Protein Kinase C Epsilon Deletion in Adipose Tissue, but Not in Liver, Improves Glucose Tolerance.
Cell Metab
; 29(1): 183-191.e7, 2019 01 08.
Article
em En
| MEDLINE
| ID: mdl-30318338
ABSTRACT
Protein kinase C epsilon (PKCÉ) activation in the liver is proposed to inhibit insulin action through phosphorylation of the insulin receptor. Here, however, we demonstrated that global, but not liver-specific, deletion of PKCÉ in mice protected against diet-induced glucose intolerance and insulin resistance. Furthermore, PKCÉ-dependent alterations in insulin receptor phosphorylation were not detected. Adipose-tissue-specific knockout mice did exhibit improved glucose tolerance, but phosphoproteomics revealed no PKCÉ-dependent effect on the activation of insulin signaling pathways. Altered phosphorylation of adipocyte proteins associated with cell junctions and endosomes was associated with changes in hepatic expression of several genes linked to glucose homeostasis and lipid metabolism. The primary effect of PKCÉ on glucose homeostasis is, therefore, not exerted directly in the liver as currently posited, and PKCÉ activation in this tissue should be interpreted with caution. However, PKCÉ activity in adipose tissue modulates glucose tolerance and is involved in crosstalk with the liver.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Tecido Adiposo
/
Proteína Quinase C-épsilon
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Glucose
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Insulina
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Fígado
Limite:
Animals
Idioma:
En
Revista:
Cell Metab
Assunto da revista:
METABOLISMO
Ano de publicação:
2019
Tipo de documento:
Article
País de afiliação:
Austrália