The Hepatokine TSK does not affect brown fat thermogenic capacity, body weight gain, and glucose homeostasis.
Adipose Tissue, Brown
/ metabolism
Animals
Body Weight
/ physiology
Female
Glucose
/ metabolism
Homeostasis
/ genetics
Intercellular Signaling Peptides and Proteins
/ genetics
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Obesity
/ metabolism
Proteoglycans
/ metabolism
Thermogenesis
/ genetics
Weight Gain
/ genetics
Brown adipose tissue
Glucose homeostasis
Hepatokine
Obesity
Thermogenesis
Tsukushi
Journal
Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
09
07
2019
revised:
13
09
2019
accepted:
29
09
2019
entrez:
27
11
2019
pubmed:
27
11
2019
medline:
24
6
2020
Statut:
ppublish
Résumé
Hepatokines are proteins secreted by the liver that impact the functions of the liver and various tissues through autocrine, paracrine, and endocrine signaling. Recently, Tsukushi (TSK) was identified as a new hepatokine that is induced by obesity and cold exposure. It was proposed that TSK controls sympathetic innervation and thermogenesis in brown adipose tissue (BAT) and that loss of TSK protects against diet-induced obesity and improves glucose homeostasis. Here we report the impact of deleting and/or overexpressing TSK on BAT thermogenic capacity, body weight regulation, and glucose homeostasis. We measured the expression of thermogenic genes and markers of BAT innervation and activation in TSK-null and TSK-overexpressing mice. Body weight, body temperature, and parameters of glucose homeostasis were also assessed in the context of TSK loss and overexpression. The loss of TSK did not affect the thermogenic activation of BAT. We found that TSK-null mice were not protected against the development of obesity and did not show improvement in glucose tolerance. The overexpression of TSK also failed to modulate thermogenesis, body weight gain, and glucose homeostasis in mice. TSK is not a significant regulator of BAT thermogenesis and is unlikely to represent an effective target to prevent obesity and improve glucose homeostasis.
Identifiants
pubmed: 31767170
pii: S2212-8778(19)30917-2
doi: 10.1016/j.molmet.2019.09.014
pmc: PMC6889588
pii:
doi:
Substances chimiques
Intercellular Signaling Peptides and Proteins
0
Proteoglycans
0
TSKU protein, human
0
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
184-191Subventions
Organisme : CIHR
Pays : Canada
Informations de copyright
Copyright © 2019 The Author(s). Published by Elsevier GmbH.. All rights reserved.
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