The findings, based on an animal model, reveal that the absence of this protein leads to an early failure in appetite regulation and disrupts lipid metabolism in several tissues. This increases the risk of developing obesity – a global health issue linked to cardiovascular disease, diabetes and other metabolic disorders.

The study was coordinated by UIC Barcelona’s Neurolipids Group, led by Núria Casals and Rosalía Rodríguez, in collaboration with researchers from Laura Herrero’s group at the University of Barcelona, as well as other teams within the Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición (Biomedical Research Centre in Physiopathology of Obesity and Nutrition) (CIBEROBN).

Titled “CPT1C deficiency in SF1 neurons impairs early metabolic adaptation to dietary fats, leading to obesity”, the study explores how the brain senses nutrients and adjusts the body’s metabolic functions accordingly. “We found that without CPT1C, hypothalamic neurons are unable to properly detect fatty acids, which triggers imbalances in hunger regulation and metabolism,” explains researcher Núria Casals.  “As a result, mice lacking this protein accumulate body fat more easily, even though they eventually normalise their food intake and maintain a steady energy expenditure.”

The research team also observed that the lack of CPT1C not only alters how SF1 neurons perceive lipids, but also leads to an increase in endocannabinoids in the hypothalamus and a disruption of the melanocortin system – two key mechanisms in appetite and weight control. “These findings position CPT1C as a critical lipid sensor in maintaining energy balance and preventing obesity in the context of high-calorie diets,” says Laura Herrero, group leader at CIBEROBN.