title: Changes in Brain 14-3-3 Proteins in Response to Insulin Resistance Induced by a High Palatable Diet.
abstract: The 14-3-3 protein family takes part in a wide range of cellular processes and is expressed in all eukaryotic organisms. In mammals, seven isoforms (β, ε, η, γ, τ, ζ, and σ) have been identified. 14-3-3 proteins are suggested to modulate the insulin-signaling cascade in the brain. The aim of this study was to investigate whether insulin resistance state induced by high palatable diet modulates expression of the 14-3-3 proteins in brain. Wistar male rats (n = 8) were divided into two experimental groups: insulin resistant (IR), induced by high palatable diet, and control (CO) group. Biochemical parameters (glucose tolerance test and plasma lipid profile) were evaluated after 130 days. Brain structures (cortex and hippocampus) were dissected for evaluation of messenger RNA (mRNA) and protein levels of different 14-3-3 proteins. Statistical analyses included Student t test and Pearson correlation. Significant decrease was observed in Ywhah and in Ywahq mRNA levels in the cortex of IR group, while no changes were observed in the hippocampus. Significant increase of θ isoform was observed in hippocampus IR group by immunodetection, while no differences were detected in the remaining isoforms. Inverse correlation was observed between blood glucose levels in cortex IR group and both Ywhah and Ywhaq mRNA levels. Protein levels of Creb and phosphatidylinositide 3-kinases (PI3K) showed to be increased in the hippocampus. These alterations may be due to a compensatory effect of impaired insulin signaling. We demonstrated differential expression of 14-3-3 isoforms throughout brain regions of rats with IR. As a whole, our results indicate that brain 14-3-3 levels are influenced by different diets.
authors.affiliation: Laboratório de Identificação Genética-Centro de Pesquisa Experimental e Serviço de Genética Médica-Hospital de Clínicas de Porto Alegre (HCPA), Porto Alegre, Brazil.
authors.forename: Hugo
authors.initials: H
authors.lastname: Bock
authors.forename: Aline Rigon
authors.initials: AR
authors.lastname: Zimmer
authors.forename: Eduardo Rigon
authors.initials: ER
authors.lastname: Zimmer
authors.forename: Diogo Onofre Gomes
authors.initials: DO
authors.lastname: de Souza
authors.forename: Luis Valmor Cruz
authors.initials: LV
authors.lastname: Portela
authors.forename: Maria Luiza
authors.initials: ML
authors.lastname: Saraiva-Pereira
mesh_terms: D048948:14-3-3 Proteins / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D015153:Blotting, Western; D001921:Brain / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D004032:Diet; D004195:Disease Models, Animal; D005951:Glucose Tolerance Test; D006624:Hippocampus / Q000378:metabolism; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008297:Male; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D020033:Protein Isoforms / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D017208:Rats, Wistar
chemical_list: D048948:14-3-3 Proteins; D001786:Blood Glucose; D017362:Cyclic AMP Response Element-Binding Protein; D008055:Lipids; D020033:Protein Isoforms; D012333:RNA, Messenger; D019869:Phosphatidylinositol 3-Kinases