Islet inflammation: a unifying target for diabetes treatment?
Trends Endocrinol Metab
; 24(7): 351-60, 2013 Jul.
Article
en En
| MEDLINE
| ID: mdl-23484621
ABSTRACT
In the past decade, islet inflammation has emerged as a contributor to the loss of functional ß cell mass in both type 1 (T1D) and type 2 diabetes (T2D). Evidence supports the idea that overnutrition and insulin resistance result in the production of proinflammatory mediators by ß cells. In addition to compromising ß cell function and survival, cytokines may recruit macrophages into islets, thus augmenting inflammation. Limited but intriguing data imply a role of adaptive immune response in islet dysfunction in T2D. Clinical trials have validated anti-inflammatory therapies in T2D, whereas immune therapy for T1D remains challenging. Further research is required to improve our understanding of islet inflammatory pathways and to identify more effective therapeutic targets for T1D and T2D.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Islotes Pancreáticos
/
Mediadores de Inflamación
/
Diabetes Mellitus Tipo 1
/
Diabetes Mellitus Tipo 2
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Trends Endocrinol Metab
Asunto de la revista:
ENDOCRINOLOGIA
/
METABOLISMO
Año:
2013
Tipo del documento:
Article
País de afiliación:
Estados Unidos