Abrupt decrease in serum testosterone levels after an oral glucose load in men: implications for screening for hypogonadism

Authors

  • Lisa M. Caronia,

    1. Reproductive Endocrine Unit of the Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
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    • These two authors contributed equally to this work.

  • Andrew A. Dwyer,

    1. Endocrinology, Diabetes, & Metabolism Service, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland
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    • These two authors contributed equally to this work.

  • Douglas Hayden,

    1. Department of Biostatistics, General Clinical Research Center, Massachusetts General Hospital, Boston, MA, USA
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  • Francesca Amati,

    1. Department of Physiology, University of Lausanne, Lausanne, Switzerland
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  • Nelly Pitteloud,

    1. Endocrinology, Diabetes, & Metabolism Service, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland
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  • Frances J. Hayes

    Corresponding author
    1. Department of Endocrinology, St. Vincent's University Hospital, Dublin, Ireland
    • Reproductive Endocrine Unit of the Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
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Correspondence: Frances J. Hayes, Department of Endocrinology, St. Vincent's University Hospital, Elm Park, Dublin 4, Ireland. Tel.: +353 1 221 4407; Fax +353 1 221 4981; E-mail: f.hayes@st-vincents.ie

Summary

Objective

This study examines the physiological impact of a glucose load on serum testosterone (T) levels in men with varying glucose tolerance (GT).

Design

Cross-sectional study.

Patients and Methods

74 men (19–74 years, mean 51·4 ± 1·4 years) underwent a standard 75-g oral glucose tolerance test with blood sampling at 0, 30, 60, 90 and 120 min. Fasting serum glucose, insulin, total T (and calculated free T), LH, SHBG, leptin and cortisol were measured.

Results

57% of the men had normal GT, 30% had impaired GT and 13% had newly diagnosed type 2 diabetes. Glucose ingestion was associated with a 25% decrease in mean T levels (delta = −4·2 ± 0·3 nm, P < 0·0001). T levels remained suppressed at 120 min compared with baseline (13·7 ± 0·6 vs 16·5 ± 0·7 nm, P < 0·0001) and did not differ across GT or BMI. Of the 66 men with normal T levels at baseline, 10 (15%) had levels that decreased to the hypogonadal range (<9·7 nm) at one or more time points. SHBG, LH and cortisol levels were unchanged. Leptin levels decreased from baseline at all time points (P < 0·0001).

Conclusions

Glucose ingestion induces a significant reduction in total and free T levels in men, which is similar across the spectrum of glucose tolerance. This decrease in T appears to be because of a direct testicular defect, but the absence of compensatory changes in LH suggests an additional central component. Men found to have low nonfasting T levels should be re-evaluated in the fasting state.

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