RGD Reference Report - Berberine Ameliorates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease in Rats via Activation of SIRT3/AMPK/ACC Pathway.

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Berberine Ameliorates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease in Rats via Activation of SIRT3/AMPK/ACC Pathway.
Authors:	Zhang, Yu-Pei Deng, Yuan-Jun Tang, Kai-Rui Chen, Run-Sen Liang, Shu Liang, Yin-Ji Han, Li Jin, Ling Liang, Zi-En Chen, Yan-Ning Yang, Qin-He
Citation:	Zhang YP, etal., Curr Med Sci. 2019 Feb;39(1):37-43. doi: 10.1007/s11596-019-1997-3. Epub 2019 Mar 13.
RGD ID:	25823184
Pubmed:	PMID:30868489 (View Abstract at PubMed)
DOI:	DOI:10.1007/s11596-019-1997-3 (Journal Full-text)
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.

Biological Process

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
Cpt1a	Rat	response to alkaloid		IEP		Berberine	RGD
Cpt1a	Rat	response to nutrient levels		IEP		High-fat diet	RGD

RGD Manual Annotations

Only show annotations with direct experimental evidence (0 objects hidden)

Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
CPT1A	Human	adenosine monophosphate-activated protein kinase (AMPK) signaling pathway		ISO	Cpt1a (Rattus norvegicus)		RGD
Cpt1a	Rat	adenosine monophosphate-activated protein kinase (AMPK) signaling pathway		IEP			RGD
Cpt1a	Mouse	adenosine monophosphate-activated protein kinase (AMPK) signaling pathway		ISO	Cpt1a (Rattus norvegicus)		RGD

Genes (Rattus norvegicus)


Cpt1a (carnitine palmitoyltransferase 1A)

Genes (Mus musculus)


Cpt1a (carnitine palmitoyltransferase 1a, liver)

Genes (Homo sapiens)


CPT1A (carnitine palmitoyltransferase 1A)

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Berberine Ameliorates High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease in Rats via Activation of SIRT3/AMPK/ACC Pathway.

RGD Manual Annotations