Growth hormone response to growth hormone releasing factor in diabetic men.
Kopelman. P G PG; Mason. A C AC; Noonan. K K; Monson. J P JP
Key Findings
- Fasting GH levels were similar across all groups (lean, obese, diabetic, non‑diabetic).
- Lean men and lean diabetics had comparable peak GH increases after GRF‑1‑29 (around 20‑25 mU/L).
- Obese men, regardless of diabetes status, had a dramatically lower peak GH response (around 4‑6 mU/L).
- The blunted GH response in obesity was independent of fasting insulin or glucose concentrations.
Practical Outcomes
- For biohackers using GRF‑1‑29 to boost GH, obesity may limit its effectiveness, so weight loss could be a prerequisite for a strong response. Monitoring GH spikes after a test dose can help gauge individual sensitivity. Adjusting expectations or dosing in obese individuals is advisable, but no new dosing protocol is required.
Summary
A study looked at how men’s growth hormone (GH) spikes after a single dose of the peptide GRF‑1‑29. It found that lean men—whether healthy or diabetic—had a normal GH surge, but obese men (both healthy and diabetic) showed a much weaker response. The reduced response wasn’t linked to blood sugar or insulin levels.
Abstract
Increased plasma concentrations of growth hormone (GH) are reported in diabetes and it is suggested that this may be important in the development of complications. We have investigated fasting GH levels and the response to 100 micrograms i.v. growth hormone releasing factor, GRF(1-29)NH2, in age-matched men: six normal weight controls, six obese controls, six insulin-dependent diabetics, six normal weight non-insulin dependent diabetics and six obese non-insulin dependent diabetics. None of the diabetic men had clinical evidence of diabetic complications. Fasting GH values did not differ significantly between the five groups. The peak GH response to GRF was similar in the controls, insulin-dependent diabetics (IDD) and non-insulin dependent (NIDD) normal weight diabetics (mean peak +/- SEM: controls 25.5 +/- 5 mU/l, IDD 26.5 +/- 6 mU/l, NIDD 19.7 +/- 5 mU/l) but was significantly reduced in the two obese groups (obese 6.4 +/- 3 mU/l, obese diabetics 4.5 +/- 1 mU/l, P less than 0.01). This impairment of GH secretion was unrelated to either fasting plasma insulin or glucose concentration. We conclude that our results do not confirm the previous reports of abnormal GH secretion in diabetes but do demonstrate a markedly impaired GH response to GRF to be a feature of obesity.
Study Information
pubmed
1988
1988-01-01T00:00:00.000Z
10.1111/j.1365-2265.1988.tb01200.x
32
27