Study wrapper · #587
Stimulation of endogenous pulsatile growth hormone secretion by activation of growth hormone secretagogue receptor reduces the fat accumulation and improves the insulin sensitivity in obese mice.
Editor's note
In hyperphagic obese mice (melanocortin-4-receptor knockouts) fed a matched diet, researchers infused hexarelin, a synthetic GHS-receptor agonist, for three to four weeks. Hexarelin increased pulsatile growth-hormone secretion without raising basal GH, and this was accompanied by increased fat breakdown and oxidation, reduced liver fat synthesis, less visceral fat, and improved whole-body insulin sensitivity, all without changing IGF-1 or insulin levels. The framing, that stimulating the body's own pulsatile GH may avoid some of the glucose side effects seen with GH injections, is the interesting angle. Caveats are substantial: this is a single genetic obesity model over a few weeks, glucose tolerance itself did not change, and the mechanism is inferred from tissue gene expression. These are preclinical findings; human data are needed before any clinical conclusions can be drawn.
Plain-language abstract
Researchers studied hexarelin, a lab-made peptide that triggers the body's own growth hormone, in obese mice that overeat because of a genetic change. Mice received a steady infusion of hexarelin or an inactive control for three to four weeks while being fed equal amounts of food. Hexarelin boosted the natural pulsing release of growth hormone but not its baseline level. Treated mice burned more fat, made less fat in the liver, carried less belly fat, and used insulin more effectively, yet their insulin and IGF-1 levels did not change and their overall glucose tolerance stayed the same. The authors suggest that nudging the body's own growth hormone might improve fat handling while avoiding some downsides of injected growth hormone. These are preclinical findings in a single mouse model; human studies would be needed before drawing conclusions.