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Mechanistic insights into the aetiology of post-prandial decline in testosterone in reproductive-aged men.

Authors
  • Tremellen, Kelton1, 2
  • Hill, Amy1, 3
  • Pearce, Karma3
  • 1 Department of Obstetrics Gynaecology and Reproductive Medicine, Flinders University, Adelaide, South Australia, Australia. , (Australia)
  • 2 Repromed, Dulwich, South Australia, Australia. , (Australia)
  • 3 School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia. , (Australia)
Type
Published Article
Journal
Andrologia
Publisher
Wiley (Blackwell Publishing)
Publication Date
Nov 01, 2019
Volume
51
Issue
10
Identifiers
DOI: 10.1111/and.13418
PMID: 31475727
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

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. © 2019 Blackwell Verlag GmbH.

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