Open AccessTestosterone replacement therapy in insulin‐sensitive hypogonadal men restores phosphatidylcholine levels by regulation of arachidonic acid metabolism
Author(s) -
Fanelli Giuseppina,
Belardo Antonio,
Savino Rocco,
Rinalducci Sara,
Zolla Lello
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15392
Subject(s) - lysophosphatidylcholine , arachidonic acid , endocrinology , medicine , testosterone (patch) , phosphatidylcholine , phospholipase a2 , chemistry , thromboxanes , metabolism , insulin , biochemistry , phospholipid , enzyme , membrane
Abstract Male hypogonadism is notoriously associated with altered lipid metabolism. In this study, we performed an untargeted mass spectrometry–based profiling of plasma lipids from twenty healthy and twenty hypogonadal men before and after testosterone replacement therapy (TRT) for 60 days. Results demonstrated that hypogonadism was associated with a significant increase in sphingomyelin (SM), whereas phosphatidylcholine (PC) was mainly cleaved by activated phospholipase‐A2 into lysophosphatidylcholine (LPC). In hypogonadal patients, arachidonic acid (AA), also produced through the latter cleavage, was prevalently bio‐transformed into leukotriene B4 (LTB4) and not into endoperoxides from which prostaglandins and thromboxanes are derived. Interestingly, upon testosterone treatment SM, PC and LPC returned to levels similar to controls. Also, AA was newly converted into prostaglandin‐A2, thromboxane‐A2 and 5(S)‐hydroxyeicosatetraenoic acid (HETE), suggesting that testosterone probably plays a role in controlling hypogonadal alterations above reported.