Inhibiting TRIM8 alleviates adipocyte inflammation and insulin resistance by regulating the DUSP14/MAPKs pathway.
Adipocyte
; 13(1): 2381262, 2024 Dec.
Article
en En
| MEDLINE
| ID: mdl-39039652
ABSTRACT
Obesity is a low-grade chronic inflammation induced by the pathological expansion of adipocytes which allows the development of obesity-associated metabolic diseases like type 2 diabetes mellitus (T2D) and non-alcoholic fatty liver disease (NAFLD). However, mechanisms regulating adipocyte inflammation remain poorly understood. Here, we observed that TRIM8 was upregulated in adipocyte inflammation and insulin resistance while DUSP14 was downregulated. TRIM8 deficiency and DUSP14 over-expression decreased the level of inflammatory cytokines, increased glucose uptake content, and improved insulin signalling transduction compared to LPS treatment alone. Conversely, silencing DUSP14 increased the expression of inflammatory cytokines. It decreased the glucose uptake content and the phosphorylation level of proteins involved in insulin signalling, further impairing insulin signalling and aggravating insulin resistance. Furthermore, The decreased level of inflammatory cytokines, increased glucose uptake, and improved insulin signalling transduction caused by TRIM8 deficiency were reversed by down-regulated DUSP14. Collectively, our findings revealed that TRIM8 can regulate adipocyte inflammation and insulin resistance by regulating the MAPKs pathway which is dependent on DUSP14.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Resistencia a la Insulina
/
Adipocitos
/
Fosfatasas de Especificidad Dual
/
Inflamación
Límite:
Animals
Idioma:
En
Revista:
Adipocyte
Año:
2024
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Estados Unidos