When Watson and Crick cracked the mystery of DNA, I don’t think they could have ever imagined how far-reaching the implications of this tiny double helix would be. The study of genetics has led scientists to some of the most profound revelations on the nature of life discovered by any of the major scientific disciplines.
That tradition continues with a new study, published today in the journal Cell Metabolism, that shows a genetic heritability of a particular mutation in the gene pro-opiomelanocortin, or POMC, which causes a disruption in the endorphin coding sequence of the body, leading to a propensity for heavier body weights, adiposity(the body’s inclination to store fat), and appetite increase.
The researchers took 310 Labrador retrievers and had them weighed by an independent veterinary professional who then assigned the dogs with a body condition score(BCS). This measure of canine obesity is used throughout the dog world to assess overall fitness level.
The authors of the study then examined candidate genes in the hypothalamic melanocortin pathway to determine if there were any mutations that were significantly distributed between the obese and lean groups of dogs.
They found that a specific deletion mutation in the POMC gene of 14 base pairs (adenine-cytosine, thymine-guanine) was found in 10/15 obese dogs and only 2/18 lean dogs. Showing a strong correlation between dog’s obesity and having the mutation.
The study goes on to show that the deletion mutation in the POMC gene causes a loss of production of β-MSH and β-endorphin, both linked to melanocortin receptors. Problems with melanocortin receptors in humans has been shown to correlate to obesity.
This research provides dog owners with some insight into why certain breeds may have a tendency towards obesity. It will allow the owner to consult with their veterinarian to construct a feeding schedule that will be beneficial for the dog in the long run.