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AICAR


The Salk Institute discovered that AICAR significantly improves the performance of mice in endurance-type exercise by converting fast-twitch muscle fibers to the more energy-efficient, fat-burning, slow-twitch type. They also found that AICAR and GW1516, when given to "sedentary" mice, activated 40% of the genes that were turned on when mice were given GW1516 and made to exercise. As a result a publicity storm about "exercise pills" and "exercise in a pill" ensued. The World Anti-Doping Agency now lists both compounds on their prohibited list (since 2009), and the lead researcher of the breakthrough study cooperated in providing data to make possible a urinalysis test to detect AICAR.[4][5]

AICAR, aminoimidazole carboxamide ribonucleotide, acts as an agonist to AMP-activated protein kinase; AMP-activated protein kinase, also known as AMPK, is an enzyme with an important role in cellular homeostasis and energy regulation.[1] AMPK acts through a variety of means to ultimately stimulate liver fatty oxidation, ketogenesis, beta-cell modulation of insulin secretion, and other functions within the body. AICAR has been shown to stimulate glucose uptake and reduce apoptosis by reducing reactive oxygen compounds within cells.[2][3]


AICAR has a number of other experimental/clinical and research chemical uses as it is expressed in a variety of tissue types. Bai et al found that "data demonstrate that AICAR-initiated AMPK activation may represent a promising alternative to our current approaches to suppressing intestinal inflammation in IBD."[6]


Guo et al found "results suggest[ing] a mechanism by which AICAR inhibits the proliferation of EGFRvIII expressing glioblastomas and point toward a potential therapeutic strategy for targeting EGFR-activated cancers."[7]


An original study by Pold et al offers additional hope that AICAR could offer important treatment potential for humans:


Five-week-old, pre-diabetic ZDF rats underwent daily treadmill running or AICAR treatment over an 8-week period and were compared with an untreated group. In contrast to the untreated, both the exercised and AICAR-treated rats did not develop hyperglycemia during the intervention period. Whole-body insulin sensitivity, as assessed by a hyperinsulinemic-euglycemic clamp at the end of the intervention period, was markedly increased in the exercised and AICAR-treated animals compared with the untreated ZDF rats (P < 0.01). In addition, pancreatic beta-cell morphology was almost normal in the exercised and AICAR-treated animals, indicating that chronic AMPK activation in vivo might preserve beta-cell function. Our results suggest that activation of AMPK may represent a therapeutic approach to improve insulin action and prevent a decrease in beta-cell function associated with type 2 diabetes.[8]



References:

[1]Corton JM, Gillespie JG, Hawley SA, Hardie DG. "5-aminoimidazole-4-carboxamide ribonucleoside. A specific method for activating AMP-activated protein kinase in intact cells?". Eur. J. Biochem. 229 (2): 558–65. 1995.

[2]Lemieux K, Konrad D, Klip A, Marette A. "The AMP-activated protein kinase activator AICAR does not induce GLUT4 translocation to transverse tubules but stimulates glucose uptake and p38 mitogen-activated protein kinases alpha and beta in skeletal muscle". Faseb J. 17 (12): 1658–65. 2003.

[3]Kim JE, Kim YW, Lee IK, Kim JY, Kang YJ, Park SY. "AMP-activated protein kinase activation by

5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) inhibits palmitate-induced endothelial cell apoptosis through reactive oxygen species suppression". J. Pharmacol. Sci. 106 (3): 394–403. 2008.

[4]Narkar VA, Downes M, Yu RT, Embler E, Wang YX, Banayo E, Mihaylova MM, Nelson MC, Zou Y, Juguilon H, Kang H, Shaw RJ, Evans RM. "AMPK and PPARdelta agonists are exercise mimetics". Cell 134 (3): 405–15. 2008. [5]WADA 2009 Prohibited List: WADA PROHIBITED LIST PDF (PDF Document).

[6]Bai A, Yong M, Ma Y, Ma A, Weiss C, Guan Q, Bernstein C, Peng Z. Novel Anti-Inflammatory Action of 5-Aminoimidazole-4-carboxamide ribonucleoside with protective effect in DSS-induced acute and chronic colitis. J Pharmacol Exp Ther. 2010 Mar 17.

[7]Guo D, Hildebrandt IJ, Prins RM, Soto H, Mazzotta MM, Dang J, Czernin J, Shyy JY, Watson AD, Phelps M, Radu CG, Cloughesy TF, Mischel PS. The AMPK agonist AICAR inhibits the growth of EGFRvIII-expressing glioblastomas by inhibiting lipogenesis.Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):12932-7.

[8]Pold R, Jensen LS, Jessen N, Buhl ES, Schmitz O, Flyvbjerg A, Fujii N, Goodyear LJ, Gotfredsen CF, Brand CL, Lund S. Long-term AICAR administration and exercise prevents diabetes in ZDF rats. Diabetes. 2005 Apr;54(4):928-34.





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