(Illustrated by Wang Chia-Chen)

Labradors and humans share the same obesity genes – new study

刊出日期 2025.03.27

‌
‌
‌
‌
‌

We led a study to find out how genes have such a significant influence on why humans (and dogs) become overweight. It was their reputation for greediness that led us to focus on labrador retrievers. Genes are responsible for 40%-70% of human obesity – the rest is related to life experience.
We extracted DNA from samples of saliva sent in by interested pet owners. More than ten years after the first dog slobber arrived in the post, the results of our study are striking: dogs don’t just share a home with their human owners, they share obesity genes too. Each of the top five genes that increased the risk of weight gain in labradors were also implicated in human obesity.
Such crossover is not astonishing; both dogs and humans evolved to deal with cycles of food glut and famine. Both have brain mechanisms that drive hunger and satiety to ensure food intake meets our daily energy requirements.
And although we often think of fat as a problem, it does make sense to have some – it is an energy reserve to draw upon in times when food is scarce. Genes influence those mechanisms, but how?
The answer lies in the highly selective nature of dog breeding. A side effect of dog breeding is that it is remarkably straightforward to identify the genes which cause traits – even those like obesity, which come from the net effect of lots of changes along our DNA.
As a vet, I know obesity is a real problem for many of my patients, so we study dogs both for their own sake and as a “model” of human disease.
The genes we found were most important in determining obesity in labradors were not frontrunners in genetic studies of obesity in people. Rather, they were also-rans, with a minor impact on human weight gain.
Normally they wouldn’t interest us, but the dog results told us they can have a big effect on body weight and made them worth investigating. That was true of our top labrador obesity gene, DENND1B. Dogs who carried the problem version of this gene had around 8% more body fat, but the effect in humans is only subtle.
It turns out that DENND1B has a previously unrecognised role in the brain’s regulation of body weight, for dogs and humans. Leptin is a hormone produced from fat cells in the body. More fat, more leptin.
It acts in the brain by activating “melanocortin receptors” to reduce hunger and increase energy use. The system drives food intake in times of starvation and reduces it when the body has good energy reserves.
We showed DENND1B is produced alongside melanocortin receptors in the brain and alters signalling by them.
There is a lot we still need to learn about DENND1B, but this was a great start, especially since it is notoriously difficult to go from finding a genetic association to providing a molecular link to how the gene is acting in the body. Although not the target of the latest wave of anti-obesity drugs, there are obesity medicines which target melanocortin receptors, so there is real value in understanding the nuances of that brain pathway.
As well as learning about DENND1B function, we also scored dogs in the study as having a high or low obesity risk relating to a larger number of genetic changes. We used a questionnaire asking owners to put a number on their dogs’ appetite, their activity levels and the degree to which their owners limited what they got to eat.
This told us that the genetic risk was largely down to increased appetite – our high-risk dogs were more likely to pester their owners for food, scavenge for scraps, and would eat pretty much anything.
Genes making staying slim harder
Low-risk dogs in our study were all slim or only marginally overweight. But their owners don’t get the credit – this group tended to stay at a healthy weight even if owners didn’t pay much attention to how they regulated their dogs’ diet and exercise.
High-risk dogs can be kept slim, but it is much harder work. These owners need to be vigilant at all times to ensure their chow-hounds don’t get opportunities to snack and must steel themselves to resist the “big, brown eye treatment” that is such an effective way to beg for food.
The same is true in people. If you are unlucky enough to get genes that make you prone to obesity, they manifest in greater appetites, making it harder to resist overindulging. Slim people aren’t morally superior – they just don’t need to exert as much willpower to stay at a healthy weight.
So should we try to get rid of these obesity genes? Certainly not, and the reason why brings us back to Pippa, fixated on her treat. The guide dogs in our study had a higher genetic risk than pet labradors.
Since they are the elite performers of the canine world, this maybe gives us a clue as to why greediness has become hard-wired into the labrador genome. “I love these dogs,” says owner Chris, “Because they’re so easy to train – they’ll do anything for a biscuit.”
（To read the Chinese version of this article, please click: 〈新研究指出：拉不拉多和人類擁有相同的肥胖基因〉）
＊This article is republished from The Conversation under a Creative Commons license. Read the original article.

About The Conversation
The Conversation was founded in Melbourne, Australia in 2011. It is a unique collaboration between academics and journalists that in a decade has become the world’s leading publisher of research-based news and analysis.

常用關鍵字

# 健康 # 國際 # 動物 # 英文新聞 # 科學

誰幫我們完成這篇文章

艾莉諾．拉芬（Eleanor Raffan）

作者

University Assistant Professor in Systems Physiology, University of Cambridge. Veterinary surgeon (BVM&S, 2002) with postgraduate training and specialism in small animal medicine (Royal College of Veterinary Surgeons Specialist). PhD from Cambridge Uni 2014 in the genetics of human metabolic disease. Since 2014 I have run my own research group in Cambridge, first at the Institute of Metabolic Science then as an assistant professor at the Dept. Physiology, Development and Neuroscience, both University of Cambridge. 劍橋大學系統生理學助理教授。於2002年獲得獸醫學士學位的專科獸醫，並且完成了皇家獸醫外科學院提供的小型動物醫學專業研究所訓練。2014年，我在劍橋大學獲得博士學位，研究的是人類代謝疾病的遺傳學。自2014年開始，我在劍橋大學領導自己的研究團隊，最初是在代謝科學研究所，後來又轉任生理學、發育與神經科學系的助理教授。

了解更多