# Kisspeptin and bone turnover

> Bone turnover in the Meno Peptides notebook — Meno Peptides looks closely at kisspeptin bone markers in healthy men and a separate mouse bone-loss experiment, with no menopause benefit assumed.

This is the chapter whose small print most deserves a wide margin: who was studied, and what moved in the blood.

## The acute study in healthy men

In an [acute kisspeptin study in 26 healthy eugonadal men](https://pubmed.ncbi.nlm.nih.gov/35244717/), researchers measured bone-formation markers during a 90-minute intravenous infusion. They reported a 20.3% maximal rise in total osteocalcin and a 24.3% rise in carboxylated osteocalcin.

Osteocalcin is the bone-formation marker being measured here. For this experiment, the particular measurements deserve priority over a broad phrase such as bone support. They give the experiment a defined result, in healthy men, over a brief observation period.

I initially underestimated this experiment. Its narrowness seemed like a weakness until I considered the precision of the question: can administering kisspeptin alter these markers acutely? The reported increases make a possible skeletal action worth pursuing. That is the research lead that interests me.

![Two osteocalcin increases shown side by side for the acute study in healthy men](images/bone-markers.svg)

*Bone-formation markers from the [acute human experiment](https://pubmed.ncbi.nlm.nih.gov/35244717/); the percentages refer to different osteocalcin measures.*

## Bone removal in the mouse experiment

A separate [mouse study examined kisspeptin-10 and osteoclast activity](https://pubmed.ncbi.nlm.nih.gov/38346942/). Osteoclasts are the cells involved in bone resorption, the removal of bone. Kisspeptin-10 binding to Gpr54 upregulated Dusp18 in the reported pathway and suppressed osteoclast activity. Mice lacking Kiss1, Gpr54 or Dusp18 showed osteoclast hyperactivation and bone loss; kisspeptin-10 abrogated bone loss in vivo.

That is a mouse result. The bone-removal findings draw me into this mouse experiment; the human experiment measured markers of formation. The papers approach skeletal biology from different directions. I would be cautious about flattening them into a single percentage or a single advertised benefit.

## The menopause question

The [human study concerns an acute response in healthy men](https://pubmed.ncbi.nlm.nih.gov/35244717/), and the [bone-loss intervention concerns mice](https://pubmed.ncbi.nlm.nih.gov/38346942/). A study enrolling postmenopausal women would have to supply its own results.

I am left with concrete questions. Would a change in these markers persist? Would the bone-loss findings translate into a useful outcome in women? Those questions make this a worthwhile chapter to follow, even while the answer for menopause remains unwritten.

That separation also clarifies my enthusiasm. The biology excites me; a benefit for a particular group still needs evidence from that group. On kisspeptin and bone, that is as far as my confidence currently reaches. The [reproductive-signalling chapter](/kisspeptin-signals) supplies some of the molecule's less tidy history.

---

At Meno Peptides I pursue the unfinished menopause chapter in published research, with curiosity to spare and no medical advice to offer.