Search Results
You are looking at 1 - 2 of 2 items for
- Author: Natalia Pascuali x
- Refine by access: All content x
Search for other papers by Mariana Di Pietro in
Google Scholar
PubMed
Search for other papers by Natalia Pascuali in
Google Scholar
PubMed
Search for other papers by Fernanda Parborell in
Google Scholar
PubMed
Search for other papers by Dalhia Abramovich in
Google Scholar
PubMed
Polycystic ovary syndrome (PCOS) is the most prevalent endocrine pathology among women in reproductive age. Its main symptoms are oligo or amenorrhea, hyperandrogenism and the presence of ovarian cysts. It is also associated with infertility, obesity and insulin resistance. Mainly due to its heterogeneity, PCOS treatments are directed to manage its symptoms and to prevent associated diseases. The correct formation and regression of blood vessels during each ovarian cycle is indispensable for proper follicular development, ovulation and corpus luteum formation. The importance of these processes opened a new and promising field: ovarian angiogenesis. Vascular alterations characterize numerous pathologies, either with increased, decreased or abnormal angiogenesis. In the last years, several anomalies of ovarian angiogenesis have been described in women with PCOS. Therefore, it has been suggested that these alterations may be associated with the decreased – or lack of – ovulation rates and for the formation of cysts in the PCOS ovaries. Restoration of a proper vessel formation in the ovaries may lead to improved follicular development and ovulation in these patients. In the present review, we attempt to summarize the alterations in ovarian angiogenesis that have been described in women with PCOS. We also discuss the therapeutic approaches aimed to correct these alterations and their beneficial effects on the treatment of infertility in PCOS.
Search for other papers by Candela Velazquez in
Google Scholar
PubMed
Search for other papers by Mayra Bordaquievich in
Google Scholar
PubMed
Search for other papers by Yamila Herrero in
Google Scholar
PubMed
Search for other papers by Débora Juana Cohen in
Google Scholar
PubMed
Search for other papers by María Silvia Bianchi in
Google Scholar
PubMed
Search for other papers by Patricia Cuasnicu in
Google Scholar
PubMed
Search for other papers by Katherine Prost in
Google Scholar
PubMed
Department of Pathology, College of Medicine, University of Illinois at Chicago (UIC), Chicago, Illinois, USA
Search for other papers by Natalia Pascuali in
Google Scholar
PubMed
Search for other papers by Fernanda Parborell in
Google Scholar
PubMed
Search for other papers by Dalhia Abramovich in
Google Scholar
PubMed
In brief
The hypoglycemic drug metformin has shown reproductive effects in women, although its mechanism of action is not fully understood. In this study, we demonstrate the direct effects of metformin on the ovary of healthy mice, with no alterations in fertility.
Abstract
Metformin is a hypoglycemic drug widely used in type-2 diabetes (T2D) patients. In recent years, this drug has been suggested as a treatment for gestational diabetes and recommended to women with ovarian hyperstimulation syndrome (PCOS) to increase the chances of pregnancy or avoid early miscarriages. However, the exact effects of metformin on the female reproductive tract in general, and on the ovary in particular, are still not completely understood. In this study, we analyzed the effect of metformin on fertility and ovarian physiology in healthy female mice. We found that this drug altered the estrous cycle, early follicular development, serum estradiol and progesterone levels, and ovarian steroidogenic enzyme expression. Moreover, ovarian angiogenesis was lower in metformin-treated animals compared with untreated ones, whereas natural or gonadotropin-induced fertilization rates remained unchanged. However, offspring of metformin-treated animals displayed decreased body weight at birth. In this work, we unraveled the main effects of metformin on the ovary, isolated from other conditions such as hyperglycemia and hyperandrogenism, which is essential for a better understanding of metformin’s mechanisms of action on reproduction and fertility.
