Department of Medicine/Endocrinology, University of New Mexico School of Medicine,
Albuquerque 87131-5271, USA.

OBJECTIVE: To increase lean body mass and improve health status in patients with wasting
associated with the acquired immunodeficiency syndrome (AIDS) by treatment with recombinant
human growth hormone (rhGH), recombinant human insulin-like growth factor 1 (rhIGF-1), or both. DESIGN: Randomized, double-blind, placebo-controlled clinical trial. SETTING: University of New Mexico Clinical Research Center and University of Texas Southwestern Medical Center. PATIENTS: 60 patients with AIDS and wasting as defined by the Centers for Disease Control and Prevention. Patients were divided into four groups of 15 patients each. INTERVENTION: Group 1
received 1.4 mg of rhGH once daily plus placebo twice daily; group 2 received 5 mg of rhIGF-1
twice daily plus placebo once daily; group 3 received 5 mg of rhIGF-1 twice daily plus 1.4 mg of
rhGH once daily; and group 4 received placebo three times daily. MEASUREMENTS: Body
weight, body composition, muscle strength, protein catabolism, quality of life, and immune status
were assessed at baseline, and changes in these variables were measured at 6 and 12 weeks.
RESULTS: At 6 weeks, lean body mass had increased and total fat mass had decreased in the
groups receiving rhGH, rhIGF-1, or both. Group 3 had the greatest changes in lean body mass
(mean +/- SE, 3.2 +/- 0.59 kg; P < 0.001); only in this group were changes in body mass maintained at 12 weeks. Only patients in group 1 had improvement in muscular strength of the knees and upper body (P = 0.04) and quality of life (P = 0.01). Immunologic function did not improve in any group. CONCLUSIONS: Growth factor therapy had significantly increased lean body mass and decreased fat mass by 6 weeks, but these improvements persisted for 12 weeks only in group 3. Growth factor therapy at the dosages used in this study is not recommended because the magnitude of weight gain was modest and improvements in quality-of-life measures varied.

Publication Types:

Clinical trial
Multicenter study
Randomized controlled trial

It sounds to me that the IGF when taken by itself stops exerting anabolic effects after 6 weeks and the hGH and IGF together were the only ones to continue yielding positive effects after this time. Also they are talking about the dose around 5mg twice a day for a total daily dose of 10mg/day but the email Mr. N had forwarded to me from you had said that the dose you were recommending was in the area of 50-100mcg's/day. Can you clarify for me the difference. Also I had some questions on the effects when taken with insulin. Is IGF going to increase my chance of hyperglycemia and therefore cause an increased risk if taken with insulin? If so how can this be controlled.

Note, that's because it wasn't the long r3 version that they had to use so much.

Different effects of IGF-I on insulin-stimulated glucose uptake in adipose tissue and skeletal muscle
Fredrik Frick1, Jan Oscarsson1, Kerstin Vikman-Adolfsson1, Malin Ottosson2, Noriko Yoshida2, and Staffan Edén1
1 Department of Physiology and Pharmacology and 2 Wallenberg Laboratory, Göteborg University, S-405 30 Goteborg, Sweden

The effect of insulin-like growth factor I (IGF-I) on insulin-stimulated glucose uptake was studied in adipose and muscle tissues of hypophysectomized female rats. IGF-I was given as a subcutaneous infusion via osmotic minipumps for 6 or 20 days. All hypophysectomized rats received L-thyroxine and cortisol replacement therapy. IGF-I treatment increased body weight gain but had no effect on serum glucose or free fatty acid levels. Serum insulin and C-peptide concentrations decreased. Basal and insulin-stimulated glucose incorporation into lipids was reduced in adipose tissue segments and isolated adipocytes from the IGF-I-treated rats. In contrast, insulin treatment of hypophysectomized rats for 7 days increased basal and insulin-stimulated glucose incorporation into lipids in isolated adipocytes. Pretreatment of isolated adipocytes in vitro with IGF-I increased basal and insulin-stimulated glucose incorporation into lipids. These results indicate that the effect of IGF-I on lipogenesis in adipose tissue is not direct but via decreased serum insulin levels, which reduce the capacity of adipocytes to metabolize glucose. Isoproterenol-stimulated lipolysis, but not basal lipolysis, was enhanced in adipocytes from IGF-I-treated animals. In the soleus muscle, the glycogen content and insulin-stimulated glucose incorporation into glycogen were increased in IGF-I-treated rats. In summary, IGF-I has opposite effects on glucose uptake in adipose tissue and skeletal muscle, findings which at least partly explain previous reports of reduced body fat mass, increased body cell mass, and increased insulin responsiveness after IGF-I treatment.

insulin-like growth factor I; soleus muscle; glycogen; triglyceride; lipid; free fatty acids; C-peptide; L-thyroxine; cortisol