switzerland
ID NLM: 101521595
Informations de publication
Date de publication:
14 Oct 2024
14 Oct 2024
Historique:
received:
11
09
2024
revised:
07
10
2024
accepted:
10
10
2024
medline:
26
10
2024
pubmed:
26
10
2024
entrez:
26
10
2024
Statut:
epublish
Résumé
( Hepatic steatosis was induced by a free fatty acid mixture in HepG2 cells. Thereafter, different HMC concentrations (10, 30, and 50 µM) or fenofibrate (10 µM, a PPARα agonist, positive control) was treated in HepG2 cells. HMC markedly decreased lipid accumulation and triglyceride content in free fatty acid-treated HepG2 cell; it (10 and 50 μM) markedly upregulated protein expressions of pAMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase. HMC (10 and 50 μM) markedly inhibited the expression of sterol regulatory element-binding protein-1c, fatty acid synthase, and stearoyl-coA desaturase 1, which are the enzymes involved in lipid synthesis. Furthermore, HMC (10 and 50 μM) markedly upregulated the protein expression of peroxisome proliferator-activated receptor alpha (PPARα) and enhanced the protein expressions of carnitine palmitoyl transferase 1 and acyl-CoA oxidase 1. HMC inhibits lipid accumulation and promotes fatty acid oxidation by AMPK and PPARα pathways in free fatty acid-treated HepG2 cells, thereby attenuating hepatic steatosis.
Sections du résumé
BACKGROUND
BACKGROUND
(
METHODS
METHODS
Hepatic steatosis was induced by a free fatty acid mixture in HepG2 cells. Thereafter, different HMC concentrations (10, 30, and 50 µM) or fenofibrate (10 µM, a PPARα agonist, positive control) was treated in HepG2 cells.
RESULTS
RESULTS
HMC markedly decreased lipid accumulation and triglyceride content in free fatty acid-treated HepG2 cell; it (10 and 50 μM) markedly upregulated protein expressions of pAMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase. HMC (10 and 50 μM) markedly inhibited the expression of sterol regulatory element-binding protein-1c, fatty acid synthase, and stearoyl-coA desaturase 1, which are the enzymes involved in lipid synthesis. Furthermore, HMC (10 and 50 μM) markedly upregulated the protein expression of peroxisome proliferator-activated receptor alpha (PPARα) and enhanced the protein expressions of carnitine palmitoyl transferase 1 and acyl-CoA oxidase 1.
CONCLUSION
CONCLUSIONS
HMC inhibits lipid accumulation and promotes fatty acid oxidation by AMPK and PPARα pathways in free fatty acid-treated HepG2 cells, thereby attenuating hepatic steatosis.
Identifiants
pubmed: 39458470
pii: nu16203475
doi: 10.3390/nu16203475
pii:
doi:
Substances chimiques
PPAR alpha
0
AMP-Activated Protein Kinases
EC 2.7.11.31
Fatty Acids, Nonesterified
0
Triglycerides
0
PPARA protein, human
0
Isoflavones
0
Sterol Regulatory Element Binding Protein 1
0
Acetyl-CoA Carboxylase
EC 6.4.1.2
Carnitine O-Palmitoyltransferase
EC 2.3.1.21
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : National Research Foundation of Korea
ID : NRF-2020R1A2B5B01001547