Difference between revisions of "Moreira 2017 MiP2017"
(Created page with "{{Abstract |title=left|90px|Mitochondrial Physiology Society|MiPsociety |info=MiP2017 |year=2017 |event=MiP2017 |abstract=Image:MITOEAGLE-lo...") Ā |
Ā |
||
Line 1: | Line 1: | ||
{{Abstract | {{Abstract | ||
|title=[[Image: | |title=[[Image:MoreiraB.jpg|left|90px|Bruno Moreira]] Leptin role in Sertoli cells mitochondria ā a novel mechanism with possible implications in the male reproductive potential of obese individuals. | ||
|info=[[MiP2017]] | |info=[[MiP2017]] | ||
|authors=Moreira BP, Martins AD, Monteiro MP, Sousa M, Oliveira PF, Alves MG | |||
|year=2017 | |year=2017 | ||
|event=MiP2017 | |event=MiP2017 | ||
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]] | |abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]] | ||
Metabolic diseases such as obesity have been on the rise during the last decades, reaching worrying levels. Several statistics point towards an even worse future, where several European countries are expected to reach 70% of obese population, in the next 15 years. Obesity is characterized by an abnormal accumulation of fat and is associated with other co-morbidities, such as diabetes. Several causes are appointed for this vertiginous increase including sedentarism and an increased intake of energy-dense foods rich in carbohydrates. Following an inverse trend, fertility rates and sperm parameters of reproductive-aged men are decreasing, evidencing a relationship between both events. In fact, reproductive function is sensitive to energy balance; however, the molecular mechanisms that associate obesity and reproductive dysfunction are still undisclosed [1]. Leptin, an adipocyte-derived hormone, is upregulated in overweight and obese individuals [2]. Besides the well-described actions in the hypothalamus, leptin has important actions in several peripheral tissues. However, despite the focus in leptin during the last two decades, its role in testicular cells is still undisclosed. Recently, our group has identified the leptin receptor in human Sertoli cells (SCs) and demonstrated that leptin modulates human SCs glycolytic profile [3]. Furthermore, several studies have reported leptinās ability to modulate mitochondrial biogenesis and dynamics [4]. | |||
In this study, we studied the potential role of leptin in mitochondrial dynamics and biogenesis in rat and human SCs. SerW3, a rat Sertoli cell line, and Cloneticsā¢ human SCs cultures were established. Once rat SCs reached 80% confluence, they were divided in 4 different groups and incubated with different leptin concentrations during 24h. One group was treated with Sertoli cell medium without addition of leptin while the other groups were treated with 3 different leptin concentrations (5 ng/mL ā normal plasmatic concentration, 25 ng/mL āconcentration found in obese individuals and 50 ng/mL ā supraphysiological concentration). This procedure was repeated for human SCs.Ā In human SCs the concentration of 50 ng/mL mimics the levels found in morbidly obese individuals. Afterwards, cells were tested for mitochondrial membrane potential (JC-1 assay), protein expression of mitochondrial complexes (Western blot) and expression of genes involved in mitochondrial biogenesis (qPCR). | |||
Our results suggest that leptin modulates mitochondrial membrane potential in a concentration of 50 ng/mL in rat SCs. Leptin exposure had no effect in levels of mitochondrial complexes and mRNA levels of mitochondrial biogenesis markers in these cells (Fig. 1). In human SCs, protein levels of complex II presented changes in the groups treated with 5 and 50 ng/mL. Additionally, mRNA levels of ''SIRT1'' presented changes in the group treated with 50 ng/mL (Fig. 2). | |||
Our results show that high concentrations of leptin, found in morbidly obese individuals, modulate mitochondrial function in rat SCs. This could illustrate a novel mechanism through which leptin affects the male reproductive potential in obese male individuals. Notably, some differences obtained are species-dependent illustrating different responses to leptin exposure from rat and human SCs. These differences, particularly in ''SIRT1'' mRNA levels, could also suggest leptinās involvement in the metabolic control of spermatogenesis. | |||
|editor=[[Kandolf G]] | |editor=[[Kandolf G]] | ||
}} | }} | ||
{{Labeling}} | {{Labeling | ||
|area=mt-Biogenesis;mt-density, Comparative MiP;environmental MiP, Exercise physiology;nutrition;life style, Pharmacology;toxicology | |||
|diseases=Obesity | |||
|organism=Human | |||
|tissues=Genital | |||
|enzymes=Complex II;succinate dehydrogenase | |||
}} | |||
== Figures == | |||
[[File:Moreira_figure1_MiP2017.jpg|left|450px]] | |||
[[File:Moreira_figure2_MiP2017.jpg|left|450px]] | |||
Ā | |||
== Affiliations == | == Affiliations == | ||
::::Moreira BP(1,2,3), Martins AD(2,3), Monteiro MP(3,4), Sousa M(2,3), Oliveira PF(3,5,6), Alves MG(2,3) | |||
::::#Health Sciences Research Center (CICS), Univ Beira Interior, CovilhĆ£, Portugal | |||
::::#Dept Microscopy, Lab Cell Biol, Inst Biomedical Sciences Abel Salazar (ICBAS), Univ Porto, Portugal | |||
::::#Unit Multidisciplinary Research in Biomedicine (UMIB), Inst Biomedical Sciences Abel Salazar (ICBAS), Univ Porto, Portugal | |||
::::#Dept Anatomy, Inst Biomedical Sciences Abel Salazar (ICBAS), Univ Porto, Portugal | |||
::::#Dept Genetics, Fac Medicine, Porto, Portugal | |||
::::#i3S ā Inst InvestigaĆ§Ć£o InovaĆ§Ć£o em SaĆŗde, Univ Porto, Portugal. ā brunommoreira9@gmail.com | |||
== References == | == References == | ||
::::#Oliveira PF, Sousa M, Silva BM, Monteiro MP, Alves MG (2017) Obesity, energy balance and spermatogenesis. Reproduction 153:173-85. | |||
::::#Alves MG, Jesus TT, Sousa M, Goldberg E, Silva BM, Oliveira PF (2016) Male fertility and obesity: are ghrelin, leptin and glucagon-like peptide-1 pharmacologically relevant? Curr Pharm Des 22:783-91. | |||
::::#Martins AD, Moreira AC, Sa R, Monteiro MP, Sousa M, Carvalho RA, Silva BM, Oliveira PF, Alves MG (2015) Leptin modulates human Sertoli cells acetate production and glycolytic profile: a novel mechanism of obesity-induced male infertility? Biochim Biophys Acta 1852:1824-32. | |||
::::#Blanquer-Rossello MM, Santandreu FM, Oliver J, Roca P, Valle A (2015) Leptin Modulates Mitochondrial Function, Dynamics and Biogenesis in MCF-7 Cells. J Cell Biochem 116:2039-48. |
Latest revision as of 11:39, 3 October 2017
Leptin role in Sertoli cells mitochondria ā a novel mechanism with possible implications in the male reproductive potential of obese individuals. |
Link: MiP2017
Moreira BP, Martins AD, Monteiro MP, Sousa M, Oliveira PF, Alves MG (2017)
Event: MiP2017
Metabolic diseases such as obesity have been on the rise during the last decades, reaching worrying levels. Several statistics point towards an even worse future, where several European countries are expected to reach 70% of obese population, in the next 15 years. Obesity is characterized by an abnormal accumulation of fat and is associated with other co-morbidities, such as diabetes. Several causes are appointed for this vertiginous increase including sedentarism and an increased intake of energy-dense foods rich in carbohydrates. Following an inverse trend, fertility rates and sperm parameters of reproductive-aged men are decreasing, evidencing a relationship between both events. In fact, reproductive function is sensitive to energy balance; however, the molecular mechanisms that associate obesity and reproductive dysfunction are still undisclosed [1]. Leptin, an adipocyte-derived hormone, is upregulated in overweight and obese individuals [2]. Besides the well-described actions in the hypothalamus, leptin has important actions in several peripheral tissues. However, despite the focus in leptin during the last two decades, its role in testicular cells is still undisclosed. Recently, our group has identified the leptin receptor in human Sertoli cells (SCs) and demonstrated that leptin modulates human SCs glycolytic profile [3]. Furthermore, several studies have reported leptinās ability to modulate mitochondrial biogenesis and dynamics [4].
In this study, we studied the potential role of leptin in mitochondrial dynamics and biogenesis in rat and human SCs. SerW3, a rat Sertoli cell line, and Cloneticsā¢ human SCs cultures were established. Once rat SCs reached 80% confluence, they were divided in 4 different groups and incubated with different leptin concentrations during 24h. One group was treated with Sertoli cell medium without addition of leptin while the other groups were treated with 3 different leptin concentrations (5 ng/mL ā normal plasmatic concentration, 25 ng/mL āconcentration found in obese individuals and 50 ng/mL ā supraphysiological concentration). This procedure was repeated for human SCs. In human SCs the concentration of 50 ng/mL mimics the levels found in morbidly obese individuals. Afterwards, cells were tested for mitochondrial membrane potential (JC-1 assay), protein expression of mitochondrial complexes (Western blot) and expression of genes involved in mitochondrial biogenesis (qPCR).
Our results suggest that leptin modulates mitochondrial membrane potential in a concentration of 50 ng/mL in rat SCs. Leptin exposure had no effect in levels of mitochondrial complexes and mRNA levels of mitochondrial biogenesis markers in these cells (Fig. 1). In human SCs, protein levels of complex II presented changes in the groups treated with 5 and 50 ng/mL. Additionally, mRNA levels of SIRT1 presented changes in the group treated with 50 ng/mL (Fig. 2).
Our results show that high concentrations of leptin, found in morbidly obese individuals, modulate mitochondrial function in rat SCs. This could illustrate a novel mechanism through which leptin affects the male reproductive potential in obese male individuals. Notably, some differences obtained are species-dependent illustrating different responses to leptin exposure from rat and human SCs. These differences, particularly in SIRT1 mRNA levels, could also suggest leptinās involvement in the metabolic control of spermatogenesis.
ā¢ Bioblast editor: Kandolf G
Labels: MiParea: mt-Biogenesis;mt-density, Comparative MiP;environmental MiP, Exercise physiology;nutrition;life style, Pharmacology;toxicology Pathology: Obesity
Organism: Human Tissue;cell: Genital
Enzyme: Complex II;succinate dehydrogenase
Figures
Affiliations
- Moreira BP(1,2,3), Martins AD(2,3), Monteiro MP(3,4), Sousa M(2,3), Oliveira PF(3,5,6), Alves MG(2,3)
- Health Sciences Research Center (CICS), Univ Beira Interior, CovilhĆ£, Portugal
- Dept Microscopy, Lab Cell Biol, Inst Biomedical Sciences Abel Salazar (ICBAS), Univ Porto, Portugal
- Unit Multidisciplinary Research in Biomedicine (UMIB), Inst Biomedical Sciences Abel Salazar (ICBAS), Univ Porto, Portugal
- Dept Anatomy, Inst Biomedical Sciences Abel Salazar (ICBAS), Univ Porto, Portugal
- Dept Genetics, Fac Medicine, Porto, Portugal
- i3S ā Inst InvestigaĆ§Ć£o InovaĆ§Ć£o em SaĆŗde, Univ Porto, Portugal. ā brunommoreira9@gmail.com
- Moreira BP(1,2,3), Martins AD(2,3), Monteiro MP(3,4), Sousa M(2,3), Oliveira PF(3,5,6), Alves MG(2,3)
References
- Oliveira PF, Sousa M, Silva BM, Monteiro MP, Alves MG (2017) Obesity, energy balance and spermatogenesis. Reproduction 153:173-85.
- Alves MG, Jesus TT, Sousa M, Goldberg E, Silva BM, Oliveira PF (2016) Male fertility and obesity: are ghrelin, leptin and glucagon-like peptide-1 pharmacologically relevant? Curr Pharm Des 22:783-91.
- Martins AD, Moreira AC, Sa R, Monteiro MP, Sousa M, Carvalho RA, Silva BM, Oliveira PF, Alves MG (2015) Leptin modulates human Sertoli cells acetate production and glycolytic profile: a novel mechanism of obesity-induced male infertility? Biochim Biophys Acta 1852:1824-32.
- Blanquer-Rossello MM, Santandreu FM, Oliver J, Roca P, Valle A (2015) Leptin Modulates Mitochondrial Function, Dynamics and Biogenesis in MCF-7 Cells. J Cell Biochem 116:2039-48.