Emerging Role of Corticosteroid-Binding Globulin in Glucocorticoid-Driven Metabolic Disorders.

1. Front Endocrinol (Lausanne). 2016 Dec 19;7:160. doi: 10.3389/fendo.2016.00160.
eCollection 2016.

Emerging Role of Corticosteroid-Binding Globulin in Glucocorticoid-Driven
Metabolic Disorders.

Moisan MP(1), Castanon N(1).

Author information:
(1)INRA, Nutrition and Integrative Neurobiology (NutrINeurO), UMR 1286, Bordeaux,
France; Université de Bordeaux, Nutrition and Integrative Neurobiology
(NutrINeurO), UMR 1286, Bordeaux, France.

Glucocorticoid hormones (GCs) are critical for survival since they ensure the
energy supply necessary to the body in an ever challenging environment. GCs are
known to act on appetite, glucose metabolism, fatty acid metabolism, and storage.
However, to be beneficial to the body, GC levels should be maintained in an
optimal window of concentrations. Not surprisingly, conditions of GC excess or
deficiency, e.g., Cushing’s syndrome or Addison’s disease, are associated with
severe alterations of energy metabolism. Corticosteroid-binding globulin (CBG),
through its high specific affinity for GCs, plays a critical role in regulating
plasma GC levels and their access to target cells. Genetic studies in various
species including humans have revealed that CBG is the major factor influencing
interindividual genetic variability of plasma GC levels, both in basal and stress
conditions. Some, but not all, of these genetic studies have also provided data
linking CBG levels to body composition and insulin levels. The examination of
CBG-deficient mice submitted to hyperlipidic diets unveiled specific roles for
CBG in lipid storage and metabolism. An influence of CBG on appetite has not been
reported but remains to be more finely analyzed. Finally, only male mice have
been examined under high-fat diet, while obesity is affecting women even more
than men. Overall, a role of CBG in GC-driven metabolic disorders is emerging in
recent studies. Although subtle, the influence of CBG in these diseases could
open the way to new therapeutic interventions since CBG is easily accessible in
the blood.

DOI: 10.3389/fendo.2016.00160
PMCID: PMC5165022
PMID: 28066325

Auteurs Bordeaux Neurocampus