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Altered lipid partitioning and glucocorticoid availability in CBG‐deficient male mice with diet‐induced obesity
Author(s) -
Gulfo José,
Ledda Angelo,
Serra Elisabet,
Cabot Cristina,
Esteve Montserrat,
Grasa Mar
Publication year - 2016
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21543
Subject(s) - medicine , endocrinology , adipose tissue , adipocyte , white adipose tissue , glucocorticoid , context (archaeology) , transcortin , glucocorticoid receptor , biology , chemistry , globulin , paleontology
Objective To evaluate how deficiency in corticosteroid‐binding globulin (CBG), the specific carrier of glucocorticoids, affects glucocorticoid availability and adipose tissue in obesity. Methods 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. Results 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. Conclusions 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.