Description

IGF-1 LR3 accelerates recovery, improves fat loss and body composition, boosts performance, and has potential anti-aging effects. (PMID: 37165618, PMID: 2792010, PMID: 32256674, PMID: 30557473)

IGF-1 LR3, or Insulin-Like Growth Factor-1 Long R3 Research Topics:

1. Accelerated Recovery and Healing:

   This peptide aids in the regeneration of damaged tissues, tendons, and ligaments, reducing recovery time after intense workouts or injuries. It also increases collagen production, improving the strength and integrity of connective tissues. (PMID: 37165618)

2. Improved Fat Loss and Body Composition:

   IGF-1 LR3 enhances fat metabolism, promoting lipolysis and inhibiting lipogenesis, which helps in achieving a leaner and more defined physique. (PMID: 2792010)

3. Enhanced Performance:

   The peptide improves strength, power, and endurance, allowing more intense and prolonged training sessions. It also enhances the oxygen-carrying capacity of the blood, facilitating better oxygen delivery to muscles during exercise. (PMID: 32256674)

4. Potential Anti-Aging Effects:

   By stimulating cell proliferation and development, IGF-1 LR3 may have beneficial effects on tissue renewal, contributing to its potential use in anti-aging therapies. (PMID: 30557473)

Peer-Reviewed Studies

• Action of long(R3)-insulin-like growth factor-1 on protein metabolism in beef heifers.

Hill, R. A., Hunter, R. A., Lindsay, D. B., & Owens, P. C. (1999). Domestic animal endocrinology, 16(4), 219–229. https://doi.org/10.1016/s0739-7240(99)00015-6

• Porcine growth hormone and LongR(3)IGF-I can improve recovery from surgery-induced weight loss in guinea pigs.

Conlon, M. A., & Kita, K. (2001). General and comparative endocrinology, 123(3), 332–336. https://doi.org/10.1006/gcen.2001.7674

Structure

Sequence: MFPAMPLSSL FVNGPRTLCG AELVDALQFV CGDRGFYFNK PTGYGSSSRR APQTGIVDEC CFRSCDLRRL EMYCAPLKPA KSA Molecular Formula: C400H625N111O115S9 Molecular Weight: 9117 .5 g/mol
CAS Number: 946870-92-4

IGF-1 LR3 Research

Cell Division

Like IGF-1, IGF1-LR3 is a potent stimulus for cell division and proliferation. Its primary effects are on connective tissues like muscle and bone, but it also promotes cell division in the liver, kidney, nerve, skin, lung, and blood tissues. IGF-1 is best thought of as a maturation hormone because it not only promotes cell proliferation, but differentiation as well. IGF-1 causes cells to mature, in other words, so that they can carry out their specialized functions.

Unlike IGF-1, IGF1-LR3 remains in the bloodstream for a long period of time. This property makes IGF1- LR3 a much more potent molecule. A dose of IGF1-LR3 provides approximately three times as much cell activation as a similar dose of IGF-1. Note that IGF1-LR3 and all IGF-1 derivatives do not promote cell enlargement (hypertrophy), but rather promote cell division and proliferation (hyperplasia). In the case of muscle, for instance, IGF1-LR3 does not cause muscle cells to get larger, but it does increase total number of muscle cells.

Fat Metabolism and Diabetes

IGF1-LR3 boosts fat metabolism in an indirect manner by binding to both the IGF-1R receptor and the insulin receptor. These actions increase glucose uptake from the blood by muscle, nerve, and liver cells. This results in an overall decrease in blood sugar levels, which then triggers adipose tissue as well as the liver to begin breaking down glycogen and triglycerides. Overall, this produces a net decrease in adipose tissue and net energy consumption (i.e. net catabolism).

Given its role in reducing blood sugar levels, it should come as no surprise that IGF1-LR3 reduces insulin levels as well as the need for exogenous insulin in diabetes. In most cases, this translates into a 10% decrease in insulin requirements to maintain the same blood sugar levels. This fact may help scientists understand how to decrease insulin doses in individuals who have decreased insulin sensitivity and may even offer insight into preventing type 2 diabetes in the first place.

Impairs Myostatin

Myostatin (a.k.a. growth differentiation factor 8) is a muscle protein that primarily inhibits the growth and differentiation of muscle cells. While this function is important to prevent unregulated hypertrophy and ensure proper healing following injury, there are times when inhibiting myostatin could be of benefit. The ability to stop myostatin from functioning could be useful in conditions like Duchenne muscle dystrophy (DMD) or in people who suffer muscle loss during prolonged immobility. In these cases, inhibiting this natural enzyme could help to slow muscle breakdown, maintain strength, and stave off morbidity.

In mouse models of DMD, it has been found that IGF1-LR3 and other IGF-1 derivatives are capable of counteracting the negative effects of myostatin to protect muscle cells and prevent apoptosis. IGF1-LR3, thanks to its long half-life, is highly effective in counteracting myostatin and appears to work by activating a muscle protein called MyoD [1],[2]. MyoD is the protein normally activated by exercise (e.g. weight lifting) or tissue damage and is responsible for muscle hypertrophy.

IGF1-LR3 Longevity Research

IGF1-LR3 promotes tissue repair and maintenance throughout the body, making it a protective molecule against cell damage and the effects of aging. Research in cows and pigs indicates that IGF1-LR3 administration may be an effective solution for offsetting the effects of cellular aging. Ongoing research in mice seeks to determine if IGF1-LR3 might be useful in preventing the progression of a wide range of conditions such as dementia, muscle atrophy, and kidney disease. This research reveals that IGF-1 administration can prolong life and reduce disability [3],[4],[5].

Glucocorticoid Signaling

Glucocorticoids, secreted primarily by the adrenal glands, are important clinical drugs used to control pain and reduce inflammation in autoimmune diseases, neurological injury, cancer, and more.

Unfortunately, glucocorticoids have a number of undesirable side effects such as muscle wasting, fat gain, and deterioration of bone density. There is some interest in using IGF1-LR3 to reduce the side effects of glucocorticoids and thus allow for more effective therapy [6].

IGF1-LR3 exhibits minimal to moderate side effects, and low oral and excellent subcutaneous bioavailability in mice. Per kg, dosage in mice does not scale to humans. IGF1-LR3 for sale at Life Link Research is limited to educational and scientific research only, not for human consumption. Only buy IGF1-LR3 if you are a licensed researcher.

Article Author

The above literature was researched, edited, and organized by Dr. E. Logan, M.D. Dr. E. Logan holds a doctorate from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Scientific Journal Author

Dr. Anastasios Philippou, Ph.D. focused on Experimental Physiology at the National & Kapodistrian University of Athens Medical School. He is now a National Center Manager and Assistant Professor, however his extensive studying and documented research pertaining to the effects of muscle regeneration, the role of IGF-1 in skeletal muscle physiology, the expression of IGF-1 isoforms after exercise-induced muscle damage in humans, characterization of the MGF E peptide actions in vitro, and epigenetic regulation on gene expression induced by physical exercise are most impressive.

Dr. Anastasios Philippou, Ph.D. is being referenced as one of the leading scientists involved in the research and development of IGF1-LR3. 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 Life Link Research 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. Anastasios Philippou, Ph.D. is listed in [7] and [8] under the referenced citations.

Referenced Citations

1. “Adipose Tissue-Derived Stem Cell Secreted IGF-1 Protects Myoblasts from the Negative Effect of Myostatin.” [Online]. Available: https://www.hindawi.com/journals/bmri/2014/1 29048/. [Accessed: 16-May-2019].
2. N. Li, Q. Yang, R. G. Walker, T. B. Thompson, M. Du, and B. D. Rodgers, “Myostatin Attenuation In Vivo Reduces Adiposity, but Activates Adipogenesis,” Endocrinology, vol. 157, no. 1, pp. 282-291,Jan. 2016.
3. E. Corpas, S. M. Harman, and M. R. Blackman, “Human growth hormone and human aging,” Endocr. Rev., vol. 14, no. 1, pp. 20-39, Feb. 1993.
4. W. E. Sonntag, A. Csiszar, R. deCabo, L. Ferrucci, and z. Ungvari, “Diverse roles of growth hormone and insulin-like growth factor-1 in mammalian aging: progress and controversies,” J. Gerontol. A. Biol. Sci. Med. Sci., vol. 67, no. 6, pp. 587-598, Jun. 2012.
5. “IGF-I/IGFBP system: metabolism outline and physical exercise. – PubMed – NCBI.”
   [Online]. Available: https://www.ncbi.nlm.nih.gov/pubmed/227140 57. [Accessed: 16-May-2019].
6. B. Y. Hanaoka, C. A. Peterson, C. Horbinski, and L. J. Crofford, “Implications of glucocorticoid therapy in idiopathic inflammatory myopathies,” Nat. Rev. Rheumatol., vol. 8, no. 8, pp. 448-457, Aug. 2012.
7. A Philippou, A Halapas, M Maridaki, M Koutsilieris – J Musculoskelet Neuronal Interact, 2007 [Semantic Scholar]
8. A Philippou, E Papageorgiou, G Bogdanis, A Halapas … – In vivo, 2009 [liar Journals]