Study summary · research use only
AMPK activation by AICAR reduces diet induced fatty liver in C57BL/6 mice
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study using C57BL/6 mice, fatty liver was induced in two groups by a high fat high fructose diet (HFFD) for 10 weeks while two groups received normal pellet feed. During the final two weeks, some groups received the AMPK activator AICAR (150 mg/kg bw/day, i.p.) while others received saline. AICAR administration was associated with decreased fatty liver, decreased circulating glucose and insulin, reduced triglyceride and collagen accumulation, and reduced markers of oxidative stress in HFFD-fed mice. AICAR treatment was also associated with upregulated FOXO3 and p-AMPK expression and reduced p-mTOR expression. The authors state that further characterization of AMPK, mTOR, and FOXO3 crosstalk in non-alcoholic fatty liver disease is needed.
Abstract
Dysregulation of 5'-adenosine monophosphate-activated protein kinase (AMPK) occurs in metabolic disorders including non-alcoholic fatty liver disease (NAFLD) which makes it a molecular target for treatment. An AMPK activator, 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR) alleviates NAFLD in experimental rats, however the specific mechanism remains to be explored. We aimed to study the effect of AICAR on lipid levels, oxidant-antioxidant balance, AMPK and mTOR activation and FOXO3 gene expression in liver of mice model. Fatty liver was induced in two groups of C57BL/6 mice (groups 2 and 3) by providing a high fat high fructose diet (HFFD) for 10 weeks while groups 1 and 4 animals were fed normal pellet. For the last two weeks, groups 3 and 4 were administered AICAR (150 mg/kg bw/day, i.p.) while groups 1 and 2 were administered saline. AICAR decreased fatty liver, decreased glucose and insulin in circulation, prevented the accumulation of triglycerides and collagen and ameliorated oxidative stress in HFFD fed mice. At the molecular level, AICAR upregulated FOXO3 and p-AMPK expression and reduced p-mTOR expression. AMPK activation may involve FOXO3 in protection against NAFLD. The role of AMPK, mTOR and FOXO3 crosstalk in NAFLD needs to be characterised in future.
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