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- Title
Altered lipid partitioning and glucocorticoid availability in CBG-deficient male mice with diet-induced obesity.
- Authors
Gulfo, José; Ledda, Angelo; Serra, Elisabet; Cabot, Cristina; Esteve, Montserrat; Grasa, Mar
- Abstract
<bold>Objective: </bold>To evaluate how deficiency in corticosteroid-binding globulin (CBG), the specific carrier of glucocorticoids, affects glucocorticoid availability and adipose tissue in obesity.<bold>Methods: </bold>C57BL/6 (WT) and CBG-deficient (KO) male mice were fed during 12 weeks with standard or hyperlipidic diet (HL). Glucocorticoid availability and metabolic parameters were assessed.<bold>Results: </bold>Body weight and food intake were increased in KO compared with WT mice fed a standard diet and were similar when fed a HL diet. Expression of CBG was found in white adipose tissue by immunochemistry, real-time PCR, and Western blot. In obesity, the subcutaneous depot developed less in KO mice compared with WT, which was associated with a minor adipocyte area and peroxisome proliferator-activated receptor-γ expression. Conversely, the epididymal depot displayed higher weight and adipocyte area in KO than in WT mice. CBG deficiency caused a fall of hepatic 11β-hydroxysteroid dehydrogenase type 2 expression and an increase in epidymal adipose tissue, particularly in HL mice.<bold>Conclusions: </bold>Deficiency in CBG drives lipid partitioning from subcutaneous to visceral adipose depot under a context of lipid excess and differentially modulates 11β-hydroxysteroid dehydrogenase type 2 expression.
- Subjects
OBESITY; GLUCOCORTICOIDS; GLOBULINS; DIET; LABORATORY mice; FAT cells; PEROXISOME proliferator-activated receptors; ADIPOSE tissues; ANIMAL experimentation; BIOLOGICAL models; FATIGUE (Physiology); GENETIC disorders; MICE; OXIDOREDUCTASES
- Publication
Obesity (19307381), 2016, Vol 24, Issue 8, p1677
- ISSN
1930-7381
- Publication type
journal article
- DOI
10.1002/oby.21543