Whole Body
AMP-Activated Protein Kinase Kinases
/ metabolism
Aging
/ genetics
Animals
Energy Metabolism
Gene Deletion
Insulin Resistance
Male
Mice
Mice, Inbred C57BL
Phosphotransferases (Phosphate Group Acceptor)
/ genetics
Proto-Oncogene Proteins c-akt
/ metabolism
Uncoupling Protein 1
/ metabolism
Weight Gain
IP6K1
adipose tissue browning
aging
insulin resistance
metabolism
weight gain
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
12 Feb 2022
12 Feb 2022
Historique:
received:
15
12
2021
revised:
05
02
2022
accepted:
10
02
2022
entrez:
26
2
2022
pubmed:
27
2
2022
medline:
11
3
2022
Statut:
epublish
Résumé
(1) Background: We previously demonstrated that disruption of IP6K1 improves metabolism, protecting mice from high-fat diet-induced obesity, insulin resistance, and non-alcoholic fatty liver disease and steatohepatitis. Age-induced metabolic dysfunction is a major risk factor for metabolic diseases. The involvement of IP6K1 in this process is unknown. (2) Methods: Here, we compared body and fat mass, insulin sensitivity, energy expenditure and serum-, adipose tissue- and liver-metabolic parameters of chow-fed, aged, wild type (
Identifiants
pubmed: 35216174
pii: ijms23042059
doi: 10.3390/ijms23042059
pmc: PMC8878859
pii:
doi:
Substances chimiques
Ucp1 protein, mouse
0
Uncoupling Protein 1
0
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
AMP-Activated Protein Kinase Kinases
EC 2.7.11.3
Phosphotransferases (Phosphate Group Acceptor)
EC 2.7.4.-
IP6K1 protein, human
EC 2.7.4.21
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIH HHS
ID : NIDDK-R01DK103746
Pays : United States
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