Oral fat sensitivity (OFS), the ability to taste fat, is associated with eating habits in humans, including daily fatty food consumption; namely, proper OFS is important for health. In addition, lifestyle factors, such as stress and sleep, may affect fat intake. However, correlations between OFS, stress management, and sleep are largely unknown. Thus, we investigated the associations of OFS with lifestyle factors regarding stress management and daytime sleepiness in healthy young adult men. We measured OFS, sensitivities for three prototypical tastes (sweet, salty, and sour), and BMI in 22 subjects (27.2 ± 6.0 years), who also completed a self-reported questionnaire on health, including lifestyle-related questions. The correlations of taste sensitivities with stress management and daytime sleepiness were analyzed. We thus found that the number of mentors for personal concerns (a question regarding stress management, social support) was positively associated with OFS (P = 0.041), but not the other taste sensitivities. In contrast, other lifestyle factors related to stress management (frequency of relaxation, frequency of eating when irritated or worried, and degree of satisfaction with one's sleep) and daytime sleepiness were not significantly associated with OFS, similar to that observed for other tested taste sensitivities. These results characterize the unique association of OFS with the degree of social support in healthy young men and provide novel insights into the nature of individual OFS differences. Thus, measuring the degree of social support may be helpful for the evaluation of OFS impairment, thereby contributing to the prevention of stress-induced overeating.

This study evaluated the mechanism of temperature-controlled repeated thermal stimulation (TRTS)-mediated neuronal differentiation. We assessed the effect of SP600125, a c-Jun N-terminal kinase (JNK) inhibitor, on neuronal differentiation of rat PC12-P1F1 cells, which can differentiate into neuron-like cells by exposure to TRTS or neurotrophic factors, including bone morphogenetic protein (BMP) 4. We evaluated neuritogenesis by incubating the cells under conditions of TRTS and/or SP600125. Cotreatment with SP600125 significantly enhanced TRTS-mediated neuritogenesis, whereas that with other selective mitogen-activated protein kinase (MAPK) inhibitors did not—e.g., extracellular signal-regulated kinase (ERK)1/2 inhibitor U0126, and p38 MAPK inhibitor SB203580. We tried to clarify the mechanism of SP600125 action by testing the effect of U0126 and the BMP receptor inhibitor LDN193189 on the SP600125-mediated enhancement of intracellular signaling. SP600125-enhanced TRTS-induced neuritogenesis was significantly inhibited by U0126 or LDN193189. Gene expression analysis revealed that TRTS significantly increased β3-Tubulin, MKK3, and Smad7 gene expressions. Additionally, Smad6 and Smad7 gene expressions were substantially attenuated through SP600125 co-treatment during TRTS. Therefore, SP600125 may partly enhance TRTS-induced neuritogenesis by attenuating the negative feedback loop of BMP signaling. Further investigation of the mechanisms underlying the effect of SP600125 during TRTS-mediated neuritogenesis may contribute to the future development of regenerative neuromedicine.