Role of Fermented Goat Milk on Liver Gene and Protein Profiles Related to Iron Metabolism during Anemia Recovery
Metadatos
Afficher la notice complèteAuteur
Moreno Fernández, Jorge; Muñoz Alférez, María José; López Aliaga, María Inmaculada; Díaz Castro, JavierEditorial
MDPI
Materia
Fermented cow and goat milk Anemia Iron homeostasis Iron repletion Gene and protein expression
Date
2020-05Referencia bibliográfica
Moreno-Fernandez, J., Alférez, M. J., López-Aliaga, I., & Díaz-Castro, J. (2020). Role of Fermented Goat Milk on Liver Gene and Protein Profiles Related to Iron Metabolism during Anemia Recovery. Nutrients, 12(5), 1336. [DOI: 10.3390/nu12051336]
Patrocinador
Ministry of Education, Culture and Sport (Spain); Spanish Government; Traslados Temporales FPU (University of Kings College of London)Résumé
Despite the crucial role of the liver as the central regulator of iron homeostasis, no studies
have directly tested the modulation of liver gene and protein expression patterns during iron deficiency
instauration and recovery with fermented milks. Fermented goat milk consumption improves the
key proteins of intestinal iron metabolism during iron deficiency recovery, enhancing the digestive
and metabolic utilization of iron. The aim of this study was to assess the influence of fermented
goat or cow milk consumption on liver iron homeostasis during iron-deficiency anemia recovery
with normal or iron-overload diets. Analysis included iron status biomarkers, gene and protein
expression in hepatocytes. In general, fermented goat milk consumption either with normal or high
iron content up-regulated liver DMT1, FPN1 and FTL1 gene expression and DMT1 and FPN1 protein
expression. However, HAMP mRNA expression was lower in all groups of animals fed fermented
goat milk. Additionally, hepcidin protein expression decreased in control and anemic animals fed
fermented goat milk with normal iron content. In conclusion, fermented goat milk potentiates the
up-regulation of key genes coding for proteins involved in iron metabolism, such as DMT1, and
FPN1, FTL1 and down-regulation of HAMP, playing a key role in enhanced iron repletion during
anemia recovery, inducing a physiological adaptation of the liver key genes and proteins coordinated
with the fluctuation of the cellular iron levels, favoring whole-body iron homeostasis.