Frequency-tagged EEG reveals category-selective responses to face race.

Obesity is one of the most prevalent and pressing health concerns in companion animals, affecting an estimated 30–60% of pet dogs globally (). Excessive adiposity in dogs often visibly impairs normal behavior and physical function. Obese dogs are frequently reported to exhibit reduced willingness to exercise, difficulty rising or moving comfortably, and a diminished capacity to engage in natural behaviors such as play, exploration, and social interaction. In addition to these welfare concerns, obesity is now recognized as a complex and chronic inflammatory condition that significantly impairs quality of life and predisposes animals to a spectrum of co-morbidities, such as orthopedic disease, insulin resistance, cardiovascular dysfunction, cancer, and steatotic liver disease (, ). Obesity has been linked to reduced lifespan, with obese dogs living up to 1.5 years less than their lean counterparts (). Moreover, the financial and psychological burden of managing obesity-related diseases in pets can be substantial, disproportionately affecting households with lower socioeconomic status (). Current large-scale epidemiological studies have highlighted that the risk of being overweight or obese varies considerably by life stage, breed, and reproductive status (, ). Recent findings in Labrador retrievers have identified DENND1B as a key obesity-associated gene that modulates melanocortin 4 receptor (MC4R) signaling, a pathway central to appetite regulation in both dogs and humans. The same gene is also linked to body mass index in large human cohorts and severe childhood obesity, highlighting a shared genetic basis across species, positioning the dog as a powerful translational model (). These genetic predispositions, combined with lifestyle factors such as feeding and physical inactivity, help explain the rising prevalence of obesity even in juvenile life stages (). While obesity in dogs has been associated with systemic inflammation, insulin resistance, dyslipidemia, and alterations in gut microbiota composition (, , ), the mechanistic understanding of these processes in companion animals remains limited. In dogs, high-fat diets have been linked to colonic microbiota deviations characterized by Proteobacteria overgrowth, mucosal inflammation, and increased epithelial apoptosis, suggesting early disruption of gut immune homeostasis. However, pathophysiological mechanisms underlying obesity and its comorbidities have been extensively delineated in humans and rodent models but not in companion animals. Microbiota deviations combined with disruption of gut barrier integrity lead to microbial translocation, particularly lipopolysaccharide (LPS), and activation of pro-inflammatory signaling cascades (e.g., TLR4 - NF-κB) that drive systemic inflammation and hepatic dysfunction (). Bile acid dysregulation has emerged as a central driver of metabolic disease, with altered bile acid pools and impaired FXR and TGR5 signaling linked to increased intestinal permeability, dysregulated lipid and glucose metabolism, reduced GLP-1 secretion, and exacerbation of chronic inflammation (). Whether such an integrated gut–liver–metabolic axis involving bile acid signaling operates similarly in dogs remains to be established.