Back to Search
Start Over
Wnt10b inhibits obesity in ob/ob and agouti mice.
- Source :
-
Diabetes [Diabetes] 2007 Feb; Vol. 56 (2), pp. 295-303. - Publication Year :
- 2007
-
Abstract
- The Wnt family of secreted signaling molecules has profound effects on diverse developmental processes, including the fate of mesenchymal progenitors. While activation of Wnt signaling blocks adipogenesis, inhibition of endogenous Wnt/beta-catenin signaling by Wnt10b promotes spontaneous preadipocyte differentiation. Transgenic mice with expression of Wnt10b from the FABP4 promoter (FABP4-Wnt10b) have less adipose tissue when maintained on a normal chow diet and are resistant to diet-induced obesity. Here we demonstrate that FABP4-Wnt10b mice largely avert weight gain and metabolic abnormalities associated with genetic obesity. FABP4-Wnt10b mice do not gain significant body weight on the ob/ob background, and at 8 weeks of age, they have an approximately 70% reduction in visceral and subcutaneous adipose tissues compared with ob/ob mice. Similarly, on the lethal yellow agouti (A(y)) background, FABP4-Wnt10b mice have 50-70% less adipose tissue weight and circulating leptin at 5 months of age. Wnt10b-Ay mice are more glucose tolerant and insulin sensitive than A(y) controls, perhaps due to reduced expression and circulation of resistin. Reduced expression of inflammatory cytokines may also contribute to improved glucose homeostasis.
- Subjects :
- Agouti Signaling Protein
Animals
Blood Glucose physiology
Disease Models, Animal
Energy Intake physiology
Female
Intercellular Signaling Peptides and Proteins genetics
Leptin deficiency
Leptin genetics
Male
Mice
Mice, Transgenic
Obesity genetics
Oxygen Consumption physiology
Panniculitis physiopathology
Adipose Tissue physiology
Fatty Acid-Binding Proteins physiology
Insulin Resistance physiology
Obesity physiopathology
Proto-Oncogene Proteins physiology
Wnt Proteins physiology
Subjects
Details
- Language :
- English
- ISSN :
- 0012-1797
- Volume :
- 56
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Diabetes
- Publication Type :
- Academic Journal
- Accession number :
- 17259372
- Full Text :
- https://doi.org/10.2337/db06-1339