What question did this study set out to answer?

This study aims to determine how AMP-activated kinase (AMPK) regulates glycerolipid synthesis and fatty acid oxidation in liver and muscle tissues.

March 8, 1999Biochemical JournalOpen Access

AMP-activated kinase reciprocally regulates triacylglycerol synthesis and fatty acid oxidation in liver and muscle: evidence that sn-glycerol-3-phosphate acyltransferase is a novel target

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Randomized trial evaluates AMPK's role in lipid metabolism, suggesting a new target for treatment.

This study aims to determine how AMP-activated kinase (AMPK) regulates glycerolipid synthesis and fatty acid oxidation in liver and muscle tissues.
Lipid metabolism was analyzed in cultured rat hepatocytes and isolated mouse soleus muscle with AICA riboside treatment.
Mitochondrial GPAT activity was measured following incubation with AMPK activator AICA riboside.
C2C12 myoblasts and differentiated myotubes were also evaluated for similar metabolic effects.
In cultured hepatocytes, AICA riboside decreased [14C]oleate incorporation into TAG by 50% and [3H]glycerol by 38%.
AICA riboside increased fatty acid oxidation in mouse soleus by 48% and decreased TAG incorporation by 37%.
AMPK inhibited mitochondrial GPAT activity by 22-34% without affecting other lipid metabolic pathways.

Muoio et al. (1999) studied this question.

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