KPNBeta1 promotes palmitate-induced insulin resistance via NF-kappaB signaling in hepatocytes
J. physiol. biochem
; 71(4): 763-772, dic. 2015.
Artigo
em Inglês
| IBECS
| ID: ibc-145728
Biblioteca responsável:
ES1.1
Localização: BNCS
ABSTRACT
It has been intensively studied that inflammation contributes to the insulin resistance development in obesity-induced type 2 diabetes mellitus (T2DM). In this study, we assessed the effect of karyopherin Beta1 (KPNBeta1) in hepatic insulin resistance and the underlying mechanisms using high-fat diet (HFD) fed mice and palmitate (PA)-stimulated hepatocytes (HepG2). KPNBeta1 expression is increased in the HFD fed mice liver. PA upregulated KPNBeta1 expression in HepG2 cells in a time-dependent manner. PA also increased pro-inflammatory cytokines expression, including tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), and interleukin 1Beta (IL-1Beta). KPNBeta1 knockdown reversed PA-induced pro-inflammatory cytokines expression and insulin-stimulated glucose uptake in HepG2 cells. In addition, KPNBeta1 knockdown reduced intracellular lipid accumulation. Mechanistically, KPNBeta1 transports nuclear factor kB (NF-kappaB) p65 from the cytoplasm to the nucleus to increase pro-inflammatory genes expression. In summary, KPNBeta1 acts as a positive regulator in the NF-kappaB pathway to enhance palmitate-induced inflammation response and insulin resistance in HepG2 cells
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Coleções:
Bases de dados nacionais
/
Espanha
Base de dados:
IBECS
Assunto principal:
Resistência à Insulina
/
Hepatócitos
/
Carioferinas
/
Diabetes Mellitus Tipo 2
Limite:
Animais
Idioma:
Inglês
Revista:
J. physiol. biochem
Ano de publicação:
2015
Tipo de documento:
Artigo
Instituição/País de afiliação:
Affiliated Hospital of Nantong University/China