PMID- 36637439
OWN - NLM
STAT- MEDLINE
DCOM- 20230117
LR  - 20240102
IS  - 1557-7600 (Electronic)
IS  - 1096-620X (Print)
IS  - 1096-620X (Linking)
VI  - 26
IP  - 1
DP  - 2023 Jan
TI  - Sodium Propionate or Sodium Butyrate Promotes Fatty Acid Oxidation in HepG2 Cells 
      Under Oxidative Stress.
PG  - 74-79
LID - 10.1089/jmf.2021.0120 [doi]
AB  - The beneficial effects of sodium butyrate (NaB) and sodium propionate (NaP) on 
      fatty acid oxidation (FAO) genes and production of proinflammatory cytokines 
      related to nonalcoholic fatty liver disease (NAFLD) were evaluated using HepG2 
      human liver hepatocellular carcinoma cells exposed to palmitate/oleate or 
      lipopolysaccharides (LPSs) as a model. The results showed that NaP or NaB was 
      able to promote FAO, regulate lipolysis, and reduce reactive oxygen species 
      production by significantly increasing the mRNA expression of peroxisome 
      proliferator-activated receptor gamma coactivator 1 alpha (PGC-1alpha), peroxisome 
      proliferator-activated receptor alpha (PPARalpha), adipose triglyceride lipase 
      (ATGL), carnitine palmitoyltransferase 1 alpha (CPT1alpha), fibroblast growth factor 
      21 (FGF21), and uncoupling protein 2 (UCP2) in HepG2 cells. Together, NaP and NaB 
      may produce greater effects by increasing CPT1alpha, PPARalpha, and UCP2 mRNA expression 
      in LPS-treated HepG2 cells and by increasing CPT1alpha and ATGL mRNA expression in 
      palmitate-/oleate-treated HepG2 cells. Only NaP treatment significantly increased 
      FGF21 mRNA expression in palmitate-/oleate-treated HepG2 cells. The enzyme-linked 
      immunosorbent assay results revealed that only pretreatment with LPSs and not 
      palmitate/oleate significantly increased tumor necrosis factor alpha (TNF-alpha) 
      expression in HepG2 cells. NaP alone or in combination with NaB significantly 
      decreased TNF-alpha expression in LPS-induced HepG2 cells. The expression of 
      interleukin-8 in both models showed no significant differences in all treatments. 
      NaP and NaB show potential for in vivo studies on NAFLD.
FAU - Cook, Kristina J
AU  - Cook KJ
AUID- ORCID: 0000-0002-8644-8927
AD  - Pennington Biomedical Research Center, Louisisna State University System, Baton 
      Rouge, Louisiana, USA.
FAU - Coulter, Ann
AU  - Coulter A
AUID- ORCID: 0000-0002-3103-601X
AD  - School of Nutrition and Food Sciences, Louisisna State University System, Baton 
      Rouge, Louisiana, USA.
FAU - Keenan, Michael
AU  - Keenan M
AUID- ORCID: 0000-0003-1282-8756
AD  - Pennington Biomedical Research Center, Louisisna State University System, Baton 
      Rouge, Louisiana, USA.
FAU - Greenway, Frank
AU  - Greenway F
AUID- ORCID: 0000-0002-1766-6111
AD  - School of Nutrition and Food Sciences, Louisisna State University System, Baton 
      Rouge, Louisiana, USA.
FAU - Losso, Jack N
AU  - Losso JN
AUID- ORCID: 0000-0002-8187-7757
AD  - Pennington Biomedical Research Center, Louisisna State University System, Baton 
      Rouge, Louisiana, USA.
LA  - eng
GR  - U54 GM104940/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - J Med Food
JT  - Journal of medicinal food
JID - 9812512
RN  - 107-92-6 (Butyric Acid)
RN  - DK6Y9P42IN (sodium propionate)
RN  - 2UMI9U37CP (Oleic Acid)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (PPAR alpha)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha)
SB  - IM
MH  - Humans
MH  - *Non-alcoholic Fatty Liver Disease/metabolism
MH  - Butyric Acid/pharmacology
MH  - Hep G2 Cells
MH  - Oleic Acid
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
MH  - PPAR alpha/genetics/metabolism
MH  - Lipopolysaccharides
MH  - Oxidative Stress
MH  - RNA, Messenger/metabolism
MH  - Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism
PMC - PMC9889010
OTO - NOTNLM
OT  - HepG2 cells
OT  - butyrate
OT  - fatty acid oxidation
OT  - oxidative stress
OT  - propionate
COIS- No competing financial interests exist.
EDAT- 2023/01/14 06:00
MHDA- 2023/01/18 06:00
PMCR- 2024/01/01
CRDT- 2023/01/13 10:52
PHST- 2023/01/13 10:52 [entrez]
PHST- 2023/01/14 06:00 [pubmed]
PHST- 2023/01/18 06:00 [medline]
PHST- 2024/01/01 00:00 [pmc-release]
AID - 10.1089/jmf.2021.0120 [pii]
AID - 10.1089/jmf.2021.0120 [doi]
PST - ppublish
SO  - J Med Food. 2023 Jan;26(1):74-79. doi: 10.1089/jmf.2021.0120.