Lipocalin 2 Deficiency Diminishes the Metabolic Effect of Ketogenic Diet in Female Mice

Obesity is a worldwide public health concern, and prevalence in the United States continuously increasing. Treatment of obesity ranges from dietary approaches to gastric surgery; there no one-size-fits-all approach. In recent years, ketogenic diet (KD) has become popular approach for weight loss metabolic promotion. The main mechanism caused by this promote body use fat as its primary form energy drastically reducing carbohydrate intake. Understanding molecular mechanisms that contribute effect KD critical determining appropriateness At cellular level, been known activate mitochondrial function thermogenesis thermogenic adipose tissue stimulate utilization. However, specific molecules genes are involved regulation remain largely unknown. Lipocalin-2 (LCN2) characterized an adipokine our group others. previous studies, LCN2 suggested regulator metabolism. knockout (KO) mice exhibit impaired well exacerbated diet-induced inflammation. It interest know if plays role KD-induced study, wild type (WT) KO female at 10 months age were fed either or regular chow (RCD) weeks, followed assessments including food intake, weight, mass, histology tissues. Our results showed was significant difference daily intake between WT under RCD KD. we did find thatafter weeks KD, had ~15% significantly decreased inguinal gonadal mass when compared with control RCD. Interestingly, on not observed mice; depots different RCD- KD-fed mice. From liver tissue, led increased small adipocytes mice, suggesting healthy remodeling tissue. Intriguingly, completely absent Moreover, found lipid accumulation This reflects utilization fatty acids production ketones. More strikingly, resulted more profoundly which may be due dysfunction defective acid oxidation absence LCN2. Together, demonstrate deficiency diminishes suggests regulating metabolism, thermogenesis, other unknown physiological activities important leads improved health.