Study wrapper · #220
Growth hormone (GH)-independent stimulation of adiposity by GH secretagogues.
Editor's note
A mouse study with a counterintuitive result worth flagging. GH itself is lipolytic, so one might expect GH secretagogues to reduce fat. Instead, twice-daily ipamorelin (and GHRP-6) increased body fat in both GH-deficient (lit/lit) and GH-intact mice, alongside higher serum leptin and food intake, an effect that occurred independent of GH. The authors attribute the fat gain partly to increased feeding, consistent with the appetite-stimulating (orexigenic) side of GHS-R1a activation. This is a useful corrective to the common assumption that these peptides drive fat loss: in this model the net effect on adiposity went the other way. Caveats are the usual ones, a rodent model, short duration, and mechanisms in mice need not map to humans. For Ipamorelin and GHRP-6, which lack controlled human body-composition trials, this is a mechanistic signal, not a clinical outcome. Human data are needed before conclusions can be drawn.
Plain-language abstract
Growth hormone tends to break down fat, so scientists tested whether drugs that raise growth hormone, the peptides ipamorelin and GHRP-6, would reduce body fat in mice. They gave the peptides twice daily by injection under the skin to two kinds of mice: those that cannot make normal growth hormone and those with normal growth hormone. Unexpectedly, ipamorelin caused a small (about 15%) rise in body weight and increased fat-pad size in both groups. Body-fat scans confirmed that two weeks of either peptide raised relative body fat in the normal mice. Growth hormone alone did the opposite, lowering fat in the deficient mice. The peptides, but not growth hormone, also raised the appetite-related hormone leptin and increased how much the mice ate. The researchers concluded that these peptides can increase body fat through a route that does not depend on growth hormone, likely by boosting appetite. This is an animal study and does not show what happens in people.