# Olfactory Capacity and Obesity: A Narrative Review of the Literature
## 3 Results
### Studies on Animals and Insets  
Animal studies have shown that olfactory behavior and sensitivity are more active during fasting compared to a state of satiety [28; 29]. These changes are associated with an increase in orexigenic molecules (ghrelin, neuropeptide Y, and orexins) during fasting and, conversely, a decrease in anorexigenic molecules (insulin, cholecyst, and leptin) [17; 30].  
On the other hand, after food intake, olfactory sensitivity decreases, a process regulated by satiety signals [31]. Additionally, previous studies have demonstrated that impaired olfactory function correlates with overweight and obesity, suggesting that reduced olfactory function may delay satiety and lead to increased body weight [32]. Research suggests that the olfactory system is closely linked to neural systems that regulate food intake by  
Figure 2: Smell and hypothalamic regulation of energy balance.  
detecting metabolic states [33]. Moreover, the olfactory bulb contains receptors for various hormones and neuromodulators involved in food intake regulation, including insulin, leptin, ghrelin, orexin, and endocannabinoids [33] (Figure 1). Thus, the sense of smell is potentially modulated in response to changing levels of molecules such as ghrelin, orexins, neuropeptide Y, insulin, leptin, and cholecystinin [33]. While it is known that these peptides and their receptors modulate the olfactory system, how changes in adiposity influence olfactory function remains unclear.  
Changes in taste perception have also been observed across different body mass index (BMI) levels [10; 34]. However, it remains unclear how olfactory abilities are related to adiposity (or vice versa) by directly impacting eating behavior [35; 36; 37]. Currently, much of the knowledge about pro-olfactory neuroanatomical pathways comes from animal models. It is hypothesized that odor-evoked responses originate from first-order neurons in the nasal mucosa, which project to the olfactory bulb (OB). This olfactory information is then transmitted to the anterior olfactory nucleus, piriform cortex, and amygdala, which together are considered the primary olfactory cortex. This complex neural network plays a fundamental role in individual olfactory performance, odor-driven behaviors, and food consumption [17]. To some extent, this gap in knowledge reflects the relative complexity of the mammalian olfactory system [32; 38; 39].  
An animal study showed that mice with conditional ablation of mature olfactory sensory neurons (OSNs) were more resistant to diet-induced obesity and showed increased thermogenesis in brown and inguinal fat. Loss of sense of smell after obesity not only prevented weight gain, but also improved fat mass and insulin resistance. The results suggest that reducing olfactory input activates the sympathetic nervous system, causing lipolysis to occur in adipocytes. In contrast, ablation of the IGF1 receptor in OSNs improved olfactory performance and increased adiposity and insulin resistance. These findings reveal a dual role of the olfactory system in the regulation of energy homeostasis [40].  
A study conducted on Drosophila melanogaster flies showed that defects in olfactory sensory neurons reduced food intake, increased triglyceride levels, enhanced resistance to hunger and desiccation, and decreased cold stress. Additionally, the disruption of the neuropeptide F receptor or insulin signaling in olfactory sensory neurons also modulated food intake and the stress response to hunger [41]. Moreover, reduced insulin signaling in hungry flies triggers short neuropeptide F receptor (sNPFR) production to increase sNPF signaling, enhancing the response to odors [30].