Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 475, Issue 1-2, Pages 261-276Publisher
SPRINGER
DOI: 10.1007/s11010-020-03879-4
Keywords
Ovariectomy; Menopause model; Metabolic syndrome; Hypoestrogenism
Categories
Funding
- Consejo Nacional de Ciencia y Tecnologia (CONACYT)
- PAPIIT, DGAPA, UNAM [IN227116]
Ask authors/readers for more resources
Bilateral ovariectomy is the best characterized and the most reported animal model of human menopause. Ovariectomized rodents develop insulin resistance (IR) and visceral obesity, the main risk factors in the pathophysiology of metabolic syndrome (MS). These alterations are a consequence of hypoestrogenic status, which produces an augment of visceral fat, high testosterone levels (hyperandrogenism), as well as inflammation, oxidative stress, and metabolic complications, such as dyslipidemia, hepatic steatosis, and endothelial dysfunction, among others. Clinical trials have reported that menopause per se increases the severity and incidence of MS, and causes the highest mortality due to cardiovascular disease in women. Despite all the evidence, there are no reports that clarify the influence of estrogenic deficiency as a cause of MS. In this review, we provide evidence that ovariectomized rodents can be used as a menopausal metabolic syndrome model for evaluating and discovering new, safe, and effective therapeutic approaches in the treatment of cardiometabolic complications associated to MS during menopause.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available