Impaired growth hormone response to growth hormone releasing factor and insulin-hypoglycaemia in obesity.
Kopelman. P G PG; Noonan. K K; Goulton. R R; Forrest. A J AJ
Key Findings
- Obese women showed a much lower GH spike after an IV dose of GHRF compared to lean women (â9âŻÂ”/L vs 28âŻÂ”/L).
- Both obese groups (prolactin responders and nonâresponders) had similarly reduced GH responses to GHRF, but nonâresponders had an especially weak GH rise to insulinâinduced hypoglycaemia.
- The data point to a hypothalamicâpituitary dysfunction linked to obesity, affecting how the body reacts to GHâreleasing signals.
Practical Outcomes
- If youâre using sermorelin or similar GHâreleasing peptides, excess body fat may blunt the expected GH boost. Weight loss or strategies that improve hypothalamic function could enhance peptide effectiveness. Consider monitoring GH levels and possibly adjusting dose if youâre obese, and be aware that the response may be less predictable.
Summary
In obese women, the body doesnât release as much growth hormone (GH) when given a hormoneâlike peptide that normally triggers GH (like sermorelin), and this blunted response is even worse in those who also have a weak prolactin reaction to lowâbloodâsugar tests. This suggests that excess weight can mess up the brainâpituitary signals that control GH.
Abstract
We have previously reported an impaired growth hormone (GH) response and abnormal prolactin release to insulin-hypoglycaemia in obesity. We suggested that obese women with an absent prolactin response to hypoglycaemia ('non-responders') have a disorder of hypothalamic function. We have now investigated the GH response to i.v. growth hormone releasing factor, GHRF (1-29)NH2, in 14 obese women and nine age-matched normal-weight women. We found a significantly reduced GH response to GHRF in the obese women as compared with controls (mean peak +/- SEM: obese 8.9 +/- 2 mu/l, controls 28 +/- 2 mu/l; P less than 0.01). When the obese women were divided on the basis of their prolactin response to insulin-hypoglycaemia (seven 'non-responders', mean weight 102 +/- 5 kg; seven responders, mean weight 108 +/- 8 kg) a similar GH response to GHRF was found between the two groups but the GH response to hypoglycaemia was significantly less in the 'non-responder' women (mean peak 'non-responders' 10.5 +/- 3 mu/l, responders 27 +/- 4 mu/l; P less than 0.05). We conclude that obesity may be characterized by an impaired GH response to both i.v. GHRF and insulin-hypoglycaemia, which suggests altered hypothalamic-pituitary function. The finding that the GH response to hypoglycaemia is significantly less in the obese prolactin 'non-responder' women supports the hypothesis for a hypothalamic disorder.
Study Information
pubmed
1985
10.1111/j.1365-2265.1985.tb00187.x