MartinsAD 2018 MiPschool Tromso E2
Event: MiPschool Tromso-Bergen 2018
Degradation of lifestyle habits is the major cause for the increase of obesity. This disease is characterized by an accumulation of adipose tissue in the body and is associated with other metabolic conditions, such as diabetes. The rising in the number of individuals with obesity becomes a worldwide problem that is increasing even in undeveloped countries. Some reports provide evidence for the fact that an incidence of metabolic diseases is associated with a decrease in sperm quality and birth rates. The effects of body energy balance in the reproductive function are evident, however the mechanisms behind this remain to be elucidated. In the organism, food intake and energy homeostasis are under the hormonal control of leptin-ghrelin axis, and the levels of these hormones are a reflex of the energy status of the subject. In the testis, the somatic Sertoli cells are the major checkpoint for spermatogenesis, and also an important hormonal target. Since, the effects of leptin and ghrelin in Sertoli cells are still unclear, we aim to disclose the effects of these hormones in the mitochondrial dynamics of human Sertoli cells (hSCs).
CloneticsTM hSCs and hSCs from testicular biopsies were exposed to leptin (0, 5, 25, 50 ng/mL) and ghrelin (0, 20, 100 and 500 pM) during 24h, respectively. The concentrations were chosen mimicking the levels reported in obese, normal weight, and severely undernourished or morbidly obese individuals. Protein expression of mitochondrial complexes was assessed by western blot in hSCs exposed to both hormones. We also evaluated mitochondrial membrane potential by JC-1 assay in hSCs exposed to leptin. The expression of genes involved in mitochondrial biogenesis was also measured by qualitative PCR.
Human SCs exposed to 5 and 50 ng/mL of leptin presented a decrease in protein levels of complex II compared with non-exposed cells. Transcript levels of Sirtuin 1 presented an increase in hSCs exposed to 50 ng/mL of leptin when compared with the other conditions. Ghrelin was able to modulate the protein expression of complex I, III and V in hSCs exposed to this hormone. Regarding the mitochondrial membrane potential, hSCs exposed to 100 pM of ghrelin showed a decrease in JC-1 ratio when compared with non-exposed cells. Finally, hSCs exposed to 500 pM of ghrelin presented an increase in JC-1 ratio when compared with cells exposed to 100 pM.
Leptin and ghrelin modulate mitochondrial complexes of hSCs, as well as mitochondrial dynamics. An alteration in mitochondrial dynamics of hSCs can be reflected in pivotal changes on spermatogenesis. Nevertheless, the role of leptin and ghrelin in mitochondria of hSCs remains to be elucidated and further experiments will be necessary.
• Bioblast editor: Plangger M
Martins AD(1#), Moreira BP(1#), Monteiro MP(1,2), Jarak I(1,3,4), Silva BM(4), Carvalho RA(4), Sousa M(1,5), Oliveira PF(1,6), Alves MG(1)
- Dept Microscopy, Lab Cell Biology, Unit Multidisciplinary Research Biomedicine, Inst Biomedical Sciences Abel Salazar
- Dept Anatomy, Unit Multidisciplinary Research Biomedicine, Inst Biomedical Sciences Abel Salazar; Univ Porto
- Fac Health Sciences, Univ Beira Interior, Covilhã
- Centre Functional Ecology, Univ Coimbra
- Centre Reproductive Genetics Professor Alberto Barros, Porto
- i3S Inst Investigação Inovação em Saúde, Univ Porto; Portugal. - email@example.com
# Both authors contributed equally
Labels: MiParea: Pharmacology;toxicology Pathology: Obesity
Organism: Human Tissue;cell: Genital
Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III, Complex V;ATP synthase