Obesity of mice lacking VAP-1/SSAO by Aoc3 gene deletion is reproduced in mice expressing a mutated vascular adhesion protein-1 (VAP-1) devoid of amine oxidase activity.
Adipose tissue
Biogenic amines
Cholesterol
Copper-containing amine oxidases
Lipogenesis
Low-grade inflammation
Journal
Journal of physiology and biochemistry
ISSN: 1877-8755
Titre abrégé: J Physiol Biochem
Pays: Spain
ID NLM: 9812509
Informations de publication
Date de publication:
Feb 2021
Feb 2021
Historique:
received:
28
11
2019
accepted:
29
06
2020
pubmed:
28
7
2020
medline:
5
8
2021
entrez:
27
7
2020
Statut:
ppublish
Résumé
The product of Aoc3 gene is known as vascular adhesion protein-1 (VAP-1), a glycoprotein contributing to leukocyte extravasation and exhibiting semicarbazide-sensitive amine oxidase activity (SSAO). Regarding the immune functions of VAP-1/SSAO, it is known that mice bearing Aoc3 gene knock-out (AOC3KO) exhibit defects in leukocyte migration similar to those of mice expressing a mutated VAP-1 lacking functional SSAO activity (knock-in, AOC3KI). However, it has not been reported whether these models differ regarding other disturbances. Thus, we further compared endocrine-metabolic phenotypes of AOC3KO and AOC3KI mice to their respective control. Special attention was paid on adiposity, glucose and lipid handling, since VAP-1/SSAO is highly expressed in adipose tissue (AT). In both mouse lines, no tissue SSAO activity was found, while Aoc3 mRNA was absent in AOC3KO only. Although food consumption was unchanged, both AOC3KO and AOC3KI mice were heavier and fatter than their respective controls. Other alterations commonly found in adipocytes from both lines were loss of benzylamine insulin-like action with unchanged insulin lipogenic responsiveness and adiponectin expression. A similar downregulation of inflammatory markers (CD45, IL6) was found in AT. Glucose handling and liver mass remained unchanged, while circulating lipid profile was distinctly altered, with increased cholesterol in AOC3KO only. These results suggest that the lack of oxidase activity found in AOC3KI is sufficient to reproduce the metabolic disturbances observed in AOC3KO mice, save those related with cholesterol transport. Modulation of SSAO activity therefore constitutes a potential target for the treatment of cardiometabolic diseases, especially obesity when complicated by low-grade inflammation.
Identifiants
pubmed: 32712883
doi: 10.1007/s13105-020-00756-y
pii: 10.1007/s13105-020-00756-y
doi:
Substances chimiques
Cell Adhesion Molecules
0
Amine Oxidase (Copper-Containing)
EC 1.4.3.21
semicarbazide-sensitive amine oxidase-vascular adhesion protein-1, mouse
EC 1.4.3.21
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
141-154Références
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