High-fat diet causes mitochondrial damage and downregulation of mitofusin-2 and optic atrophy-1 in multiple organs.
high-fat diet
hyperlipidemia
mitochondria
mitofusin-2
optic atrophy-1
Journal
Journal of clinical biochemistry and nutrition
ISSN: 0912-0009
Titre abrégé: J Clin Biochem Nutr
Pays: Japan
ID NLM: 8700907
Informations de publication
Date de publication:
Jul 2023
Jul 2023
Historique:
received:
01
07
2022
accepted:
19
02
2023
medline:
3
8
2023
pubmed:
3
8
2023
entrez:
3
8
2023
Statut:
ppublish
Résumé
High-fat consumption promotes the development of obesity, which is associated with various chronic illnesses. Mitochondria are the energy factories of eukaryotic cells, maintaining self-stability through a fine-tuned quality-control network. In the present study, we evaluated high-fat diet (HFD)-induced changes in mitochondrial ultrastructure and dynamics protein expression in multiple organs. C57BL/6J male mice were fed HFD or normal diet (ND) for 24 weeks. Compared with ND-fed mice, HFD-fed mice exhibited increased body weight, cardiomyocyte enlargement, pulmonary fibrosis, hepatic steatosis, renal and splenic structural abnormalities. The cellular apoptosis of the heart, liver, and kidney increased. Cellular lipid droplet deposition and mitochondrial deformations were observed. The proteins related to mitochondrial biogenesis (TFAM), fission (DRP1), autophagy (LC3 and LC3-II: LC3-I ratio), and mitophagy (PINK1) presented different changes in different organs. The mitochondrial fusion regulators mitofusin-2 (MFN2) and optic atrophy-1 (OPA1) were consistently downregulated in multiple organs, even the spleen. TOMM20 and ATP5A protein were enhanced in the heart, skeletal muscle, and spleen, and attenuated in the kidney. These results indicated that high-fat feeding caused pathological changes in multiple organs, accompanied by mitochondrial ultrastructural damage, and MFN2 and OPA1 downregulation. The mitochondrial fusion proteins may become promising targets and/or markers for treating metabolic disease.
Identifiants
pubmed: 37534099
doi: 10.3164/jcbn.22-73
pii: DN/JST.JSTAGE/jcbn/22-73
pmc: PMC10390808
doi:
Types de publication
Journal Article
Langues
eng
Pagination
61-76Informations de copyright
Copyright © 2023 JCBN.
Déclaration de conflit d'intérêts
No potential conflicts of interest were disclosed.
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