Study summary · research use only
The effects of human GH and its lipolytic fragment (AOD9604) on lipid metabolism following chronic treatment in obese mice and beta(3)-AR knock-out mice
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study in obese mice and beta(3)-adrenergic receptor (beta(3)-AR) knock-out mice examined human growth hormone (hGH) and its C-terminal fragment AOD9604 given intraperitoneally for 14 days. In obese mice, both compounds reduced body weight and body fat and were associated with increased beta(3)-AR RNA expression, raising it toward levels seen in lean mice. In beta(3)-AR knock-out mice, long-term hGH and AOD9604 treatment did not produce the body-weight and lipolysis changes seen in wild-type mice, though acute AOD9604 dosing did increase energy expenditure and fat oxidation in the knock-out mice. The authors conclude the lipolytic actions of hGH and AOD9604 are not directly mediated through beta(3)-AR, despite both increasing its expression. Species: mice.
Abstract
Both human GH (hGH) and a lipolytic fragment (AOD9604) synthesized from its C-terminus are capable of inducing weight loss and increasing lipolytic sensitivity following long-term treatment in mice. One mechanism by which this may occur is through an interaction with the beta-adrenergic pathway, particularly with the beta(3)-adrenergic receptors (beta(3)-AR). Here we describe how hGH and AOD9604 can reduce body weight and body fat in obese mice following 14 d of chronic ip administration. These results correlate with increases in the level of expression of beta(3)-AR RNA, the major lipolytic receptor found in fat cells. Importantly, both hGH and AOD9604 are capable of increasing the repressed levels of beta(3)-AR RNA in obese mice to levels comparable with those in lean mice. The importance of beta(3)-AR was verified when long-term treatment with hGH and AOD9604 in beta(3)-AR knock-out mice failed to produce the change in body weight and increase in lipolysis that was observed in wild-type control mice. However, in an acute experiment, AOD9604 was capable of increasing energy expenditure and fat oxidation in the beta(3)-AR knock-out mice. In conclusion, this study demonstrates that the lipolytic actions of both hGH and AOD9604 are not mediated directly through the beta(3)-AR although both compounds increase beta(3)-AR expression, which may subsequently contribute to enhanced lipolytic sensitivity.
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