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Chronic hypercortisolism causes more persistent visceral adiposity than HFD-induced obesity.

Abstract

Excessive and prolonged glucocorticoid (GC) exposure, resulting from either prescribed or endogenous hypercortisolism, is associated with a high cardiovascular and metabolic burden (Cushing's syndrome). Although previous studies in humans and mice have reported heterogeneous data about the persistence of metabolic syndrome features after remission of hypercortisolism, there is still controversy as to whether this is due to the deleterious changes induced by GCs during active disease or the result of various other factors interfering in the recovery period. In order to study metabolic effects after remission, we used a reversible mouse model of corticosterone (CORT) (100 µg/ml) administration in drinking water for five weeks, followed by a 10-week recovery period. We compared CORT-induced effects at these time points with a high-fat diet-treated group (HFD 45%) and a vehicle group (VEH). Plasma CORT, 11β-HSD activity, food intake, glucose levels, interscapular brown adiposity, hepatic triglycerides and muscle mass were found altered during CORT treatment but normalized after recovery. Although hyperinsulinemia and insulin resistance were increased during CORT and HFD treatment, insulin homeostasis remained altered following the recovery period only in CORT-treated mice. Subcutaneous and visceral adipose tissues (SAT and VAT) were enlarged during HFD and CORT treatment as measured by MRI. However, increased muscle lipid content, adiposity and macrophage infiltration in VAT were only present in the CORT group following recovery. Taken together, CORT-induced insulin alterations were more potent than HFD-induced ones during the same period of treatment, and also more persistent long term . Moreover, we demonstrated that CORT treatment induces more long-lasting visceral adipose tissue enlargement than HFD.

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  • Authors+Show Affiliations

    ,

    G Garcia-Eguren, Group of Endocrine Disorders, Institut d'Investigacions Biomediques August Pi i Sunyer, Barcelona, Spain.

    ,

    O Giró, Group of Encocrine Disorders, Institut d'Investigacions Biomediques August Pi i Sunyer, Barcelona, Spain.

    ,

    M Romero, Biochemistry and Molecular Medicine, Universitat de Barcelona Facultat de Biologia, Barcelona, Spain.

    ,

    M Grasa, Biochemistry and Molecular Medicine, Universitat de Barcelona Facultat de Biologia, Barcelona, Spain.

    F Hanzu, Endocrinology and Nutrition, Hospital Clinic de Barcelona, Barcelona, Spain.

    Source

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    31117053

    Citation

    Garcia-Eguren, Guillermo, et al. "Chronic Hypercortisolism Causes More Persistent Visceral Adiposity Than HFD-induced Obesity." The Journal of Endocrinology, 2019.
    Garcia-Eguren G, Giró O, Romero MDM, et al. Chronic hypercortisolism causes more persistent visceral adiposity than HFD-induced obesity. J Endocrinol. 2019.
    Garcia-Eguren, G., Giró, O., Romero, M. D. M., Grasa, M., & Hanzu, F. A. (2019). Chronic hypercortisolism causes more persistent visceral adiposity than HFD-induced obesity. The Journal of Endocrinology, doi:10.1530/JOE-19-0168.
    Garcia-Eguren G, et al. Chronic Hypercortisolism Causes More Persistent Visceral Adiposity Than HFD-induced Obesity. J Endocrinol. 2019 May 1; PubMed PMID: 31117053.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Chronic hypercortisolism causes more persistent visceral adiposity than HFD-induced obesity. AU - Garcia-Eguren,Guillermo, AU - Giró,Oriol, AU - Romero,Maria Del Mar, AU - Grasa,Mar, AU - Hanzu,Felicia Alexandra, Y1 - 2019/05/01/ PY - 2019/02/15/received PY - 2019/05/20/accepted PY - 2019/5/23/pubmed PY - 2019/5/23/medline PY - 2019/5/23/entrez JF - The Journal of endocrinology JO - J. Endocrinol. N2 - Excessive and prolonged glucocorticoid (GC) exposure, resulting from either prescribed or endogenous hypercortisolism, is associated with a high cardiovascular and metabolic burden (Cushing's syndrome). Although previous studies in humans and mice have reported heterogeneous data about the persistence of metabolic syndrome features after remission of hypercortisolism, there is still controversy as to whether this is due to the deleterious changes induced by GCs during active disease or the result of various other factors interfering in the recovery period. In order to study metabolic effects after remission, we used a reversible mouse model of corticosterone (CORT) (100 µg/ml) administration in drinking water for five weeks, followed by a 10-week recovery period. We compared CORT-induced effects at these time points with a high-fat diet-treated group (HFD 45%) and a vehicle group (VEH). Plasma CORT, 11β-HSD activity, food intake, glucose levels, interscapular brown adiposity, hepatic triglycerides and muscle mass were found altered during CORT treatment but normalized after recovery. Although hyperinsulinemia and insulin resistance were increased during CORT and HFD treatment, insulin homeostasis remained altered following the recovery period only in CORT-treated mice. Subcutaneous and visceral adipose tissues (SAT and VAT) were enlarged during HFD and CORT treatment as measured by MRI. However, increased muscle lipid content, adiposity and macrophage infiltration in VAT were only present in the CORT group following recovery. Taken together, CORT-induced insulin alterations were more potent than HFD-induced ones during the same period of treatment, and also more persistent long term . Moreover, we demonstrated that CORT treatment induces more long-lasting visceral adipose tissue enlargement than HFD. SN - 1479-6805 UR - https://www.unboundmedicine.com/medline/citation/31117053/Chronic_hypercortisolism_causes_more_persistent_visceral_adiposity_than_HFD-induced_obesity L2 - https://joe.bioscientifica.com/doi/10.1530/JOE-19-0168 DB - PRIME DP - Unbound Medicine ER -