CTRP12 ablation differentially affects energy expenditure, body weight, and insulin sensitivity in male and female mice.
Adipokines
/ genetics
Adipose Tissue
/ metabolism
Adiposity
/ genetics
Animals
Body Weight
/ genetics
Diet, High-Fat
Endoplasmic Reticulum Stress
/ genetics
Energy Metabolism
/ genetics
Fatty Acids, Nonesterified
/ metabolism
Female
Fibrosis
/ genetics
Gene Expression
Gene-Environment Interaction
Insulin Resistance
/ genetics
Lipid Metabolism
/ genetics
Liver
/ pathology
Male
Mice
Mice, Knockout
Organ Size
Oxidative Stress
/ genetics
Sex Factors
Triglycerides
/ metabolism
Tumor Necrosis Factor-alpha
/ metabolism
Weight Gain
/ genetics
C1q/TNF-related protein
CTRP12
diabetes
insulin resistance
lipid metabolism
obesity
secreted hormone
Journal
American journal of physiology. Endocrinology and metabolism
ISSN: 1522-1555
Titre abrégé: Am J Physiol Endocrinol Metab
Pays: United States
ID NLM: 100901226
Informations de publication
Date de publication:
01 07 2020
01 07 2020
Historique:
pubmed:
19
5
2020
medline:
27
10
2020
entrez:
19
5
2020
Statut:
ppublish
Résumé
Secreted hormones facilitate tissue cross talk to maintain energy balance. We previously described C1q/TNF-related protein 12 (CTRP12) as a novel metabolic hormone. Gain-of-function and partial-deficiency mouse models have highlighted important roles for this fat-derived adipokine in modulating systemic metabolism. Whether CTRP12 is essential and required for metabolic homeostasis is unknown. We show here that homozygous deletion of
Identifiants
pubmed: 32421370
doi: 10.1152/ajpendo.00533.2019
pmc: PMC7468785
doi:
Substances chimiques
Adipokines
0
C1qtnf12 protein, mouse
0
Fatty Acids, Nonesterified
0
Tnf protein, mouse
0
Triglycerides
0
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
E146-E162Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK084171
Pays : United States
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