AICAR 50mg

AICAR is a molecule that has similar action to adenosine monophosphate (AMP), a nucleotide characterized by its active role in cellular energy metabolism. Researchers have studied this peptide for its ability to minimize damage from blood flow restriction (reperfusion injury) and to sustain different metabolic processes.

Another important compound often mentioned in relation to AICAR is AMPK. This one can balance energy levels by turning off energy-consuming processes, like protein and fat synthesis, and turning on energy-producing ones, such as glucose and protein synthesis.

Researchers also believe that aica ribonucleotide may affect other important processes, including cell maintenance (autophagy), generation of new mitochondria (mitochondrial biogenesis), and control of inflammation and stress responses. These wide-ranging implications suggest that AMPK is an important force in keeping the cellular function and protecting overall bodily health.

By stimulating AMPK, AICAR has been found to possibly enhance the uptake of glucose in muscle cells, increase insulin sensitivity, and increase glucose tolerance. It's also believed to have anti-inflammatory properties and enhance exercise performance in certain animal models..

What Does AICAR Do?

AICAR Peptide and Tissue Protection

This peptide is believed to have the capacity to protect tissues from damage, especially in conditions like ischemia and reperfusion. In animal experiments, AICAR has been linked with lower cases of heart attacks (myocardial infarctions) and overall better heart function which is related to such damage.

One meta-analysis examined AICAR's potential protective effects in cardiovascular tissues. The review compared five randomized, double-blind, placebo-controlled clinical trials. Overall results suggested that AICAR may lessen the severity of heart tissue damage, lower cardiac cell death, and enhance overall cardiovascular outcomes.

Researchers believe that this protective feature is likely related to AICAR's effect on cellular energy metabolism. By stimulating AMPK, AICAR may help the cells become less sensitive to low oxygen levels, in part by increasing delivery of glucose that heart cells are able to use even when there isn't enough oxygen available. In isolated mouse hearts, AICAR appeared to trigger the breakdown of glycogen (glycogenolysis) in the heart muscle, making more glucose available as an energy source. Interestingly, in triggering breakdown of glycogen, AICAR didn't significantly affect glycogen synthesis. This would imply a possible role for AMPK in selectively enhancing glycogenolysis.

The second finding was the increase of ZMP levels (5-aminoimidazole-4-carboxamide ribonucleotide), the intracellular active form of AICAR. ZMP may be able to activate the enzyme glycogen phosphorylase directly, which is responsible for releasing glucose from glycogen stores. But the study found no significant alterations in such enzymes as glycogen synthase or in glucose-6-phosphate concentrations or other adenine nucleotides in cardiac tissue. This indicates that ZMP's action would be more stimulating than changing.

AICAR's possible protection is not limited to the heart. In a mouse model that suffered from alcohol-induced fatty liver disease in a different study, AICAR showed incredible success. Chronic alcohol intake typically leads to fatty liver, both in appearance and structure. But with AICAR administration, it appeared to dampen the liver fat deposition and tissue damage.

This benefit may be partly explained by AICAR's ability to reduce the proteins involved in fat production. For example, concentration of SREBP-1c (sterol regulatory element-binding protein 1c), a protein that regulates genes taking part in fat and cholesterol production, was reduced after AICAR treatment. This further seemed to minimize the expression of fatty acid synthase (FAS), a key enzyme used in producing long-chain fatty acids like palmitate. Since FAS activity is regulated by SREBP-1c, a reduction in SREBP-1c likely contributed towards the overall decline in fat synthesis.

Overall, by activating AMPK, AICAR may guard organs like the heart and liver from stress, hypoxia, or metabolic stress injury. Its ability to affect both energy metabolism as well as fat synthesis makes it a candidate with exciting potentials in metabolic and tissue-protective research.

AICAR Peptide and Glucose Sensitivity

Research has shown that AICAR can possibly have a role in increasing glucose sensitivity by stimulating AMPK, a critical enzyme that regulates intracellular energy. In the state of AMPK activation, cells increase their glucose uptake, which seems to allow better metabolic function.

Researchers in a study using an equine skeletal muscle model examined whether AICAR would stimulate increased glucose entry into muscle cells. The results were promising, AICAR appeared to lower glucose levels and raise levels of insulin, with minimal impact on lactate levels. It also appeared to raise the level of activated (phosphorylated) AMPK in muscle and increase the level of a protein called GLUT8, which helps glucose enter cells. This GLUT8 increase could be an important part of the way AICAR increases insulin sensitivity.

Another study looked at whether AICAR, with exercise, could stimulate glucose uptake in muscles. Exercise and AICAR both increased the uptake of glucose, which suggested that AICAR could mimic some of the metabolic impact of exercise. Researchers were surprised to find out that AICAR didn't affect muscles only, it was also able to stimulate glucose uptake in other tissues, which could potentially contribute to enhanced insulin sensitivity throughout the body. The study also stated that AICAR can possibly activate ERK1/2, MAP kinase/ERK pathway enzymes. The pathway is significant to cell growth, division, and response to stress, and its activation is another possible mechanism that may decrease regulation of AICAR’s glucose metabolism.

AICAR Peptide and Endurance

Scientists believe that AICAR might activate key cellular enzymes like AMPK, glycogen phosphorylase, and fructose-1,6-bisphosphatase. Research indicates that this activation could play a role in enhancing oxidative metabolism and increasing the production of mitochondria-structures responsible for generating energy in cells. Improving both the number and efficiency of mitochondria may support greater muscle endurance.

In one study involving sedentary mice, AICAR appeared to boost the expression of metabolic genes and improve running endurance by 44%. These findings suggest that compounds like AICAR might influence the AMPK-PPARδ pathway to support training adaptions or even improve endurance without exercise. PPARδ (Peroxisome Proliferator-Activated Receptor Delta) is a nuclear receptor that helps regulate genes tied to energy metabolism. It’s thought to promote fat-burning and the creation of new mitochondria. When AMPK and PPARδ are activated together, they may mimic the effects of endurance training at the cellular level-leading to more mitochondria and a shift toward slow-twitch, endurance-oriented muscle fibers.

Another mouse study found that activating AMPK with a specific compound increased endurance beyond what was seen in animals that had undergone exercise training alone. In a model of Duchenne muscular dystrophy, AICAR appeared to enhance the benefits of physical activity and improve muscle performance, potentially by encouraging autophagy-a processes that help clear out damaged cellular components.

In human trials, infusing AICAR (also known as AICA-riboside) led to increased blood flow in the forearm in correlation with the dose given, though it didn’t affect glucose uptake in muscle. The rise in blood flow seemed to be tied to nitric oxide activity, as blocking nitric oxide synthesis reduced the effect. This suggests AICAR might help improve circulation during physical exertion, which could support endurance by delivering more oxygen and nutrients to working muscles.

References:

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