Testosterone replacement therapy in insulin‐sensitive hypogonadal men restores phosphatidylcholine levels by regulation of arachidonic acid metabolism
| Autor: | Sara Rinalducci, Giuseppina Fanelli, Lello Zolla, Antonio Belardo, Rocco Savino |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty Leukotriene B4 Hormone Replacement Therapy medicine.medical_treatment Short Communication Short Communications 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine testosterone replacement therapy Internal medicine Phosphatidylcholine medicine Humans Insulin Testosterone Arachidonic Acid Hypogonadism Lipid metabolism Cell Biology Lipid Metabolism 030104 developmental biology Endocrinology Lysophosphatidylcholine arachidonic acid metabolism Treatment Outcome chemistry Thromboxanes 030220 oncology & carcinogenesis Case-Control Studies Lipidomics Phosphatidylcholines Molecular Medicine Arachidonic acid lipids (amino acids peptides and proteins) Sphingomyelin |
| Zdroj: | Journal of Cellular and Molecular Medicine |
| ISSN: | 1582-4934 1582-1838 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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