Supplementing Genistein for Breeder Hens Alters the Growth Performance and Intestinal Health of Offspring.
genistein
intestinal health
maternal effect
microbiome
offspring
Journal
Life (Basel, Switzerland)
ISSN: 2075-1729
Titre abrégé: Life (Basel)
Pays: Switzerland
ID NLM: 101580444
Informations de publication
Date de publication:
28 Jun 2023
28 Jun 2023
Historique:
received:
01
03
2023
revised:
31
05
2023
accepted:
21
06
2023
medline:
29
7
2023
pubmed:
29
7
2023
entrez:
29
7
2023
Statut:
epublish
Résumé
Recent research revealed that dietary genistein supplementation for breeder hens can improve the immune function of offspring chicks. However, it remains unknown whether this maternal effect could improve the intestinal health of offspring. This study was conducted to explore the mechanism involved in the maternal effect of genistein on the intestinal mucosa and microbial homeostasis of chicken offspring. A total of 120 Qiling breeder hens were fed a basal diet, a 20 mg/kg genistein-supplemented diet, or a 40 mg/kg genistein-supplemented diet for 4 weeks before collecting their eggs. After hatching, 180 male offspring (60 chickens from each group) were randomly selected and divided into three groups: (1) the offspring of hens fed a basal diet (CON); (2) the offspring of hens fed a low-dose genistein-supplemented diet (LGE); (3) the offspring of hens fed a high-dose genistein-supplemented diet (HGE). At 17 d, 72 male offspring (48 chickens from CON and 24 chickens from LGE) were divided into three groups: (1) the offspring of hens fed a basal diet (CON); (2) the CON group challenged with LPS (LPS); (3) the LGE group challenged with LPS (LPS + LGE). The results showed that maternal genistein supplementation increased the birth weight and serum level of total protein (TP), followed by improved intestinal villus morphology. Continuously, the maternal effect on the body weight of chicks lasted until 21 d. Additionally, it was observed that maternal genistein supplementation exhibited protective effects against LPS-induced morphological damage and intestinal mucosal barrier dysfunction by upregulating the expression of tight junction proteins, specifically
Identifiants
pubmed: 37511844
pii: life13071468
doi: 10.3390/life13071468
pmc: PMC10381885
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : Beijing Natural Science Foundation
ID : 6222036
Organisme : National Natural Science Foundation of China
ID : 32202724
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