Endotoxin-initiated inflammation reduces testosterone production in men of reproductive age

Kelton Tremellen, Natalie McPhee, Karma Pearce, Sven Benson, Manfred Schedlowski, Harald Engler

    Research output: Contribution to journalArticlepeer-review

    55 Citations (Scopus)


    Inflammation, both acute and chronic, is associated with testosterone deficiency, raising the possibility of a direct causal link. One potential trigger for inflammation in obese men is the passage of intestinal bacteria into the circulation due to a breakdown in mucosal barrier integrity. Recently, we hypothesized that this endotoxin exposure may cause androgen deficiency in obese men. To test this hypothesis, we analyzed the relationship between serum levels of lipopo-lysaccharide-binding protein (LBP), an indirect measure of endotoxin exposure, against male reproductive hormones, inflammatory markers (C-reactive protein, IL-1β, IL-6, TNF-α), and adiposity in 75 men. Adiposity was positively correlated with endotoxin exposure (LBP) and inflammation (C-reactive protein, IL-6) and negatively correlated with testosterone. Furthermore, endotoxemia (LBP) was negatively correlated with serum testosterone but positively correlated with IL-6. Multivariate analysis revealed a significant, negative correlation between serum IL-6 and free testosterone. In a second interventional study, low-dose endotoxin challenge in lean men produced a transient inflammatory response that was followed by a decline in serum testosterone, without changes in LH or FSH, providing further evidence that endotoxin-driven inflammation may result in impaired Leydig cell function.

    Original languageEnglish
    Pages (from-to)E206-E213
    Number of pages8
    JournalAmerican Journal of Physiology - Endocrinology and Metabolism
    Issue number3
    Publication statusPublished - 1 Mar 2018


    • Endotoxin
    • Inflammation
    • Interleukin-6
    • Lipopolysaccharide
    • Obesity
    • Testosterone


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