Effect of Leptin in Human Sertoli Cells Mitochondrial Physiology

• Tipo: Artigo em Revista Científica Internacional
• Data: 2020

Autores

Moreira, BP (Autor) Outra; Silva, AM (Autor) Outra; Martins, AD (Autor) Outra; Monteiro, M (Autor) ICBAS; sousa, m (Autor) ICBAS; Oliveira, PF (Autor) FMUP; Alves, MG (Autor) Outra

Revista

Título: Reproductive Sciences

ISSN: 1933-7191

Editora: SAGE

Indexação

ISI Web of Knowledge - 0 Citações

Scopus - 1 Citação

Outras Informações

ID Authenticus: P-00S-TT7

DOI: 10.1007/s43032-020-00328-x

Abstract (EN): 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.

Idioma: Inglês

Tipo (Avaliação Docente): Científica

Nº de páginas: 12