Scientists have now explained how, over the last century, humans have grown taller and reached sexual maturity earlier. Scientists have identified how the MC3R receptor in the brain senses the nutritional situation of the body, regulates puberty and growth rate in children, and promotes lean muscle mass. The research was published in the scientific journal Nature. The average height climbed by roughly 10 cm in the United Kingdom and up to 20 cm in other countries during the twentieth century. While scientists have long speculated that this phenomena could be linked to improved food security for pregnant women and children, the exact mechanism by which the body perceives its nutritional status and converts that information into growth and sexual maturation has remained a mystery.
The hormones leptin, produced in adipose (fat) cells, and insulin, released in response to changes in blood sugar levels, were already known to send messages to the brain to reflect the body’s nutritional situation. These hormones act on a tiny set of neurons that create signals termed melanocortins in the hypothalamus, a portion of the brain. Melanocortins bind to a number of different receptors, two of which are found in the brain. The melanocortin 4 receptor (MC4R), for example, has been found to regulate hunger, and a loss of MC4R leads in obesity; however, the MC4R system does not regulate the influence of diet on puberty growth and timing.
Now, a study led by researchers from the University of Cambridge‘s MRC Metabolic Diseases Unit and MRC Epidemiology Unit (both part of the Wellcome-MRC Institute of Metabolic Science) has discovered a role for the brain’s other melanocortin receptor, known as the melanocortin 3 receptor, with collaborators from Queen Mary University of London, University of Bristol, University of Michigan, and Vanderbilt University (MC3R). They discovered that the MC3R system regulates the release of critical hormones that regulate growth and sexual development in response to dietary signals.
To demonstrate the link in humans, the researchers looked for persons with naturally occurring genetic mutations that affect the function of the MC3R in the UK Biobank’s half-million volunteers. They studied a group of a few thousand people who had various mutations in the MC3R gene and discovered that they were on average shorter and entered puberty later than those who did not have the mutation. They found 812 women with the identical mutation in one of their two copies of the MC3R gene, for example. The receptor’s capacity to function was only partially harmed by this mutation. Despite this minor effect, women who carried the mutation were 4.7 months older at puberty on average than those who did not.
People with MC3R mutations were shorter and had less lean tissue, such as muscle, but it had no effect on how much fat they carried. They analysed over 6,000 participants from the Avon Longitudinal Study of Parents and Children (ALSPAC) to validate these findings in children, and found six children with MC3R mutations. Throughout childhood, the six children were shorter and had reduced lean mass and weight, indicating that this influence begins early in life. Only one of the two copies of the gene was mutated in all of the persons identified in these studies. Finding mutations in both copies of the gene is extremely rare, but the researchers were able to identify 1 individual with a very harmful mutation in both copies of the gene in another cohort of the Genes and Health project. This person was exceedingly short and did not reach puberty until he was 20 years old.
The researchers conducted investigations in mice to confirm that the MC3R pathway operates across species since the same phenomena linking adequate nutritional body storage to reproductive maturity is evident throughout the animal kingdom. Dr. Roger Cone’s study at the University of Michigan, which had previously proven a role for the MC3R in the control of growth and lean mass in mice, discovered that whereas normal mice shut off their reproductive cycle when they went without food, mice without the MC3R did not. This proved that MC3R is an important component of how the nutritional condition regulates the generation of sex hormones.
Professor Sir Stephen O’Rahilly, a senior author on the study and Director of the University of Cambridge’s MRC Metabolic Diseases Unit, said: “This finding demonstrates how the brain can detect nutrients and use that information to make subconscious decisions that affect our growth and sexual development. The discovery of the brain route that converts nutrients into growth and puberty addresses a century-long riddle for scientists: the global phenomena of increasing height and decreasing age at puberty.
“Our findings have obvious practical implications for MC3R mutation testing in children with substantial growth and pubertal development deficits.
“This study could have a broader impact than only infant development and reproductive health. The loss of lean mass, especially muscle, is linked to a variety of chronic conditions, resulting in frailty. Simple dietary supplements, such as protein-rich drinks, have little effect on this. The discovery that the MC3R pathway’s activity affects a person’s lean mass suggests that future study should look into whether medications that specifically activate the MC3R can assist patients redirect calories into muscle and other lean tissues, perhaps enhancing their physical function.”
Professor John Perry, a senior author on the paper from the University of Cambridge’s MRC Epidemiology Unit, said: “Human genetics has never been more intriguing. We can now comprehend fundamental biological processes that have remained obscure until now by analysing the DNA sequences of vast numbers of research participants. We will continue to find new insights and understand the mechanisms behind human growth and metabolic disorders by integrating these research with work in cellular and animal models.”
The National Institute for Health Research, the UK Medical Research Council, and Wellcome financed the study.
Dr. Rob Buckle, Chief Science Officer of the Medical Research Council, one of the research’s funders, said: “These findings have the potential to pave the way for future management of growth and puberty disorders, as well as improvements in the health of those suffering from frailty due to chronic conditions. This research demonstrates the importance of long-term investments in large UK population cohorts and multidisciplinary research to uncover the causes of human health and disease.”
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