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<p>Exogenous glucocorticoids are extensively used to combat a plethora of medical conditions. However, a sustained excess of exogenous glucocorticoids causes several adverse metabolic conditions, most notably Cushing’s Syndrome which presents with a well-defined phenotype. Herein we determine the ability of the non-proteogenic amino acid, beta alanine (BA) to mitigate the development of Cushing’s Syndrome. Female C57BL/6J mice were treated with high dose corticosterone or a vehicle control with or without BA for 3 weeks. Indirect calorimetry was conducted during the final week of treatment and glucose tolerance was assessed upon completion. BA partially attenuated the development of the Cushingoid phenotype with a reduction in central adipose accumulation, bodyweight gain and trended reduction in liver weight. Despite this reduction, BA also reversed the apparent corticosterone induced increase in energy expenditure (EE), whilst further restricting mice to carbohydrate utilisation. However, BA completely preserved glucose tolerance. We identify a novel therapeutic role of BA in mitigating the development of some of the symptoms associated with exogenous glucocorticoid treatment, most notably glucose intolerance. Further investigation is now required to determine the extent of BA’s protection as well as the mechanisms involved.</p>

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Beta-alanine provides partial protection against the development of symptoms driven by glucocorticoid excess

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月23日

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  • Samuel R. Heaselgrave,
  • Minghao Deng,
  • Gareth G. Lavery,
  • Craig L. Doig

摘要

Exogenous glucocorticoids are extensively used to combat a plethora of medical conditions. However, a sustained excess of exogenous glucocorticoids causes several adverse metabolic conditions, most notably Cushing’s Syndrome which presents with a well-defined phenotype. Herein we determine the ability of the non-proteogenic amino acid, beta alanine (BA) to mitigate the development of Cushing’s Syndrome. Female C57BL/6J mice were treated with high dose corticosterone or a vehicle control with or without BA for 3 weeks. Indirect calorimetry was conducted during the final week of treatment and glucose tolerance was assessed upon completion. BA partially attenuated the development of the Cushingoid phenotype with a reduction in central adipose accumulation, bodyweight gain and trended reduction in liver weight. Despite this reduction, BA also reversed the apparent corticosterone induced increase in energy expenditure (EE), whilst further restricting mice to carbohydrate utilisation. However, BA completely preserved glucose tolerance. We identify a novel therapeutic role of BA in mitigating the development of some of the symptoms associated with exogenous glucocorticoid treatment, most notably glucose intolerance. Further investigation is now required to determine the extent of BA’s protection as well as the mechanisms involved.