No hope of ever seeing this in bulk is there? It's outrageously expensive in small amounts now.

AMP-kinase activation with AICAR simultaneously increases fatty acid and glucose oxidation in resting rat soleus muscle.
http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15774530
Smith AC, Bruce CR, Dyck DJ.
University of Guelph.

5-amino-4-imidazolecarboxamide riboside (AICAR), a pharmacological activator of AMP-activated protein kinase (AMPK), acutely stimulates glucose uptake and fatty acid (FA) oxidation in skeletal muscle. However, it is not fully understood as to whether AICAR-induced changes in glucose oxidation are secondary to changes in FA oxidation (ie. glucose fatty acid cycle), as well as to what role AMPK may be playing in the regulation of intramuscular triacylglycerol (TAG) esterification and hydrolysis. We examined the acute (60 min) effects of AICAR (2 mM) on FA metabolism, glucose oxidation and pyruvate dehydrogenase activation (PDHa) in isolated resting rat soleus muscle strips, exposed to two different FA concentrations (low-fatty acid, LFA, 0.2 mM; high-fatty acid, HFA, 1 mM). AICAR significantly increased AMPK alpha2 activity (+192%; P < 0.05) over 60 min, and simultaneously increased both FA (LFA: +33%, P < 0.05; HFA: +36%, P < 0.05) and glucose (LFA: +105%, P < 0.05; HFA: +170, P < 0.001) oxidation regardless of FA availability. While there were no changes in triacylglycerol (TAG) esterification, AICAR did increase the ratio of FA partitioned to oxidation relative to TAG esterification (LFA: +15%, P < 0.05; HFA: +49%, P < 0.05). AICAR had no effect on endogenous TAG hydrolysis and oxidation in resting soleus. The stimulation of glucose oxidation with AICAR was associated with an increase in PDHa (+126%; P < 0.05) but was without effect on pyruvate, an allosteric activator of the PDH complex, suggesting that AMPK may stimulate PDH directly. In conclusion, AMPK appears to be an important regulator of both FA metabolism and glucose oxidation in resting skeletal muscle.


AICAR further increases fatty acid oxidation and blunts triacylglycerol hydrolysis in contracting rat soleus muscle.
http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15774529
Smith AC, Bruce CR, Dyck DJ.

University of Guelph.

Muscle contraction increases glucose uptake and FA metabolism in isolated rat skeletal muscle, due at least in part to an increase in AMP-activated kinase activity (AMPK). However, the extent that AMPK plays a role in regulation of substrate utilization during contraction is not fully understood. We examined the acute effects of AICAR (2 mM) on FA metabolism and glucose oxidation during high intensity tetanic contraction in isolated rat soleus muscle strips. Muscle strips were exposed to two different FA concentrations (low-fatty acid, LFA, 0.2 mM; high-fatty acid, HFA, 1 mM) to examine the role that FA availability may have on both exogenous and endogenous FA metabolism with contraction and AICAR. Synergistic increases in AMPK alpha2 activity (+45%; P < 0.05) were observed after 30 min of contraction with AICAR, which further increased exogenous FA oxidation (LFA: +71%, P < 0.05; HFA: +46%, P < 0.05) regardless of FA availability. While there were no changes in triacylglycerol (TAG) esterification, AICAR did increase the ratio of FA partitioned to oxidation relative to TAG esterification (LFA: +65%, P < 0.05). AICAR significantly blunted endogenous TAG hydrolysis (LFA: -294%, P < 0.001; HFA: -117%, P < 0.05), but had no effect on endogenous oxidation rates, suggesting a better matching between TAG hydrolysis and subsequent oxidative needs of the muscle. There was no effect of AICAR on the already elevated rates of glucose oxidation during contraction. These results suggest that FA metabolism is very sensitive to AMPK alpha2 stimulation during contraction.

PMID: 15774529 [PubMed - as supplied by publisher]