Researchers at Columbia University Medical Center conducted a mouse study that showed that a hormone secreted by bone cells can suppress appetite. This finding adds a known class of bone-secreting hormones and reveals a previously unknown appetite-regulating mechanism and provides new insights into the therapeutic targets of obesity, type 2 diabetes and other metabolic disorders.
Discovery of bone secretion hormone
In 2007, a team led by Professor Gerard Karsenty, director of the Center for Genetics and Development at Columbia University Medical Center, first discovered that bones are endocrine organs and regulate energy metabolism by releasing hormones called osteocalcin. Prior to this study, bones were known to secrete at least two hormones, FGF23 and osteocalcin, which help regulate kidney function and glucose homeostasis.
A clue to the discovery of appetite-associated hormones in bones came from 2010. The author of this article, Professor Stavroula Kousteni, found that inhibition of the FOXO1 gene in mouse osteoblasts resulted in less eating and improved glucose tolerance in mice. Since osteocalcin does not regulate appetite, Professor Kousteni believes that other unknown bone hormones are involved in this process.
Lipocalin secreted by bone is involved in suppressing appetite
In the study, researchers at the Columbia University Medical Center found that FOXO1-deficient osteoblasts expressed abnormally high amounts of lipocalin 2 . This study found a previously unknown effect of lipocalin 2. Previously, it was thought to be a small signal molecule secreted by adipose tissue, but its level in osteoblasts was more than 10 times higher than that of adipose tissue.
In the study, mice experimented with lipocalin 2-deficient mice by adipocytes or osteoblasts showed that lipocalin 2 is mainly secreted by osteoblasts and reduces appetite and body weight.
Lipocalin 2 affects not only normal-weight mice, but also the appetite and body weight of obese mice due to lack of leptin receptor and leptin signaling. In both types of mice, lipocalin 2 inhibits their appetite, improves overall metabolism and reduces body weight.
The researchers confirmed that lipocalin 2 can cross the blood-brain barrier. In the brain, this protein binds to and activates melanocortin 4 receptor (MC4R) neurons in the hypothalamus. The hypothalamus is the primary brain region that regulates appetite, and MC4R neurons are involved in triggering appetite suppression.
The clinical application prospect of this discovery
Professor Stavroula Kousteni said: "In recent years, our research with other units has shown that bone is an endocrine organ that produces hormones that affect brain development, glucose balance, kidney function and male fertility, and this study is a bone hormone. Provides a key new feature: appetite suppression, which may open the door to new treatments for metabolic diseases."
In an analysis of patients with type 2 diabetes, the researchers found that levels of lipocalin 2 in the blood were inversely related to body weight and blood A1c levels (blood A1c levels are measures of blood glucose). This preliminary finding is encouraging. Professor Kousteni said: "In other words, patients with higher levels of lipocalin 2 have lower body weight and better glucose balance."
She noted: "It is hoped that lipocalin 2 may have the same effect in humans, and our findings can be translated into possible therapies for the treatment of obesity and other metabolic disorders."
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