Labrador and people divide the same obesity genes – a up-to-date study

Pippa lists at the oven of Aga chewing on a stick. At the age of only 12 weeks, this Labrador Retriever puppy looks cute, but unaware. But when she hears the word “cookies”, her whole behavior will change. The ears are punctured, it is immediately at the foot of the owner, staring at love, sitting and even clamorous.

We conducted a study to find out how genes have such a significant impact on why people (and dogs) become overweight. It was their reputation of greed that led us to focus on Labrador Retrievers. Genes are responsible for 40-70% human obesity – the rest is associated with life experience.

We separated DNA from saliva samples sent by interested pets owners. More than ten years after the arrival of the first dog Slobber on the post, The results of our study They are striking: dogs do not share the house with human owners, they also share the genes of obesity. Each of the five best genes that increased the risk of mass growth in labradors was also involved in human obesity.

Such a crossover is not amazing; Both dogs and people have evolved To deal with cycles of food abuse and hunger. Both have brain mechanisms that drive hunger and satiety to ensure food intake that meets our daily energy demand.

And although we often consider fat as a problem, it makes sense to have some – it is an energy reserve at a time when food is not enough. Genes affect these mechanisms, but how?

The answer is about the highly selective nature of dog farming. A side effect of dog breeding is that identifying genes that cause features – is extremely plain that cause features – They even like obesitywhich result from the net effect of many changes along our DNA.

As a veterinarian, I know that obesity is a real problem for many of my patients, which is why we study dogs both because of each other and as a “model” of human disease.

The genes we found were the most crucial thing in determining obesity in labradors, they were not a leader in genetic research of obesity in humans. They were rather wounds, with little influence on weight gain.

We are usually not interested, but the dog’s results told us that they can have a great impact on body weight and made them to examine them. This is true about our best labrador, Dennd1b obesity gene. Dogs that carried the problem version of this gene had about 8% more fat, but the effect in humans is only subtle.

It turns out that Dennd1B plays an unrecognized role in regulating the body weight of the brain, dogs and people. Leptin is a hormone made of fat cells in the body. More fat, more leptin.

It works in the brain by activating “melanocortic receptors” to reduce hunger and escalate energy consumption. The system drives food intake in times of hunger and reduces it when the body has good energy reserves.

We showed that Dennd1B is produced next to melanocortin receptors in the brain and changes their signaling.

We still have to find out about Dennd1B, but it was a great start, especially since it is extremely tough to find a genetic connection to ensure a molecular connection with how the gene works in the body. Although this is not the goal of the latest wave of obesity drugs, there are obesity drugs focused on melanocortic receptors, so there is a reality in understanding the nuances of this brain trail.

In addition to learning the Dennd1B function, we also assessed dogs in the study as a high or low risk of obesity associated with a greater number of genetic changes. We used the questionnaire, asking the owners to accept the number of appetite of their dogs, the level of their activity and the degree to which their owners constrained what they had.

This told us that the genetic risk was largely with an escalate in appetite-high risk dogs more often sought their owners to throw away the gold and ate almost everything.

Genes that make it tough to remain

Low risk dogs in our study were compact or only marginally overweight. But their owners do not get recognition – this group usually remained in a hearty weight, even if the owners did not pay much attention to how they regulated the diet and exercises of their dogs.

High risk dogs can be slim, but this is a much more tough job. These owners must be vigilant all the time to make sure that their feeds are not able to snacks and have to steel to resist “vast, brown eye treatment”, which is such an effective way to plead for food.

The same applies to people. If you are unlucky to get genes that make you susceptible to obesity, they manifest in greater appetite, which makes it tough to rely on excessive deepening. Slim people are not morally better – they just don’t have to exert enough will to stay in a hearty weight.

Should we try to get rid of these genes of obesity? Certainly not, and the reason why he brings us back to Pippy, focused on her feast. Dogs of guides in our study had a higher genetic risk than pets labradors.

Because they are the elite performers of the dog of dogs, maybe it gives us a hint of why greed became challenging in the labrador genome. “I love these dogs,” says the owner Chris, “because they are so simple to train – they will do everything for a biscuit.”