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ACBP orchestrates the metabolic phenotype in Cushing’s syndrome
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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Feeding gut microbes to nourish the brain: unravelling the diet–microbiota–gut–brain axis
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Glucose limitation protects cancer cells from apoptosis induced by pyrimidine restriction and replication inhibition
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Inceptor binds to and directs insulin towards lysosomal degradation in β cells
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Cancer cachexia: multilevel metabolic dysfunction