RESUMEN
Although fluctuations in energy metabolism are known to influence intake as well as nutrient selection, there are no definitive reports on how food preferences change with changes in habitat temperature. We investigated the effects of habitat temperature on appetite and food preference and elucidated the underlying mechanism by conducting a feeding experiment and a leptin administration test on mice reared at low temperatures. Our results showed that the increased food intake and HFD preference observed in the 10°C group were induced by decrease in plasma leptin concentration. Then, a leptin administration experiment was conducted to clarify the relationship between leptin and food preference with low-temperature acclimation. The control group reared in 10°C significantly preferred the HFD, but the leptin-administered group did not. These results show that the peripheral system appetite-regulating hormone leptin not only acts to suppress appetite but also might inhibit preference for lipids in low-temperature acclimation.
Asunto(s)
Aclimatación/efectos de los fármacos , Depresores del Apetito/farmacología , Frío , Dieta Alta en Grasa , Ingestión de Alimentos/efectos de los fármacos , Preferencias Alimentarias/efectos de los fármacos , Leptina/farmacología , Animales , Apetito/efectos de los fármacos , Depresores del Apetito/sangre , Dieta de Carga de Carbohidratos , Metabolismo Energético , Leptina/sangre , Masculino , Ratones , Ratones Endogámicos C57BLRESUMEN
c-Met is a receptor-type tyrosine kinase, which is involved in a wide range of cellular responses such as proliferation, motility, migration and invasion. It has been reported to be overexpressed in various cancers. However, the role of c-Met in breast cancer stem cells (CSCs) still remains unclear. We herein, show that c-Met expression is significantly elevated in Basal-like type of breast cancer in comparison with other subtypes. High expression of c-Met strongly correlated with the expression of two CSC markers, ALDH1A3 and CD133 in breast cancers. In addition, breast cancers at tumor stage III-IV expressing both c-Methigh and ALDH1A3high had poor prognosis. Furthermore, treatment with c-Met inhibitors (Crizotinib, Foretinib, PHA-665752 and Tivantinib) in MDA-MB157 cells with high c-Met protein expression resulted in significant suppression in cell viability, contrary to MDA-MB468 cells with low c-Met protein expression. These c-Met inhibitors also suppressed cell viability and tumor-sphere formation of ALDH1high breast cancer cells with high c-Met expression. These results suggest that c-Met in ALDH1 positive CSCs seems to play an important role in breast cancer repopulation. Therefore, we conclude that c-Met is a potential therapeutic target in ALDH1 positive breast CSCs.