N.B.: Different languages can express different contents  -  (Italiano - English)


Bone was recently found to be part of the endocrine system: it releases hormones into the blood (2017-05-23)

Bone has recently emerged as a pleiotropic endocrine organ that secretes at least two hormones, FGF23, which regulate kidney function and osteocalcin, which regulate glucose homeostasis.

Researchers now identified, through molecular and genetic analyses in mice, lipocalin 2 (LCN2) as an osteoblast-enriched, secreted protein.

Lipocalin 2 is released into the blood by osteoblasts (the bone forming cells), crosses the blood-brain barrier, binds to the melanocortin 4 receptor (MC4R) in the paraventricular and ventromedial neurons of the hypothalamus, and activates a signaling pathway that suppresses appetite.

After a meal, Lipocalin 2 levels in the serum of mice rapidly increase, and this increase is required for suppression of appetite after eating.

Loss and gain-of-function experiments in mice demonstrate that osteoblast-derived LCN2 maintains glucose homeostasis by inducing insulin secretion and improves glucose tolerance and insulin sensitivity.

In addition, osteoblast-derived LCN2 inhibits foodintake.

Study author Stavroula Kousteni, Associate Professor of Medicine in Physiology and Cellular Biophysics of Columbia University thinks that all hormones that have a function in rodents also have the same function in humans.
For Lipocalin 2, researchers show that serum levels inversely correlate with body weight and the long-term blood sugar marker HbA1c in type 2 diabetes mellitus patients.

Also, there is evidence in the literature that Lipocalin 2 serum levels increase in lean humans after a meal, just as we observed in mice.

All these observations are indication of a similar type of regulation and function in humans.

These results identify LCN2 as a bone-derived hormone with metabolic regulatory effects, which suppresses appetite in a MC4R-dependent manner, and show that the control of appetite is an endocrine function of bone.

For more information
MC4R-dependent suppression of appetite by bone-derived lipocalin 2

Columbia University Medical Center
Department of Phisiology and Cellular Biophysics