Study summary · research use only
AICAR Protects against High Palmitate/High Insulin-Induced Intramyocellular Lipid Accumulation and Insulin Resistance in HL-1 Cardiac Cells by Inducing PPAR-Target Gene Expression
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this in vitro study using HL-1 cardiac cells (species not specified), the impact of the AMPK activator AICAR on cardiac metabolic adaptation was examined. The abstract reports that AICAR increased phospho-Thr172-AMPK and phospho-Ser79-ACC protein levels, and that 24-hour AICAR treatment, with or without the AMPK inhibitor Compound C, increased mRNA levels of all three PPARs, though only Ppara and Pparg regulation depended on AMPK. Under high palmitate/high insulin conditions, which the abstract associates with increased Cd36, Acot1, and Ucp3 mRNA and lipid storage, AICAR treatment increased Acadvl and Glut4 expression, which the abstract associates with reduced intramyocellular lipid buildup and reduced impairment of glucose uptake.
Abstract
Here we studied the impact of 5-aminoimidazole-4-carboxamide riboside (AICAR), a well-known AMPK activator, on cardiac metabolic adaptation. AMPK activation by AICAR was confirmed by increased phospho-Thr(172)-AMPK and phospho-Ser(79)-ACC protein levels in HL-1 cardiomyocytes. Then, cells were exposed to AICAR stimulation for 24 h in the presence or absence of the AMPK inhibitor Compound C, and the mRNA levels of the three PPARs were analyzed by real-time RT-PCR. Treatment with AICAR induced gene expression of all three PPARs, but only the Ppara and Pparg regulation were dependent on AMPK. Next, we exposed HL-1 cells to high palmitate/high insulin (HP/HI) conditions either in presence or in absence of AICAR, and we evaluated the expression of selected PPAR-targets genes. HP/HI induced insulin resistance and lipid storage was accompanied by increased Cd36, Acot1, and Ucp3 mRNA levels. AICAR treatment induced the expression of Acadvl and Glut4, which correlated to prevention of the HP/HI-induced intramyocellular lipid build-up, and attenuation of the HP/HI-induced impairment of glucose uptake. These data support the hypothesis that AICAR contributes to cardiac metabolic adaptation via regulation of transcriptional mechanisms.
pepmg summarizes the peer-reviewed literature and links to every source — it sells nothing, ships nothing, and gives no medical, dosing, or human-use guidance. Don't just trust this summary: follow the citation to its source and read it yourself. Research use only.