IGF-1 LR3: A Synthetic Model of the Insulin-like Growth Hormone

by | Jun 6, 2022 | Research

Insulin growth factor 1, long arginine 3 (IGF-1 LR3), is a modified, synthetic model of the insulin-like growth hormone. It functions primarily in cell proliferation, and cell-cell communication enhances fat metabolism and muscle repair by halting the actions of myostatin and cell division. Although it’s almost identical to IGF-1, it doesn’t bind to IGF-binding proteins as the IGF. As a result, it lasts in the blood 120 times longer than IGF, suggesting that IGF has a prolonged after-life compared to its counterpart – IGF-1.


Cell Division and Potential Benefits

IGF-1 LR3 peptide is a powerful cell proliferation/division stimulant. It primarily functions in bone, liver, kidney, nerve, skin, blood tissues, and lungs. It is considered a maturation hormone because it promotes cell proliferation and differentiation.

Consequent to IGF-1 LR3’s prolonged half-life, it is considered a more potent molecule because a dose of IGF-1 LR3 initiates cell activation 3 times compared to the same dose of IGF-1.

IGF-1 LR3 and IGF-1 derivatives promote cell division and proliferation rather than cell enlargement (hypertrophy)


The effect of IGF-1 LR3 on Myostatin

Myostatin is a muscle growth inhibitor. Myostatin is essential for proper healing during an injury and monitoring hypertrophy to prevent over-action. While this function is vital, the inhibition of myostatin can be beneficial, as seen in Duchenne Muscle Dystrophy. It helps slow down muscle degradation, sustain strength, protect muscles, prevent apoptosis, and keep morbidity at bay.

The counter-reactive effect of IGF-3 LR3 on myostatin is a result of its long half-life, and this action is via the activation of a muscle protein – MyoD. MyoD regulates muscle dystrophy and is activated during tissue damage and exercise.


The role of IGF-1 LR3 in Fat Metabolism and Diabetes

By binding to the IGF-1R receptor and the insulin receptor, IGF-1 LR3 enhances fat metabolism indirectly. These actions cause an increase in glucose uptake by the liver, muscle, and nerve that trigger the breakdown of fatty tissues and net energy consumption because of the continuous degradation of glycogen and triglycerides.

IGF-1 LR3 may reduce blood sugar levels as well as insulin levels. In some cases, there’s a 10% decrease in insulin required to balance blood sugar levels. This decrease could enable scientists to understand how to deal with increased insulin levels in patients with low insulin sensitivity and offer an approach to preventing type 2 diabetes.


The Longevity Research

The functions of IGF-1 LR3 are not limited, as it enhances tissue repair and maintenance across the body.

Research suggests that IGF-1 LR3 may be essential in preventing the succession of disease conditions like kidney disease, dementia, and muscle atrophy.

IGF-1 LR3 research shows promising results as it increases lactation in nursing mothers.

The roles of IGF-1 LR3 on Glucocorticoid Signaling

Glucocorticoid is a hormone secreted primarily by the adrenal glands. They control pain and reduce inflammation in autoimmune diseases, cancer, neurological injuries, etc. While glucocorticoids are beneficial in some cases, they cause a decrease in bone density, muscle wasting, and fat gain.

Clinical studies show that IGF-1 LR3 may be a necessary ancillary in reducing the side effects of glucocorticoids.

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