Insulin-like growth factors (IGFs) are peptides with sequence similarities to insulin. IGF-1 is mainly secreted by the liver via stimulation of GH (growth hormone); this is the primary mechanism of IGF/GH axis. IGF-1 plays a role in cell proliferation and inhibition of apoptosis, making it important for both normal and abnormal cell growth. Recombinant human IGF refers to IGF made via genetically altered E. coli which produce the peptide bioidentical in nature to native human IGF.
IGF-1 has only been used therapeutically with any consistency in Laron syndrome (a type of dwarfism caused by GH insensitivity), although it is in trials for treatment of diabetes and neurological diseases such as Alzheimer’s and various scleroses. Conti et al state that there is inconclusive evidence about rhIGF-1 used for “insulin resistance, burns, catabolic and post-surgery states, acute and chronic renal failure, amyotrophic lateral and multiple sclerosis, brain injury, and immunoincompetence.”
Pennisi compares IGF-1 and insulin as follows: “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 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).”
From a mouse study Pennisi observes:
“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….Pyruvate and glutamine tolerance tests proved that there was a decrease in the rate of glucose appearance in MKR mice treated with rhIGF-1 suggesting a reduction in the gluconeogenic capacity of liver, kidney and small intestine. 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.”
Vaught, Contreras, and Glickman observe the following about the effect of IGF-1 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.”
In a human study a strong anabolic effect was demonstrated from rhIGF-1: “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.”
Fouque, Peng, and Shamir describe in detail the effects of combination GH/IGF-1 treatment:
“Theoretically combined administration of GH and IGF-I may be more effective than GH alone or IGF-I alone. Arguments in favor for this are: 1] Clearance of IGF-I may be markedly altered by the co-administration of GH and this will provide sustained actions of IGF-I. 2] Higher serum IGF-I levels are achieved with a combination treatment of GH and IGF-I than with GH treatment alone or IGF-I alone. In addition, combination therapy may have additive or synergistic effects. 3] The combination GH and IGF-I counteracts disadvantageous effects on glucose metabolism of either GH alone or IGF-I alone. 4] GH may exert direct actions on tissues independently from IGF-I. 5] Combination of GH and IGF-I may be more effective in improving tissue IGF-I levels. The combination therapy of GH and IGF-I might be beneficial in growth retardation, in certain specific subgroups of critically ill or catabolic patients and in the treatment of GH-deficient subjects with the metabolic syndrome and/or manifest diabetes.”
From a mouse study Janssen hypothesizes: “The present studies demonstrate that an IGFBP inhibitor mimics the behavioral effects of IGF-I and that IGFBP inhibition may represent a novel mechanism by which to increase IGF-I to treat depression and anxiety.”
Ding, Vaynman, and Akhavan explore effects of IGF-1 on biomarkers of synaptic and cognitive plasticity:
“The ability of exercise to benefit neuronal and cognitive plasticity is well recognized. 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. Our results illustrate 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.”
IGF-1 is a potent anabolic agent that can decrease catabolic effects of corticosteroids:
“GH and insulin-like growth factor I (IGF-I) are potent protein-anabolic and growth-promoting agents in vitro and in vivo. Both GH and IGF-I 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.”
Hayes, Urban, and Jiang study the effects of IGF-1 on hypogondal men:
“Severe gonadal androgen deficiency can have profound catabolic effects in man. Hypogonadal men develop a loss of lean body mass, increased adiposity, and decreased muscle strength despite normal GH and insulin-like growth factor I (IGF-I) concentrations. We designed these studies to investigate whether GH or IGF-I administration to male subjects with profound hypogonadism can diminish or abolish the catabolic effects of testosterone deficiency. We conclude that 1) rhGH and rhIGF-I both may be beneficial in preserving lean body mass and sustaining rates of protein synthesis during states of severe androgen deficiency in man; 2) GH may affect the im IGF system via an a paracrine, local production of IGF-I; 3) androgens may be necessary for the full anabolic effect of GH/IGF-I in man. These hormones, particularly GH, may play a role in the treatment of hypogonadal men rendered hypogonadal pharmacologically or those unable to take full testosterone replacement. The latter requires further study.”
rhIGF-1 remains a promising treatment despite lack of use in the medical community. In the future it could be used to treat neurological disorders and diabetes and also to prevent catabolism.
 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.
 Janssen J. “Advantages and disadvantages of GH/IGF-I combination treatment.” Rev Endocr Metab Disord. 2009; 10(2):157-62
 Malberg J., Platt B., Rizzo S. “Increasing the levels of insulin-like growth factor-I by an IGF binding protein inhibitor produces anxiolytic and antidepressant-like effects.” Neuropsychopharmacology. 2007; 32(11):2360-8
 Ding Q., Vaynman S., Akhavan M. “Insulin-like growth factor I interfaces with brain-derived neurotrophic factor-mediated synaptic plasticity to modulate aspects of exercise-induced cognitive function.” Neuroscience. 2006; 140(3):823-33
 Mauras N. “Can growth hormone counteract the catabolic effects of steroids?” Horm Res. 2009; 72 Suppl 1:48-54
 Hayes VY., Urban R., Jiang J. “Recombinant human growth hormone and recombinant human insulin-like growth factor I diminish the catabolic effects of hypogonadism in man: metabolic and molecular effects.” J Clin Endocrinol Metab. 2001; 86(5):2211-9
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