HUMANS AND LABRADORS HAVE SIMILAR OBESITY GENES

We might have more in common with man’s best friend than previously thought.

Our research investigated how genetics significantly influences weight gain in both humans and dogs. We specifically chose Labrador retrievers for their well-known appetite tendencies. Genetics accounts for 40-70% of human obesity, with environmental factors responsible for the remainder.

Twelve-week-old Labrador puppy Pippa lounges beside the Aga, gnawing on a stick, appearing innocent and unassuming. But mention “biscuit,” and her transformation is immediate—ears alert, she positions herself at her owner’s feet, gazing upward attentively, sitting promptly, even barking on command.

We analyzed DNA from saliva samples provided by dog owners. A decade after receiving the first canine saliva specimen, our findings are remarkable: dogs share not just living spaces with their human companions but obesity-related genes as well. The five most significant genes increasing obesity risk in Labradors were all implicated in human obesity too.

This overlap isn’t surprising. Both species evolved navigating feast-and-famine cycles, developing brain mechanisms regulating hunger and satiety to match energy intake with requirements. While we often view fat negatively, it serves as a crucial energy reserve during food scarcity. But how exactly do genes influence these mechanisms?

The answer lies in selective dog breeding practices. An unintended benefit of dog breeding is the relative ease of identifying trait-causing genes—even for complex conditions like obesity that result from numerous DNA variations.

As a veterinarian, I recognize obesity as a significant health concern for many patients, motivating our study of dogs both for their welfare and as human disease models.

Interestingly, the genes we identified as most significant for Labrador obesity weren’t primary candidates in human obesity genetic research. Rather, they were secondary findings with minor effects on human weight regulation. Typically these wouldn’t warrant investigation, but our canine findings revealed their potential significance. This proved true with our top Labrador obesity gene, DENND1B. Dogs carrying the problematic variant showed approximately 8% higher body fat, though its effect in humans is subtle.

We discovered DENND1B plays a previously unrecognized role in brain regulation of body weight in both species. Leptin, produced by fat cells (more fat means more leptin), acts in the brain by activating melanocortin receptors to suppress hunger and increase energy expenditure. This system regulates food intake—increasing during scarcity and decreasing when energy reserves are adequate.

Our research demonstrated that DENND1B is produced alongside melanocortin receptors in the brain and modifies their signaling.

While much remains to learn about DENND1B, this represents significant progress, especially considering the challenges of connecting genetic associations with molecular mechanisms. Although not targeted by newest anti-obesity medications, some existing treatments do target melanocortin receptors, making deeper understanding of this brain pathway valuable.

Beyond exploring DENND1B function, we assessed dogs’ obesity risk scores based on multiple genetic variations. Using owner questionnaires rating canine appetite, activity levels, and feeding restrictions, we determined genetic risk primarily manifests through increased appetite—high-risk dogs more frequently begged for food, scavenged scraps, and showed indiscriminate eating habits.

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