Categorías:Péptidos y sus dosis
Fuente: PubChem
Secuencia: ribonucleósido de 5-aminoimidazol-4-carboxamida
Fórmula molecular: C9H15N4O8P
Peso molecular: 338,213 g/mol
CID de PubChem: 65110
Número CAS: 3031-94-5
Sinónimos: ribonucleótido AICA, nucleótido Z
Efectos AICAR
AICAR y resistencia a la insulina
La investigación en ratones muestra que AICAR, incluso en dosis bajas, reduce la inflamación en el tejido adiposo. La inflamación de la grasa se asocia con una mayor resistencia a la insulina y la reducción de la inflamación conduce a una mejor homeostasis de la glucosa y una mayor sensibilidad a la insulina incluso sin ningún cambio en el peso corporal. Parece que AICAR tiene varias vías a través de las cuales afecta la inflamación en el tejido adiposo, y al menos una de esas vías involucra SIRT1 y macrófagos [1].
El impacto de AICAR sobre la inflamación adiposa no es inesperado. Se ha descubierto que AMPK atenúa las respuestas inflamatorias en trastornos metabólicos tanto en ratones sanos como diabéticos. En una investigación en ratones, se descubrió que la activación de AMPK, causada por AICAR, mejora la sensibilidad a la insulina, la homeostasis energética, el metabolismo de los lípidos y los marcadores inflamatorios.
El ejercicio aumenta la cantidad de receptores de insulina GLUT-4 que están presentes en la superficie de las células musculares. Es uno de los medios más eficaces para aumentar la absorción de glucosa por las células musculares y reduce eficazmente tanto los niveles de glucosa como la resistencia a la insulina. Resulta que AICAR imita los efectos del ejercicio con mucha precisión y que la administración repetida de AICAR tiene efectos similares a los del ejercicio prolongado[3].
AICAR y la investigación del cáncer
AMPK desempeña un papel complejo en el crecimiento y la metástasis del cáncer, ya que ralentiza y acelera el crecimiento de los tumores en diversas circunstancias. En general, las investigaciones indican que la activación prolongada de la enzima eventualmente conduce a la muerte de las células cancerosas al desacelerar el metabolismo de las células cancerosas y hacer que las células cancerosas sean más susceptibles a las agresiones ambientales. Esto ha sido demostrado tanto en cultivos celulares como en ratas[4, p. 5], [5]. Los científicos están investigando la capacidad de AICAR para trabajar en conjunto con otros agentes quimioterapéuticos para aumentar la eficacia. La idea es que AICAR podría:
reducir los efectos secundarios,
permitir dosis más bajas de fármacos quimioterapéuticos, y
mejorar los resultados en tumores quimiorresistentes[6].
AICAR inhibe el crecimiento clonal de glioma (C6) y células de próstata.
Fuente: Revista de Química Biológica
La investigación en células de cáncer de tiroides indica que AICAR también puede funcionar provocando apoptosis (muerte celular programada). Parece que esta actividad está mediada por la inducción de la acumulación de p21 y la eventual activación de la caspasa 3. El efecto general es la inhibición de la proliferación y supervivencia de las células cancerosas [7].
AMPK activators, like AICAR, influence a number of pathways that can impact cancer growth.
Source: PubMed
AICAR Anti-inflammatory Properties
AMPK activators have been shown to play an important role in inflammation at the cellular level. Research into metformin, a common and long-used diabetes medication, indicates that at least part of the reason the drug is effective is that it reduces inflammation and boosts the function of the pancreas. AICAR has a similar effects, playing a protective role in inflammatory conditions like acute lung injry, asthma, colitis, atherosclerosis, and hepatitis[8].
There is ongoing research into the use of AICAR to mediate the effects of auto-immune diseases and other inflammatory conditions. For instance, studies in mice indicate that ACIAR may be effective in reducing inflammation in colitis. It appears that AICAR acts as a central inhibitor of immune responses in this setting by reducing NF-kappaB activation in macrophages as well as TH1- and TH17-type cytokines[9].
AICAR Research and the Heart
Much of heart disease is related to inflammation. The ability to control inflammation could reduce the progression of vascular disease, including atherosclerosis. Research in rabbit models of atherosclerosis indicated that AICAR suppression vascular smooth muscle proliferation. This is not only an important component of cardiovascular disease, but is also one of the reasons that cardiac stents fail over time. Controlling vascular inflammation could reduce both short-term and long-term complications of stent placement without the need for drugs that increase the risk of bleeding[10].
Research also suggests that AMPK activation can suppression certain immune responses that lead to atherosclerosis. The buildup of LDL, often referred to as “bad cholesterol,” leads to macrophage proliferation. This process is integral to the formation of plaques that can eventually lead to heart attack[11]. Anything that can mitigate this proliferation has the potential to reduce heart disease and even heart attack prevalence.
AICAR Research and Fertility
A great deal of AICAR research has revolved around the ability of the peptide to improve sperm motility, energy metabolism, and fertilizing ability. Research in both cats, goats, and chickens indicates that AMPK activators like AICAR can improve sperm motility by improving energy metabolism[12]. It appears that AICAR regulates the activity of energetic enzymes in spermatozoa and therefore impacts overall fertilizing ability[13].
AICAR exhibits minimal side effects, low oral and excellent subcutaneous bioavailability in mice. Per kg dosage in mice does not scale to humans. AICAR for sale at PEPTIDE GURUS is limited to educational and scientific research only, not for human consumption. Only buy AICAR if you are a licensed researcher.
Article Author
The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.
Scientific Journal Author
Spencer Gaskin, M.D., Ph.D. is an American Board of Internal Medicine certified cardiologist and medical practitioner. His expertise of Internal medicine and cardiology sources from UT Southwestern Cardiology, Washington University Interventional Cardiology, and the Mid America Heart Institute. Dr. Gaskin led a study that examined the prevention of Postischemic Leukocyte Rolling and Adhesion via preconditioning with AICAR.
Spencer Gaskin, M.D., Ph.D. is being referenced as one of the leading scientists involved in the research and development of AICAR. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between PEPTIDE GURUS and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide. Dr. Gaskin is listed in [14] under the referenced citations.
Referenced Citations
Z. Yang et al., “The full capacity of AICAR to reduce obesity-induced inflammation and insulin resistance requires myeloid SIRT1,” PloS One, vol. 7, no. 11, p. e49935, 2012.
K. Pan et al., “AMPK activation attenuates inflammatory response to reduce ambient PM2.5-induced metabolic disorders in healthy and diabetic mice,” Ecotoxicol. Environ. Saf., vol. 179, pp. 290–300, Sep. 2019.
N. Jessen, R. Pold, E. S. Buhl, L. S. Jensen, O. Schmitz, and S. Lund, “Effects of AICAR and exercise on insulin-stimulated glucose uptake, signaling, and GLUT-4 content in rat muscles,” J. Appl. Physiol. Bethesda Md 1985, vol. 94, no. 4, pp. 1373–1379, Apr. 2003.
J. Zhuge, “Overexpression of CYP2E1 induces HepG2 cells death by the AMP kinase activator 5’-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR),” Cell Biol. Toxicol., vol. 25, no. 3, pp. 253–263, Jun. 2009.
R. Rattan, S. Giri, A. K. Singh, and I. Singh, “5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside inhibits cancer cell proliferation in vitro and in vivo via AMP-activated protein kinase,” J. Biol. Chem., vol. 280, no. 47, pp. 39582–39593, Nov. 2005.
M. M. H. Yung, H. Y. S. Ngan, and D. W. Chan, “Targeting AMPK signaling in combating ovarian cancers: opportunities and challenges,” Acta Biochim. Biophys. Sin., vol. 48, no. 4, pp. 301–317, Apr. 2016.
W. G. Kim, H.-J. Choi, T. Y. Kim, Y. K. Shong, and W. B. Kim, “The effect of 5-aminoimidazole-4-carboxamide-ribonucleoside was mediated by p38 mitogen activated protein kinase signaling pathway in FRO thyroid cancer cells,” Korean J. Intern. Med., vol. 29, no. 4, pp. 474–481, Jul. 2014.
X.-W. Peng, H.-H. Zhou, J. Dai, and L. Zhang, “[Advances on the anti-inflammatory and protective effect of AMPK activators],” Sheng Li Xue Bao, vol. 71, no. 2, pp. 319–326, Apr. 2019.
A. Bai et al., “Novel anti-inflammatory action of 5-aminoimidazole-4-carboxamide ribonucleoside with protective effect in dextran sulfate sodium-induced acute and chronic colitis,” J. Pharmacol. Exp. Ther., vol. 333, no. 3, pp. 717–725, Jun. 2010.
M. Igata et al., “Adenosine monophosphate-activated protein kinase suppresses vascular smooth muscle cell proliferation through the inhibition of cell cycle progression,” Circ. Res., vol. 97, no. 8, pp. 837–844, Oct. 2005.
M. Sakai, S. Kobori, A. Miyazaki, and S. Horiuchi, “Macrophage proliferation in atherosclerosis,” Curr. Opin. Lipidol., vol. 11, no. 5, pp. 503–509, Oct. 2000.
P. Thuwanut, P. Comizzoli, K. Pruksananonda, K. Chatdarong, and N. Songsasen, “Activation of adenosine monophosphate-activated protein kinase (AMPK) enhances energy metabolism, motility, and fertilizing ability of cryopreserved spermatozoa in domestic cat model,” J. Assist. Reprod. Genet., May 2019.
Z. Zhu et al., “5’-AMP-Activated Protein Kinase Regulates Goat Sperm Functions via Energy Metabolism In Vitro,” Cell. Physiol. Biochem. Int. J. Exp. Cell. Physiol. Biochem. Pharmacol., vol. 47, no. 6, pp. 2420–2431, 2018.
F. Spencer Gaskin, Kazuhiro Kamada, Mozow Yusof, William Durante, Garrett Gross & Ronald J. Korthuis (2009) AICAR Preconditioning Prevents Postischemic Leukocyte Rolling and Adhesion: Role of KATP Channels and Heme Oxygenase, Microcirculation, 16:2, 167-176, DOI: 10.1080/10739680802355897
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