Full text
| |
| Author(s): |
Gisele de Castro
Total Authors: 1
|
| Document type: | Master's Dissertation |
| Press: | Limeira, SP. |
| Institution: | Universidade Estadual de Campinas (UNICAMP). Faculdade de Ciências Aplicadas |
| Defense date: | 2013-09-08 |
| Examining board members: |
Patrícia de Oliveira Prada;
Eduardo Rochete Ropelle;
Jackson Cioni Bittencourt
|
| Advisor: | Patrícia de Oliveira Prada |
| Abstract | |
Insulin acts in hypothalamus decreasing food intake (FI) by IR/PI3K/Akt pathway. This pathway is impaired in obese animals and endoplasmic reticulum (ER) stress and low grade inflammation are possible mechanisms involved in this impairment. Here, we highlighted amygdala as an important brain site of FI regulation in response to insulin. This regulation was dependent on PI3K/AKT pathway similar to the hypothalamus. Insulin was able to decrease NPY and increase oxytocin mRNA levels in the amygdala via PI3K, which may contribute to hypophagia. Additionally, obese rats did not reduce FI in response to insulin and AKT phosphorylation was decreased in the amygdala, suggesting insulin resistance. Insulin resistance was associated with ER stress and low grade inflammation in this brain region. The inhibition of ER stress with PBA reverses insulin action/signaling, decreases NPY and increases oxytocin mRNA levels in the amygdala from obese rats, suggesting that ER stress is probably one of the mechanisms that induce insulin resistance in the amygdala (AU) | |
| FAPESP's process: | 11/15013-5 - THE REGULATION OF INSULIN AND LEPTIN SIGNALING IN THE STRIATUM: EFFECTS ON FOOD INTAKE, INFLAMATORY PATHWAY AND ENDOPLASMATIC RETICULUM STRESS |
| Grantee: | Gisele de Castro |
| Support Opportunities: | Scholarships in Brazil - Master |