Galectin-3 gene deletion results in defective adipose tissue maturation and impaired insulin sensitivity and glucose homeostasis.
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
18 11 2020
18 11 2020
Historique:
received:
14
11
2019
accepted:
26
10
2020
entrez:
19
11
2020
pubmed:
20
11
2020
medline:
31
3
2021
Statut:
epublish
Résumé
Adiposopathy is a pathological adipose tissue (AT) response to overfeeding characterized by reduced AT expandability due to impaired adipogenesis, which favors inflammation, insulin resistance (IR), and abnormal glucose regulation. However, it is unclear whether defective adipogenesis causes metabolic derangement also independently of an increased demand for fat storage. As galectin-3 has been implicated in both adipocyte differentiation and glucose homeostasis, we tested this hypothesis in galectin-3 knockout (Lgal3
Identifiants
pubmed: 33208796
doi: 10.1038/s41598-020-76952-z
pii: 10.1038/s41598-020-76952-z
pmc: PMC7675972
doi:
Substances chimiques
Galectin 3
0
Lgals3 protein, mouse
0
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
20070Références
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