Labrador Retrievers are beloved for their playful nature and loyalty, but they’re also notorious for their seemingly endless hunger. Recent research has shed light on the genetic factors contributing to this insatiable appetite and their predisposition to obesity, findings that could have implications for both canine and human health.
Labradors are one of the most popular dog breeds globally, often employed as service animals due to their intelligence and trainability. However, their love of food often leads to obesity, a growing concern for dogs, mirroring the trend in humans. University of Cambridge scientist Eleanor Raffan and her team have been investigating the genetics of obesity and metabolic disease in dogs, focusing particularly on Labradors and their close relative, the Flat-Coated Retriever.
A 2016 study by Raffan’s team identified a link between obesity in these breeds and a mutation in the gene responsible for producing the protein pro-opiomelanocortin (POMC). This mutation appears to delete a portion of the POMC gene in affected dogs, a condition found in a quarter of Labradors and two-thirds of Flat-Coated Retrievers. Their latest research, published in Science Advances, delves into the mechanics of how these POMC mutations contribute to obesity in retrievers.
The researchers conducted a series of experiments with 87 adult Labradors, ranging in weight from healthy to slightly overweight, with some carrying the POMC mutation. In one experiment, dogs were presented with a sausage inside a transparent box with holes, allowing them to see and smell the treat. POMC-mutated Labs demonstrated greater persistence in trying to access the sausage compared to dogs without the mutation.
Another experiment involved offering the dogs unlimited food until they were satiated. Surprisingly, there was no significant difference in the amount consumed between the two groups. However, a third experiment revealed that POMC-mutated dogs had a lower resting metabolic rate, burning approximately 25% fewer calories.
These findings suggest a two-pronged effect of the POMC mutation: an increased desire to eat, coupled with a reduced calorie expenditure. This combination creates a predisposition to weight gain, making it crucial for owners of affected dogs to manage their diet and prevent access to extra food.
The absence of the POMC gene appears to hinder the production of two hormones in the brain: beta-melanocyte stimulating hormone (β-MSH) and beta-endorphin. These hormones are also present in humans, and genetic disorders linked to dysfunctional POMC mutations are known to significantly increase the risk of obesity. While lab mice are typically used to study such genes, their POMC function differs from that in dogs and humans, making the study of POMC-deficient Labradors potentially valuable for understanding obesity in humans.
While POMC is a key factor, it’s likely not the only gene contributing to obesity in Labradors. Raffan and her team are continuing their research to identify other genetic influences. These ongoing studies promise to further unravel the complex interplay of genetics and metabolism in canine obesity, potentially leading to improved strategies for weight management in both dogs and their human companions.
