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Cushing’s syndrome: a model for sarcopenic obesity

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Abstract

Purpose

Obesity and its metabolic impairments are discussed as major risk factors for sarcopenia leading to sarcopenic obesity. Cushing’s syndrome is known to be associated with obesity and muscle atrophy. We compared Cushing’s syndrome with matched obese controls regarding body composition, physical performance, and biochemical markers to test the hypothesis that Cushing’s syndrome could be a model for sarcopenic obesity.

Methods

By propensity score matching, 47 controls were selected by body mass index and gender as obese controls. Fat mass and muscle mass were measured by bioelectrical impedance analysis. Muscle function was assessed by chair rising test and hand grip strength. Biochemical markers of glucose and lipid metabolism and inflammation (hsCRP) were measured in peripheral blood.

Results

Muscle mass did not differ between Cushing’s syndrome and obese controls. However, Cushing’s syndrome patients showed significantly greater chair rising time (9.5 s vs. 7.3 s, p = 0.008) and significantly lower hand grip strength (32.1 kg vs. 36.8 kg, p = 0.003). Cushing’s syndrome patients with impaired fasting glucose have shown the highest limitations in hand grip strength and chair rising time.

Conclusions

Similar to published data in ageing medicine, Cushing’s syndrome patients show loss of muscle function that cannot be explained by loss of muscle mass. Impaired muscle quality due to fat infiltration may be the reason. This is supported by the observation that Cushing’s syndrome patients with impaired glucose metabolism show strongest deterioration of muscle function. Research in sarcopenic obesity in elderly is hampered by confounding comorbidities and polypharmacy. As Cushing’s syndrome patients are frequently free of comorbidities and as Cushing’s syndrome is potentially curable we suggest Cushing’s syndrome as a clinical model for further research in sarcopenic obesity.

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Acknowledgements

The authors want to thank the volunteer participants and John Hoppe for providing language help.

Funding

This work is part of the German Cushing registry CUSTODES and has been supported by grants from the Else Kröner-Fresenius Stiftung to MR (2012 A103 and 2015 A228).

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Authors and Affiliations

  1. Medizinische Klinik und Poliklinik IV, Schwerpunkt Akutgeriatrie, Klinikum der Universität München (LMU), Munich, Germany

    Michael Drey & Ralf Schmidmaier

  2. Medizinische Klinik und Poliklinik IV, Schwerpunkt Endokrinologie, Klinikum der Universität München (LMU), Munich, Germany

    Christina M. Berr, Martin Reincke, Julia Fazel, Jochen Seissler, Jochen Schopohl, Martin Bidlingmaier, Stefanie Zopp, Nicole Reisch, Felix Beuschlein, Andrea Osswald & Ralf Schmidmaier

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  1. Michael Drey
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  2. Christina M. Berr
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Correspondence to Michael Drey.

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The authors declare that they have no competing interests.

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All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

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Drey, M., Berr, C.M., Reincke, M. et al. Cushing’s syndrome: a model for sarcopenic obesity. Endocrine 57, 481–485 (2017). https://doi.org/10.1007/s12020-017-1370-x

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  • DOI: https://doi.org/10.1007/s12020-017-1370-x

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