Fetal programming by high-fat diet promoted the decreased of the prostate in adult Wistar albino rats.
High-fat diet
Maternal nutrition
Postnatal period
Prostate
Rats
Journal
Mechanisms of development
ISSN: 1872-6356
Titre abrégé: Mech Dev
Pays: Ireland
ID NLM: 9101218
Informations de publication
Date de publication:
12 2020
12 2020
Historique:
received:
27
03
2020
revised:
07
09
2020
accepted:
27
09
2020
pubmed:
7
10
2020
medline:
15
9
2021
entrez:
6
10
2020
Statut:
ppublish
Résumé
We investigated the effect of a high-fat diet on body metabolism and ventral prostate morphology in 4-months-old offspring. The mother was fed with a control (C) or a high-fat (HF) diet during gestation and lactation. At weaning, the offspring diet remained the same (C/C, n = 8; HF/HF, n = 8) or it was switched (C/HF, n = 8; HF/C, n = 9). Biometry, blood pressure (BP), glucose, lipid metabolism and ventral prostate were evaluated. Triacylglycerol of HF/C increased, and the C/HF group had decreased HDL-c levels (P = 0.0005 and P = 0.0100, respectively). All groups on the HF diet presented hyperglycemia (P = 0.0064). Serum testosterone diminished in the C/HF group (P = 0.0218). The HF diet, regardless of the period, reduced prostatic acinar area (P < 0.0001). The epithelium height was smaller in HF/C and HF/HF groups compared with C/C and C/HF (P < 0.0001), and the volume density of epithelium was lower in HF/C group compared with the C/C and C/HF (P = 0.0024). The volume density of smooth muscle cells diminished in C/HF and HF/C (P = 0.0013), and the volume density of connective tissue was reduced in HF/C and HF/HF (P < 0.0001). High-fat diet intake during prenatal and postnatal life leads to prostatic atrophy, which may impair prostate secretory activity and contractility, and thus disturb reproductive function in adulthood.
Identifiants
pubmed: 33022371
pii: S0925-4773(20)30054-X
doi: 10.1016/j.mod.2020.103649
pii:
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
103649Informations de copyright
Copyright © 2020 Elsevier B.V. All rights reserved.