SPARC is required for the maintenance of glucose homeostasis and insulin secretion in mice.
Aging
/ blood
Animals
Biomarkers
/ blood
Blood Glucose
/ metabolism
Diabetes Mellitus, Experimental
/ blood
Diet, High-Fat
Dietary Sucrose
Glucose Transporter Type 2
/ metabolism
Homeostasis
Insulin
/ blood
Islets of Langerhans
/ metabolism
Male
Mice, Inbred C57BL
Mice, Knockout
Osteonectin
/ deficiency
Secretory Pathway
SPARC
beta cells
diabetes
glucose homeostasis
insulin secretion
knockout mice
Journal
Clinical science (London, England : 1979)
ISSN: 1470-8736
Titre abrégé: Clin Sci (Lond)
Pays: England
ID NLM: 7905731
Informations de publication
Date de publication:
31 01 2019
31 01 2019
Historique:
received:
07
08
2018
revised:
14
12
2018
accepted:
08
01
2019
pubmed:
11
1
2019
medline:
19
11
2019
entrez:
11
1
2019
Statut:
epublish
Résumé
Obesity, metabolic syndrome, and type 2 diabetes, three strongly interrelated diseases, are associated to increased morbidity and mortality worldwide. The pathogenesis of obesity-associated disorders is still under study. Secreted protein acidic and rich in cysteine (SPARC) is a matricellular glycoprotein expressed in many cell types including adipocytes, parenchymal, and non-parenchymal hepatic cells and pancreatic cells. Studies have demonstrated that SPARC inhibits adipogenesis and promotes insulin resistance; in addition, circulating SPARC levels were positively correlated with body mass index in obese individuals. Therefore, SPARC is being proposed as a key factor in the pathogenesis of obesity-associated disorders. The aim of this study is to elucidate the role of SPARC in glucose homeostasis. We show here that SPARC null (SPARC
Identifiants
pubmed: 30626728
pii: CS20180714
doi: 10.1042/CS20180714
doi:
Substances chimiques
Biomarkers
0
Blood Glucose
0
Dietary Sucrose
0
Glucose Transporter Type 2
0
Insulin
0
Osteonectin
0
SPARC protein, mouse
0
Slc2a2 protein, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
351-365Informations de copyright
© 2019 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.