IGF-1 RH (commercial name: Increlex), also referred to as mecasermin, IGF-1, recombinant human IGF-1 and RH IGF-1, belongs to the family of peptides known as insulin-like growth factors; these peptides share similarities in sequence to insulin. The primary physiological source of IGF-1 is via the liver, due to stimulation by growth hormone (GH). This relationship is part of the “GH/IGF-1 axis.” The physiological roles of IGF-1 are diverse: cell proliferation, inhibition of apoptosis, contribution to normal and abnormal cell growth, survival, and differentiation. Clinical uses of IGF-1 include in Laron syndrome (a type of dwarfism), short stature syndrome, and in various states of GH/IGF-1 deficiency.
Conti et al (2008) cite the following areas of inquiry for future development of IGF-1, but state that evidence is inconclusive: “insulin resistance, burns, catabolic and post-surgery states, acute and chronic renal failure, amyotrophic lateral and multiple sclerosis, brain injury, and immunoincompetence.”.
Pennisi et al (2006) discuss the similarities and differences between insulin and IGF-1, and the use of IGF-1 to improve parameters of health in diabetic patients:
Insulin-like growth factor 1 (IGF-1) and insulin are structurally related polypeptides that mediate a similar pattern of biological effects via receptors that display considerably[sic] homology. Administration of recombinant human IGF-1 (rhIGF-1) has been proven to improve glucose control and liver and muscle insulin sensitivity in patients with type 2 diabetes mellitus (DM).
Pennisi also cites evidence from animal models:
MKR mice have impaired IGF-1 and insulin signaling in skeletal muscle leading to severe insulin resistance in muscle, liver and fat, developing type 2 DM at five weeks of age. Six week old MKR mice were treated either saline or rhIGF-1 for 3 weeks. Blood glucose levels were decreased in response to rhIGF-1 treatment in MKR mice. rhIGF-1 treatment also increased body weight in MKR with concomitant changes in body composition such as a decrease in fat mass and an increase in lean body mass….Taken together these results demonstrate that the improvement of the hyperglycemia was achieved by inhibition of gluconeogenesis rather than an improvement in insulin sensitivity. Also, these results suggest that a functional IGF-1R in skeletal muscle is required for IGF-1 to improve insulin sensitivity in this mouse model of type 2 DM.
Although the evidence is not conclusive regarding the potential of IGF-1 to treat diabetic patients, it is a helpful research and reference compound to better understand the underlying physiology.
Vaught, Contreras, and Glickman discuss IGF-1’s effect on motor neurons:
…data indicate that rhIGF-1 has marked effects on the survival of compromised motor neurons and the maintenance of their axons and functional connections. They also suggest the potential utility of rhIGF-1 for the treatment of diseases such as ALS and certain neuropathies.
Fouque, Peng, and Shamir (2000) discuss an anabolic effect achieved in human subjects: “Injections of rhIGF-1 induce a strong and sustained anabolic effect, as indicated by a positive nitrogen balance in CAPD patients with protein-energy malnutrition.”
Ding et al(2006) discuss “a possible mechanism by which insulin-like growth factor-I interfaces with the brain-derived neurotrophic factor system to mediate exercise-induced synaptic and cognitive plasticity”:
This study reveals that the effects of exercise on brain neuronal and cognitive plasticity are in part modulated by a central source of insulin-like growth factor-I. Exercise selectively increased insulin-like growth factor-I expression….Blocking the insulin-like growth factor-I receptor significantly reversed the exercise-induced increase in the levels of brain-derived neurotrophic factor mRNA and protein and pro-brain-derived neurotrophic factor protein, suggesting that the effects of insulin-like growth factor-I may be partially accomplished by modulating the precursor to the mature brain-derived neurotrophic factor….Blocking the insulin-like growth factor-I receptor abolished these exercise-induced increases.
According to Mauras (2009) IGF-1 “may decrease the catabolic effects of chronic steroid use in humans, particularly by enhancing lean body mass accrual and, in children, by increasing linear growth”.
 Conti E; Musumeci MB; Assenza GE; Quarta G; Autore C; Volpe M. “Recombinant human insulin-like growth factor-1: a new cardiovascular disease treatment option?” Cardiovasc Hematol Agents Med Chem. 2008; 6(4):258-71.
 Pennisi P., et al. “Recombinant Human Insulin-Like Growth Factor-I (rhIGF-1) treatment inhibits gluconeogenesis in a transgenic mouse model of type 2 Diabetes Mellitus (DM).” Endocrinology, 23 Feb 2006.
 Vaught J., Contreras P., Glicksman M. “Potential Utility of rhIGF-1 in Neuromuscular and/or Degenerative Disease.” Ciba Foundation Symposium 196 – “Growth Factors as Drugs for Neurological and Sensory Disorders.” 1996.
 Fouque D., Peng S., Shamir E. “Recombinant human insulin-like growth factor-1 induces an anabolic response in malnourished CAPD patients.” Kidney Int. 2000;57(2):646-54.
Ding Q et al. Insulin-like growth factor I interfaces with brain-derived neurotrophic factor-mediated synaptic plasticity to modulate aspects of exercise-induced cognitive function. Neuroscience. 2006 Jul 7;140(3):823-33.
 Mauras N. “Can growth hormone counteract the catabolic effects of steroids?” Horm Res. 2009; 72 Suppl 1:48-54.