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Type: Artigo de periódico
Title: Diet-induced Obesity Induces Endoplasmic Reticulum Stress And Insulin Resistance In The Amygdala Of Rats.
Author: Castro, Gisele
C Areias, Maria Fernanda
Weissmann, Lais
Quaresma, Paula G F
Katashima, Carlos K
Saad, Mario J A
Prada, Patricia O
Abstract: Insulin acts in the hypothalamus, decreasing food intake (FI) by the 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 the amygdala as an important brain region for FI regulation in response to insulin. This regulation was dependent on PI3K/AKT pathway similar to the hypothalamus. Insulin was able to decrease neuropeptide Y (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.
Subject: Agrp, Agouti-related Peptide
Amy, Amygdala
Bw, Body Weight
Cns, Central Nervous System
Crh, Corticotrophin-releasing Hormone
Er, Endoplasmic Reticulum
Endoplasmic Reticulum Stress
Fi, Food Intake
Fkbp51, Fk506 Binding Protein 51
Hfd, High-fat Diet
Hprt, Hypoxanthine Phosphoribosyl Transferase
Ikkβ, I Kappa B Kinase
Ir, Insulin Receptor
Ire1α, Inositol-requiring Kinase Alpha
Irs-1, Insulin Substrate 1
Jnk, C-jun N-terminal Kinase
Lgi, Low-grade Inflammation
Npy, Neuropeptide Y
Pba, 4-phenyl Butyric Acid
Perk, Rna-activated Protein Kinase-like Er Resident Kinase
Pi3k, Phosphoinositide 3-kinase
Pkb Or Akt, Protein Kinase B
Phosphatidylinositol 3-kinase
Citation: Febs Open Bio. v. 3, p. 443-9, 2013.
Rights: aberto
Identifier DOI: 10.1016/j.fob.2013.09.002
Date Issue: 2013
Appears in Collections:Unicamp - Artigos e Outros Documentos

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