Effect of Leptin in Human Sertoli Cells Mitochondrial Physiology
Leptin is an adipose tissue hormone that acts as energy sensor and reproductive function regulator. Recent reports suggest that leptin is involved in mitochondrial biogenesis in different tissue cells. Herein, we hypothesized that leptin could also affect Sertoli cells mitochondrial dynamics and biogenesis. Human Sertoli cells (hSCs) were cultured in the presence of different leptin concentrations (5, 25 and 50 ng/mL) or vehicle for 24 h. The three different leptin concentrations were selected to mimic the circulating levels found either in normal weight, obese, and morbidly obese individuals, respectively. Leptin receptor (LEPR) expression was evaluated as well as mitochondrial membrane potential, complexes levels, complex II activity and basal respiration. Moreover, mitochondrial DNA copy number and expression of mitochondrial biogenesis markers were assessed. In hSCs, leptin concentrations similar to those found both in lean men decreased mitochondrial complex II protein levels, but no changes in its activity were observed. This is in agreement with basal respiration and mitochondrial membrane potential assessments, which indicate no alterations in mitochondrial fitness. Furthermore, no changes in mitochondrial biogenesis markers were observed upon leptin exposure, although SIRT1/3 levels were increased after exposure to the highest leptin concentration. Overall, the increase in SIRT1/3 levels suggests a role for leptin in glycolysis, which given the relevance of SCs glycolytic flux for germ cells nutritional support further reinforces that this mechanism can be linked to obesity-related subfertility/infertility.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:28 |
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| Enthalten in: |
Reproductive sciences (Thousand Oaks, Calif.) - 28(2021), 3 vom: 30. März, Seite 920-931 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Moreira, Bruno P [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 23.11.2021 Date Revised 14.12.2021 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1007/s43032-020-00328-x |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| 100 | 1 | |a Moreira, Bruno P |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Effect of Leptin in Human Sertoli Cells Mitochondrial Physiology |
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| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Leptin is an adipose tissue hormone that acts as energy sensor and reproductive function regulator. Recent reports suggest that leptin is involved in mitochondrial biogenesis in different tissue cells. Herein, we hypothesized that leptin could also affect Sertoli cells mitochondrial dynamics and biogenesis. Human Sertoli cells (hSCs) were cultured in the presence of different leptin concentrations (5, 25 and 50 ng/mL) or vehicle for 24 h. The three different leptin concentrations were selected to mimic the circulating levels found either in normal weight, obese, and morbidly obese individuals, respectively. Leptin receptor (LEPR) expression was evaluated as well as mitochondrial membrane potential, complexes levels, complex II activity and basal respiration. Moreover, mitochondrial DNA copy number and expression of mitochondrial biogenesis markers were assessed. In hSCs, leptin concentrations similar to those found both in lean men decreased mitochondrial complex II protein levels, but no changes in its activity were observed. This is in agreement with basal respiration and mitochondrial membrane potential assessments, which indicate no alterations in mitochondrial fitness. Furthermore, no changes in mitochondrial biogenesis markers were observed upon leptin exposure, although SIRT1/3 levels were increased after exposure to the highest leptin concentration. Overall, the increase in SIRT1/3 levels suggests a role for leptin in glycolysis, which given the relevance of SCs glycolytic flux for germ cells nutritional support further reinforces that this mechanism can be linked to obesity-related subfertility/infertility | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Leptin | |
| 650 | 4 | |a Male fertility | |
| 650 | 4 | |a Mitochondria | |
| 650 | 4 | |a Sertoli cells | |
| 650 | 4 | |a Spermatogenesis | |
| 650 | 7 | |a DNA, Mitochondrial |2 NLM | |
| 650 | 7 | |a LEPR protein, human |2 NLM | |
| 650 | 7 | |a Leptin |2 NLM | |
| 650 | 7 | |a Receptors, Leptin |2 NLM | |
| 650 | 7 | |a Electron Transport Complex II |2 NLM | |
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| 650 | 7 | |a EC 3.5.1.- |2 NLM | |
| 650 | 7 | |a Sirtuin 3 |2 NLM | |
| 650 | 7 | |a EC 3.5.1.- |2 NLM | |
| 700 | 1 | |a Silva, Ana M |e verfasserin |4 aut | |
| 700 | 1 | |a Martins, Ana D |e verfasserin |4 aut | |
| 700 | 1 | |a Monteiro, Mariana P |e verfasserin |4 aut | |
| 700 | 1 | |a Sousa, Mário |e verfasserin |4 aut | |
| 700 | 1 | |a Oliveira, Pedro F |e verfasserin |4 aut | |
| 700 | 1 | |a Alves, Marco G |e verfasserin |4 aut | |
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