Publications by authors named "Marina Ercilia Dasso"
Article Synopsis
- * The study investigates how follicle-stimulating hormone (FSH) influences lipid storage and fat-related gene expression in SCs, using cultured SCs from 20-day-old rats.
- * Results showed that FSH increased lipid droplet and triacylglyceride levels in SCs and activated specific genes, suggesting it regulates lipid storage through the cAMP/PKA signaling pathway to meet energy needs.
Liraglutide, an analog of the incretin hormone glucagon-like peptide 1 (GLP-1), is widely used for obesity and type 2 diabetes treatment. However, there is scarce information about its effects on testicular function. Within the testis, Sertoli cells (SCs) provide nutritional support for germ cells; they metabolize glucose to lactate, which is delivered to germ cells to be used as a preferred energy substrate.
View Article and Find Full Text PDFIn Brief: FSH leads to glutamine dependence, which is required for mTORC1 activation and in consequence Sertoli cell proliferation.
Abstract: The spermatogenic capacity of adult individuals depends on, among other factors, the number of Sertoli cells (SCs) that result from the proliferative waves during development. FSH upregulates SC proliferation at least partly, through the activation of the PI3K/Akt/mTORC1 pathway, among other mechanisms.
Sertoli cells (SCs) are essential to maintaining germ cell development. Metformin, the main pharmacologic treatment for pediatric type 2 diabetes, is administered to children during SC maturation. The present study aimed to analyze whether metformin affects SC energy metabolism and blood-testis barrier (BTB) integrity.
View Article and Find Full Text PDFThe definitive number of Sertoli cells (SCs), achieved during the proliferative periods, defines the spermatogenic capacity in adulthood. It is recognized that FSH is the main mitogen targeting SC and that it exerts its action, at least partly, through the activation of the PI3K/Akt/mTORC1 pathway. mTORC1 controls a large number of cellular functions, including glycolysis and cell proliferation.
View Article and Find Full Text PDFPurpose: Zinc restriction during fetal and postnatal development could program cardiovascular diseases in adulthood. The aim of this study was to determine the effects of zinc restriction during fetal life, lactation, and/or post-weaning growth on cardiac inflammation, apoptosis, oxidative stress, and nitric oxide system of male and female adult rats.
Methods: Wistar rats were fed a low- or a control zinc diet during pregnancy and up to weaning.