Adipocyte Hypertrophy and Improved Postprandial Lipid Response in Beta 2 Syntrophin Deficient Mice.
Caveolin-1
Collagen
Free fatty acids
Lipid droplet
Liver
Journal
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
ISSN: 1421-9778
Titre abrégé: Cell Physiol Biochem
Pays: Germany
ID NLM: 9113221
Informations de publication
Date de publication:
2019
2019
Historique:
received:
13
08
2018
accepted:
13
12
2018
entrez:
17
4
2019
pubmed:
17
4
2019
medline:
3
5
2019
Statut:
ppublish
Résumé
Adipocyte hypertrophy in obesity is associated with inflammation and adipose tissue fibrosis which both contribute to metabolic diseases. Mechanisms regulating lipid droplet expansion are poorly understood. Knock down of the scaffold protein beta 2 syntrophin (SNTB2) increases lipid droplet size of 3T3-L1 adipocytes and the physiological relevance of SNTB2 in adipose tissue morphology and metabolic health was analyzed herein. Wild type and SNTB2 Upon high fat diet SNTB2 Current study shows that high SNTB2 in obese adipose tissues restricts adipocyte growth and thereby may contribute to metabolic diseases.
Sections du résumé
BACKGROUND/AIMS
OBJECTIVE
Adipocyte hypertrophy in obesity is associated with inflammation and adipose tissue fibrosis which both contribute to metabolic diseases. Mechanisms regulating lipid droplet expansion are poorly understood. Knock down of the scaffold protein beta 2 syntrophin (SNTB2) increases lipid droplet size of 3T3-L1 adipocytes and the physiological relevance of SNTB2 in adipose tissue morphology and metabolic health was analyzed herein.
METHODS
METHODS
Wild type and SNTB2
RESULTS
RESULTS
Upon high fat diet SNTB2
CONCLUSION
CONCLUSIONS
Current study shows that high SNTB2 in obese adipose tissues restricts adipocyte growth and thereby may contribute to metabolic diseases.
Substances chimiques
CAV1 protein, human
0
Caveolin 1
0
Dietary Fats
0
Dystrophin-Associated Proteins
0
syntrophin
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1151-1165Subventions
Organisme : German Research Foundation
ID : BU 1141/8-1
Pays : Germany
Informations de copyright
© Copyright by the Author(s). Published by Cell Physiol Biochem Press.
Déclaration de conflit d'intérêts
The authors declare to have no competing interests.