Increases the rate of cellular division
Similar to IGF-1, Receptor Grade IGF-1 LR3 stimulates cell growth and division. Connective tissues like muscle and bone are the significant targets, although it also encourages cell proliferation in the liver, intestines, and other organs. As a maturation hormone, IGF-1 increases cell proliferation and differentiation, making it an ideal candidate for use in the treatment of cancer. In other words, IGF-1 promotes cell maturation so that cells can perform their specific activities.
IGF1-LR3 has a longer half-life than IGF-1, allowing it to persist in the body for more extended periods. Because of this, IGF1-LR3 is a considerably more powerful molecule. A dosage of IGF1-LR3 activates cells three times more than a dose of IGF-1 of the same size.
It is important to note that IGF1-LR3 and other IGF-1 derivatives do not induce cell expansion (hypertrophy) but rather cell division and proliferation (hyperplasia). Because it does not enhance the size of muscle cells, IGF1-LR3 has the opposite effect on muscles.
Inhibits Type 2 Diabetes by Enhancing Fat Metabolism
Through the IGF-1R and insulin receptors, IGF1-LR3 promotes fat metabolism in a non-direct way. Muscle, neuron, and liver cells all take up more glucose from the blood when you do these things. Because of this, the liver and adipose tissue both begin to break down glycogen and triglycerides. Adipose tissue and energy consumption are reduced (i.e., net catabolism).
It should come as no surprise that IGF1-LR3 decreases insulin levels and the requirement for exogenous insulin in diabetes, given its involvement in lowering blood sugar levels. Maintaining the same blood sugar levels means a 10% reduction in insulin use. Scientists may better understand how to reduce insulin dosages in people with lower insulin sensitivity and perhaps how to prevent type 2 diabetes from developing in the first place by using this information.
Reduces the activity of the hormone myostatin
Specifically, myostatin (also known as growth differentiation factor 8 or GDF8) is a protein that suppresses muscle cell development and differentiation. There are situations when blocking myostatin might be beneficial, even though its function is critical to preventing uncontrolled hypertrophy and ensuring average recovery after damage. Duchenne muscular dystrophy (DMD) or muscle atrophy due to extended immobilization might benefit from the capacity to inhibit myostatin’s functions. This natural enzyme is inhibited by slowing muscle breakdown, maintaining strength, and preventing morbidity may be possible.
IGF1-LR3 and other IGF-1 derivatives have been discovered to counteract the deleterious effects of myostatin to protect muscle cells and prevent apoptosis in animal models of Duchenne muscular dystrophy (DMD). A muscle protein called MyoD seems to be activated by IGF1-LR3, which has a long half-life and is hence particularly effective in countering myostatin. Exercise (e.g., weightlifting) or tissue injury activates the protein MyoD, which causes muscular development.
In the Study of Longevity
Cell damage and the symptoms of aging may be prevented by IGF1-LR3’s ability to promote tissue repair and maintenance. Researchers have shown that IGF1-LR3 injections may help counteract the effects of cell aging in cows and pigs. Researchers are testing the potential of IGF1-LR3 to slow the course of many diseases, including dementia, muscular atrophy, and renal illness in mice. According to one study, taking IGF-1 supplements may extend life and lessen disability.