Study summary · research use only
Increase of fat oxidation and weight loss in obese mice caused by chronic treatment with human growth hormone or a modified C-terminal fragment
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study in obese (ob/ob) and lean C57BL/6J mice examined chronic effects of human growth hormone (hGH) and AOD9604, a C-terminal hGH fragment, on body weight and fat oxidation over 14 days of treatment via mini-osmotic pumps, alongside in vitro assays using hGH-receptor-transfected BaF-BO3 cells. Both hGH and AOD reduced body weight gain in obese mice and were associated with increased fat oxidation and higher plasma glycerol. Unlike hGH, AOD9604 did not induce elevated blood glucose or reduce insulin secretion, and it did not compete for the hGH receptor or induce cell proliferation. The authors describe the findings as further support for hGH acting as a pro-hormone. Species: mice.
Abstract
To observe the chronic effects of human growth hormone (hGH) and AOD9604 (a C-terminal fragment of hGH) on body weight, energy balance, and substrate oxidation rates in obese (ob/ob) and lean C57BL/6Jmice. In vitro assays were used to confirm whether the effects of AOD9604 are mediated through the hGH receptor, and if this peptide is capable of cell proliferation via the hGH receptor. Obese and lean mice were treated with hGH, AOD or saline for 14 days using mini-osmotic pumps. Body weight, caloric intake, resting energy expenditure, fat oxidation, glucose oxidation, and plasma glucose, insulin and glycerol were measured before and after treatment. BaF-BO3 cells transfected with the hGH receptor were used to measure in vitro 125I-hGH receptor binding and cell proliferation. Both hGH and AOD significantly reduced body weight gain in obese mice. This was associated with increased in vivo fat oxidation and increased plasma glycerol levels (an index of lipolysis). Unlike hGH, however, AOD9604 did not induce hyperglycaemia or reduce insulin secretion. AOD9604 does not compete for the hGH receptor and nor does it induce cell proliferation, unlike hGH. Both hGH and its C-terminal fragment reduce body weight gain, increase fat oxidation, and stimulate lipolysis in obese mice, yet AOD9604 does not interact with the hGH receptor. Thus, the concept of hGH behaving as a pro-hormone is further confirmed. This data shows that fragments of hGH can act in a manner novel to traditional hGH-stimulated pathways.
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