Como en años anteriores, nuestro grupo ofrece dos plazas para que estudiantes de Grado y Máster realicen prácticas en nuestro laboratorio entre el 1 de julio y el 15 de septiembre de 2023.
El propósito del programa CICERONE es acercar la investigación biomédica a los estudiantes universitarios para que puedan escoger más adecuadamente su orientación profesional.
Para inscribirse es necesario crear una cuenta en la web del CNIC antes del 28 de abril de 2023.
| Enlace | Tamaño |
|---|---|
| Bases de la convocatoria 2023 | 243 KB |
| Extracto del BOE | 167 KB |
Los dos proyectos científicos que ofrecemos este año son:
- Stress in the brain, metabolic effects: Obesity has become a new pandemic. It is known that obesity induces molecular changes in the brain that are fundamental for the development of diseases and for maintaining excess energy intake. However, little is known about how these changes appear and the molecular mechanisms that mediate them. We will study how modulating stress in the central nervous system induced by high fat diet affects the development of cardiometabolic diseases. For this purpose, genetically modified animals will be used and whole organism metabolism will be evaluated, and how the signalling of this stress in the brain affects the response of distant organs through inter-tissue communication.
- Role of adipose tissue controling whole body homeostasis: Cardiometabolic diseases (CMDs)—e.g., diabetes, steatohepatitis, and cardiomyopathy— are the leading cause of death worldwide. Adipose tissue (AT) heterogeneity and dysfunction might be involved in the CMD pathogenesis. We have recently demonstrated that i) AT regulates whole-body metabolism independently of obesity and predisposes to hepatic cancer in mice and humans; and ii) molecules secreted by AT trigger liver steatosis and insulin resistance. Our studies suggest that dysfunctional AT communicates with other organs and induces pathogenic adaptive responses through evolutionarily conserved mechanisms (rodent to humans). Our preliminary results show that AT dysfunction caused by mitochondrial alteration induces cardiomyopathy in lean mice, reinforcing that AT has a central role in controlling heart functionality.
