Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0020473 (
hyperlipidemia
)
15,891
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
This study aimed to verify the effects of berberine (BBR) on the fat metabolism proteins involved in the
sirtuin 3
(
SIRT3
)/adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) pathway in the liver tissues of rats with high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD). Forty-eight rats were randomly divided into the normal control (NC) group, HFD group or BBR group, with 16 rats in each group. After 8 and 16 weeks of treatment, serum and liver samples were collected. Subsequently, body parameters, biochemical parameters and liver pathology were examined. The expression levels of proteins involved in the
SIRT3
/AMPK/ACC pathway in the liver were detected by Western blotting. After 8 and 16 weeks of a HFD, the successful establishment of rat models with different degrees of NAFLD was confirmed by hematoxylin and eosin (H&E) and Oil Red O staining. NAFLD rat models exhibited obesity and
hyperlipidemia
, and the protein expression levels of
SIRT3
, p-AMPK, p-ACC, and CPT-1A in the liver were significantly decreased compared to those in the NC group. The concurrent administration of BBR with the HFD effectively improved serum and liver lipid profiles and ameliorated liver injury. Furthermore, the protein expression levels of
SIRT3
, p-AMPK, p-ACC, and CPT-1A in the liver were significantly increased in the BBR group as compared with those in the HFD group. In conclusion, our data suggest that the mechanism by which BBR ameliorates HFD-induced hepatic steatosis may be related to the activation of the
SIRT3
/AMPK/ACC pathway in the liver.
...
PMID:Berberine Ameliorates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease in Rats via Activation of SIRT3/AMPK/ACC Pathway. 3086 89
Hydrogen sulfide (H
2
S), a gaseous molecule, is involved in modulating multiple physiological functions, such as antioxidant, antihypertension, and the production of polysulfide cysteine. H
2
S may inhibit reactive oxygen species generation and ATP production through modulating respiratory chain enzyme activities; however, the mechanism of this effect remains unclear. In this study,
db/db
mice, neonatal rat cardiomyocytes, and H9c2 cells treated with high glucose, oleate, and palmitate were used as animal and cellular models of type 2 diabetes. The mitochondrial respiratory rate, respiratory chain complex activities, and ATP production were decreased in
db/db
mice compared with those in
db/db
mice treated with exogenous H
2
S. Liquid chromatography with tandem mass spectrometry analysis showed that the acetylation level of proteins involved in the mitochondrial respiratory chain were increased in the
db/db
mice hearts compared with those with sodium hydrosulfide (NaHS) treatment. Exogenous H
2
S restored the ratio of NAD
+
/NADH, enhanced the expression and activity of
sirtuin 3
(
SIRT3
) and decreased mitochondrial acetylation level in cardiomyocytes under hyperglycemia and
hyperlipidemia
. As a result of
SIRT3
activation, acetylation of the respiratory complexe enzymes NADH dehydrogenase 1 (ND1), ubiquinol cytochrome
c
reductase core protein 1, and ATP synthase mitochondrial F1 complex assembly factor 1 was reduced, which enhanced the activities of the mitochondrial respiratory chain activity and ATP production. We conclude that exogenous H
2
S plays a critical role in improving cardiac mitochondrial function in diabetes by upregulating
SIRT3
.
...
PMID:Exogenous H
2
S reduces the acetylation levels of mitochondrial respiratory enzymes via regulating the NAD
+
-SIRT3 pathway in cardiac tissues of
db/db
mice. 3118 32
