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AICAR is an analogue of adenosine monophosphate. It has been used clinically to protect against cardiac ischemia following heart attack. AICAR has antioxidant properties and may therefore help to slow the physiologic signs of aging. There is ongoing research into the use of AICAR to mediate the effects of diabetes, auto-immune diseases, and other inflammatory conditions.
AICAR (5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside) is a substance produced naturally by the body that stimulates AMP activated protein kinase (AMPK), a protein that regulates metabolism in a variety of ways. AMPK acts as an energy regulator and is activated during exercise or other circumstances that use up cellular energy.
Once activated by AICAR, AMPK works to make energy more available. For example, it increases the usage of fat for energy and causes cells to make more mitochondria (the cells’ powerhouses or energy creators). AMPK basically ensures that the various tissues in the body don’t run out of energy.
There are many circumstances that activate AMPK naturally, including hypoxia (low oxygen levels during exercise or at elevation), hypoglycemia (low blood sugar with exercise or fasting), the use of cellular energy during muscle contraction, and anything that disrupts energy creation within cells.
The effects of activating AMPK are extremely complex since it is involved in so many different metabolic pathways of the body. To date, the medical community has not found a way to target AMPK in a way that allows for the treatment of diseases in humans, although research has suggested it plays a role in diabetes, heart disease, and cancer.
AICAR, even at low doses, reduces inflammation in adipose tissue. Inflammation in fat is associated with increased insulin resistance and reducing inflammation leads to improved glucose homeostasis and increased insulin sensitivity even without any changes in body weight. I appears that AICAR has several pathways though which it affects inflammation in adipose tissue, with at least one of those pathways involving SIRT1 and macrophages..
AMPK activators have been shown to play an important role in inflammation at the cellular level. Research indicates that it reduces inflammation of the pancreas. AICAR has a similar effects, playing a protective role in inflammatory conditions like acute lung injry, asthma, colitis, atherosclerosis, and hepatitis.
AICAR has demonstrated antitumor activities for several types of cancers. However, the activity of AICAR on the cell growth and metastasis of prostate cancer has not been extensively studied.
The results indicated that AICAR inhibits cell growth in prostate cancer cells, but not in non-cancerous prostate cells. In addition, the results demonstrated that AICAR induces apoptosis, attenuates transforming growth factor (TGF)-β-induced cell migration, invasion and EMT-related protein expression, and enhances the chemosensitivity to docetaxel in prostate cancer cells through regulating the AMPK/mTOR-dependent pathway. These findings support AICAR as a potential therapeutic agent for the treatment of prostate cancer.
In vitro experiments revealed that AICAR activated AMPK, inhibited cell growth, and induced mitochondrial apoptosis in both osteosarcoma cell lines. In vivo, AICAR significantly reduced osteosarcoma growth without apparent body weight loss and AICAR increased both mitochondrial proliferation and apoptotic activity in treated tumor tissues. AICAR showed anticancer effects in osteosarcoma cells through an AMPK-dependent peroxisome proliferator‑activated receptor-γ coactivator-1α (PGC-1α)/mitochondrial transcription factor A (TFAM)/mitochondrial pathway. The findings in this study strongly suggest that AICAR could be considered as a potent therapeutic agent for the treatment of human osteosarcoma.
Research in thyroid cancer cells indicates that AICAR may also operate by causing apoptosis (programmed cell death). It appears that this activity is mediated through the induction of p21 accumulation and the eventual activation of caspase 3. The overall effect is inhibition of cancer cell proliferation and survival.
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. Anything that can mitigate this proliferation has the potential to reduce heart disease and even heart attack prevalence.