Global Deletion of the Prolactin Receptor Aggravates Streptozotocin-Induced Diabetes in Mice.
Front Endocrinol (Lausanne)
; 12: 619696, 2021.
Article
en En
| MEDLINE
| ID: mdl-33746901
ABSTRACT
Prolactin (PRL) levels are reduced in the circulation of rats with diabetes or obesity, and lower circulating levels of PRL correlate with increased prevalence of diabetes and a higher risk of metabolic alterations in the clinic. Furthermore, PRL stimulates ß-cell proliferation, survival, and insulin production and pregnant mice lacking PRL receptors in ß-cells develop gestational diabetes. To investigate the protective effect of endogenous PRL against diabetes outside pregnancy, we compared the number of cases and severity of streptozotocin (STZ)-induced hyperglycemia between C57BL/6 mice null for the PRL receptor gene (Prlr-/- ) and wild-type mice (Prlr+/+ ). STZ-treated diabetic Prlr-/- mice showed a higher number of cases and later recovery from hyperglycemia, exacerbated glucose levels, and glucose intolerance compared to the Prlr+/+ mice counterparts. Consistent with the worsening of hyperglycemia, pancreatic islet density, ß-cell number, proliferation, and survival, as well as circulating insulin levels were reduced, whereas α-cell number and pancreatic inflammation were increased in the absence of PRL signaling. Deletion of the PRL receptor did not alter the metabolic parameters in vehicle-treated animals. We conclude that PRL protects whole body glucose homeostasis by reducing ß-cell loss and pancreatic inflammation in STZ-induced diabetes. Medications elevating PRL circulating levels may prove to be beneficial in diabetes.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Glucemia
/
Receptores de Prolactina
/
Intolerancia a la Glucosa
/
Diabetes Mellitus Experimental
/
Insulina
Tipo de estudio:
Risk_factors_studies
Límite:
Animals
Idioma:
En
Revista:
Front Endocrinol (Lausanne)
Año:
2021
Tipo del documento:
Article
País de afiliación:
México