ACBP orchestrates the metabolic phenotype in Cushing’s syndrome: Metabolism

Mhairi Paul; Mark Nixon

doi:10.1038/s42255-024-01169-7

ACBP orchestrates the metabolic phenotype in Cushing’s syndrome: Metabolism

Mhairi Paul, Mark Nixon^*

^*Corresponding author for this work

Research output: Contribution to journal › Comment/debate › peer-review

Abstract

Cushing’s syndrome, a condition of chronic glucocorticoid excess, disrupts metabolic homeostasis, driving fat redistribution and promoting insulin resistance. New research uses a series of elegant approaches to reveal acyl-CoA-binding protein (ACBP) as a mediator of the metabolic disturbances associated with elevated glucocorticoid levels in mice.

Original language	English
Pages (from-to)	2220-2221
Number of pages	2
Journal	Nature Metabolism
Volume	6
Early online date	22 Nov 2024
DOIs	https://doi.org/10.1038/s42255-024-01169-7
Publication status	Published - Dec 2024

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abstract = "Cushing{\textquoteright}s syndrome, a condition of chronic glucocorticoid excess, disrupts metabolic homeostasis, driving fat redistribution and promoting insulin resistance. New research uses a series of elegant approaches to reveal acyl-CoA-binding protein (ACBP) as a mediator of the metabolic disturbances associated with elevated glucocorticoid levels in mice.",

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AB - Cushing’s syndrome, a condition of chronic glucocorticoid excess, disrupts metabolic homeostasis, driving fat redistribution and promoting insulin resistance. New research uses a series of elegant approaches to reveal acyl-CoA-binding protein (ACBP) as a mediator of the metabolic disturbances associated with elevated glucocorticoid levels in mice.

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ACBP orchestrates the metabolic phenotype in Cushing’s syndrome: Metabolism

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