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Mechanistic insights into the aetiology of post‐prandial decline in testosterone in reproductive‐aged men
Author(s) -
Tremellen Kelton,
Hill Amy,
Pearce Karma
Publication year - 2019
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.13418
Subject(s) - testosterone (patch) , endocrinology , medicine , leydig cell , ingestion , obesity , endocrine system , androgen , meal , hormone , luteinizing hormone
Obesity is known to be associated with impaired testicular function potentially resulting in androgen deficiency and subfertility. While the underlying cause of obesity‐related male hypogonadism is multi‐factorial, here, we investigated the impact of dietary fat on testicular endocrine function. Ingestion of a high‐fat “fast food” mixed meal, a common practice for obese men, produced a 25% fall in serum testosterone within an hour of eating, with levels remaining suppressed below fasting baseline for up to 4 hr. These changes in serum testosterone were not associated with any significant changes in serum gonadotrophins. The nadir in serum testosterone preceded the post‐prandial increase in serum IL‐6/IL‐17 by several hours, suggesting that inflammation was unlikely the cause. Furthermore, intravenous administration of fat (Intralipid) had no impact on testosterone levels, while an identical oral dose of fat did suppress testosterone. These results suggest that fat does not directly impair Leydig cell function, but rather the passage of fat through the intestinal tract elicits a response that indirectly elicits a post‐prandial fall in testosterone.