The Labrador retriever – easy to train as a service dog, including living with the blind, is the most popular canine breed for work and has been so for many years. In the US, it remains an extremely popular breed, but fashion has raised the tiny, wrinkle-faced pug to number one.
But now, new research at the University of Cambridge in the UK has discovered that around a quarter of Labrador retrievers face a double-whammy of feeling hungry all the time and burning fewer calories due to a genetic mutation. This obesity-driving combination means their owners must be very strict about feeding and exercising their pets to keep them slim.
The mutation is in a gene called POMC that plays a critical role in hunger and energy use. Around 25% of Labradors and 66% of flat-coated retrievers have this mutation that profoundly changes the way retrievers behave around food. Although they don’t need to eat more to feel full, they are hungrier between meals.
In addition, dogs with the POMC mutation were found to use around 25% less energy at rest than dogs without it, meaning they don’t need to consume as many calories to maintain a healthy body weight.
“We found that a mutation in the POMC gene seems to make dogs hungrier. Affected dogs tend to overeat because they get hungry between meals more quickly than dogs without the mutation,” said Dr. Eleanor Raffan, a researcher in the university’s physiology, development, and neuroscience department who led the study.
“People are often rude to owners of fat dogs, blaming them for not properly managing their pet’s diet and exercise, but we’ve shown that Labradors with this genetic mutation are looking for food all the time, trying to increase their energy intake. It’s very difficult to keep these dogs slim, but it can be done,” Raffan said.
Genetic mutation in humans and dogs
The POMC gene and the brain pathway it affects are similar in dogs and humans. The new findings are consistent with reports of extreme hunger in humans with POMC mutations, who tend to become obese at an early age and develop a host of clinical problems as a result. Drugs currently in development for human obesity, underactive sexual desire, and certain skin conditions target this brain pathway, so understanding it fully is important.
The POMC mutation was found to alter a pathway in the dogs’ brains linked with body-weight regulation. The mutation triggers a starvation signal that tells their body to increase food intake and conserve energy, despite this being unnecessary.
The results are published today in the journal Science Advances under the title, “Low resting metabolic rate and increased hunger due to β-MSH and β-endorphin deletion in a canine model.”
The researchers say owners can keep their retrievers distracted from this constant hunger by spreading out each daily food ration, for example, by using puzzle feeders or scattering the food around the garden so it takes longer to eat.
In the study, 87 adult pet Labs – all a healthy weight or moderately overweight – took part in several tests, including the “sausage in a box” test. First, the dogs were given a can of dog food every 20 minutes until they chose not to eat anymore. All ate huge amounts of food, but the dogs with the POMC mutation didn’t eat more than those without it. This showed that they all feel full with a similar amount of food.
Next, on a different day, the dogs were fed a standard amount of breakfast. Exactly three hours later they were offered a sausage in a box and their behavior was recorded; the box was made of clear plastic with a perforated lid, so the dogs could see and smell the sausage, but couldn’t eat it. The researchers found that dogs with the POMC mutation tried significantly harder to get the sausage from the box than dogs without it, indicating greater hunger.
The dogs were then allowed to sleep in a special chamber that measured the gases they breathed out. This revealed that dogs with the POMC mutation burn around 25% fewer calories than dogs without it.
A mutation in the POMC gene in dogs prevents the production of two chemical messengers in the dog brain, beta-melanocyte stimulating hormone (β-MSH) and beta-endorphin, but does not affect the production of a third, alpha-melanocyte stimulating hormone (α-MSH).
Further laboratory studies by the team suggest that β-MSH and beta-endorphin are important in determining hunger and moderating energy use, and their role is independent of the presence of α-MSH. Based on research in rats, this challenges the previous belief that early onset human obesity due to POMC mutations is caused only by a lack of α-MSH.