Estrogen Impairs Adipose Tissue Expansion and Cardiometabolic Profile in Obese-Diabetic Female Rats

It has been reported that 17β-estradiol (E2) can exert beneficial effects against the development of obesity, providing women with a healthier metabolic profile and conferring cardiovascular protection. However, a growing body of evidence questions this role in the context of obesity and diabetes. W...

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Detalles Bibliográficos
Autores: Martínez-Cignoni, Melanie Raquel, González-Vicens, Agustí, Morán-Costoya, Andrea, Proenza, Ana Maria, Gianotti, Magdalena, Valle, Adamo, Lladó, Isabel
Tipo de recurso: artículo
Fecha de publicación:2021
País:España
Institución:Conselleria de Salut i Consum del Govern de les Illes Balears
Repositorio:Docusalut
Idioma:inglés
OAI Identifier:oai:docusalut.com:20.500.13003/18491
Acceso en línea:https://hdl.handle.net/20.500.13003/18491
Access Level:acceso abierto
Palabra clave:Cardiovascular Diseases
Estradiol
Diabetes Mellitus
Diabetes Complications
Female
Rats
Rats, Zucker
Estrogens
Animals
Adipose Tissue
Obesity
Tejido Adiposo
Ratas Zucker
Animales
Ratas
Obesidad
Femenino
Enfermedades Cardiovasculares
Estrógenos
Complicaciones de la Diabetes
Descripción
Sumario:It has been reported that 17β-estradiol (E2) can exert beneficial effects against the development of obesity, providing women with a healthier metabolic profile and conferring cardiovascular protection. However, a growing body of evidence questions this role in the context of obesity and diabetes. We focus on the adipose tissue-heart axis to address the question of whether E2 can have metabolically detrimental effects in an obese-diabetic rat model. Female Zucker Diabetic Fatty rats were used: LEAN, fa/+; SHAM, sham-operated fa/fa; OVA, ovariectomized fa/fa, and OVA+E2, ovariectomized and E2 treated fa/fa. The secretory expression profile, tissue expansion parameters and composition of visceral adipose tissue, as well as systemic and cardiac parameters related to insulin resistance, fibrosis, and inflammation were analyzed. Ovariectomy induced an attenuation of both diabetic condition and metabolic dysfunction of adipose tissue and cardiac muscle in fa/fa rats, suggesting that E2, in the context of diabetes and obesity, loses its cardioprotective role and could even contribute to greater metabolic alterations. Adipose tissue from OVA rats showed a healthier hyperplastic expansion pattern, which could help maintain tissue function, increase adiponectin expression, and decrease pro-inflammatory adipokines. These findings should be taken into account when considering hormone replacement therapy for obese-diabetic women.