Altered lipid partitioning and glucocorticoid availability in CBG-deficient male mice with diet-induced obesity.
To evaluate how deficiency in corticosteroid-binding globulin (CBG), the specific carrier of glucocorticoids, affects glucocorticoid availability and adipose tissue in obesity.



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.



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.



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.
Department of Nutrition and Food Sciences, Faculty of Biology, University of Barcelona, Barcelona, Spain.|CIBER Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain.|Institute of Biomedicine of the University of Barcelona, Barcelona, Spain.
José
J
Gulfo
Department of Nutrition and Food Sciences, Faculty of Biology, University of Barcelona, Barcelona, Spain.|CIBER Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain.|Institute of Biomedicine of the University of Barcelona, Barcelona, Spain.
Angelo
A
Ledda
Department of Nutrition and Food Sciences, Faculty of Biology, University of Barcelona, Barcelona, Spain.
Elisabet
E
Serra
Department of Nutrition and Food Sciences, Faculty of Biology, University of Barcelona, Barcelona, Spain.
Cristina
C
Cabot
Department of Nutrition and Food Sciences, Faculty of Biology, University of Barcelona, Barcelona, Spain.|CIBER Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain.|Institute of Biomedicine of the University of Barcelona, Barcelona, Spain.
Montserrat
M
Esteve
Department of Nutrition and Food Sciences, Faculty of Biology, University of Barcelona, Barcelona, Spain.|CIBER Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain.|Institute of Biomedicine of the University of Barcelona, Barcelona, Spain.
Mar
M
Grasa
D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1 / Q000378:metabolism; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2 / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D005221:Fatigue / Q000378:metabolism*; D030342:Genetic Diseases, Inborn / Q000378:metabolism*; D005938:Glucocorticoids / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000378:metabolism*; D014156:Transcortin / Q000172:deficiency* / Q000378:metabolism
D005938:Glucocorticoids; D014156:Transcortin; D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2