Effects of a low-fat diet on the hepatic expression of adiponectin and its receptors in rats with NAFLD.
Study Goal
The researchers aimed to investigate the effects of a low-fat diet on hepatic expression of adiponectin and its receptors in rats with NAFLD.
Results Summary
The low-fat diet ameliorated steatosis, ballooning degeneration, and inflammation in NAFLD rats, while also up-regulating the expression of adiponectin and its receptors, which were down-regulated in high-fat diet groups.
Population
Male Sprague-Dawley rats with induced NAFLD.
Effective Dosage
Not specified (dietary intervention only).
Duration
8 weeks (after initial 8-week high-fat diet).
Interactions
None mentioned.
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
high-fat diet | increase | NAFLD activity score (NAS) | male SD rats | from 3.2 ± 0.45 (8th week) to 6.2 ± 0.84 (16th week) | increased | #1 |
low-fat diet | decrease | steatosis, ballooning degeneration and inflammation | male SD rats with NAFLD | - | ameliorated | #2 |
low-fat diet | increase | expression of adiponectin and its receptors | male SD rats with NAFLD | - | augmented | #3 |
high-fat diet | decrease | expression of adiponectin and its receptors | male SD rats with NAFLD | - | down-regulated | #4 |
low-fat diet | decrease | histological lesions associated with NAFLD | male SD rats with NAFLD | - | alleviated | #5 |
low-fat diet | increase | expression of adiponectin and its receptors | male SD rats with NAFLD | - | up-regulating | #6 |
BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is correlated with obesity, but specific therapeutic interventions are lacking. Adiponectin is an adipokine with anti-inflammatory activity and is considered a hepatic protector. We aimed to investigate effects of a low-fat diet on the hepatic expression of adiponectin and its receptors in rats with NAFLD. MATERIALS AND METHODS: Sixteen male SD rats were fed a high-fat diet for 8 weeks (HFD1 group) or 16 weeks (HFD2 group) to induce NAFLD, and these rats were compared with rats on a normal diet for 8 weeks (NC1 group) or 16 weeks (NC2 group). Another group of 8 rats was fed an HFD for 8 weeks and then switched to a low-fat diet (DIET group) until the 16th week. The expression of hepatic adiponectin and its receptors was detected by western blotting, immunohistochemistry and RT-qPCR. RESULTS: The NAFLD activity score (NAS) in the HFD groups increased from 3.2 ± 0.45 (8th week) to 6.2 ± 0.84 (16th week) (P < 0.001), reflecting the progression in the NAFLD histology. In contrast to the HFD2 group, the low-fat diet ameliorated the steatosis, ballooning degeneration and inflammation. Dietary intervention augmented the expression of adiponectin and its receptors, which was down-regulated in the HFD2 group. CONCLUSIONS: The NAFLD rat model was successfully developed by feeding the animals a high-fat diet. Adiponectin may play a role in the pathogenesis of NAFLD, especially in the progression from steatosis to NASH. The low-fat diet alleviated the histological lesions associated with NAFLD by up-regulating the expression of adiponectin and its receptors.