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17β-estradiol ameliorates lipotoxicity-induced hepatic mitochondrial oxidative stress and insulin resistance

Identificadores del recurso

Galmés-Pascual BM, Martínez-Cignoni MR, Morán-Costoya A, Bauza-Thorbrügge M, Sbert-Roig M, Valle A, et al. 17β-estradiol ameliorates lipotoxicity-induced hepatic mitochondrial oxidative stress and insulin resistance. Free Radic Biol Med. 2020 Apr;150:148–60.

http://hdl.handle.net/20.500.13003/18457

10.1016/j.freeradbiomed.2020.02.016

1873-4596

32105829

2-s2.0-85081006119

000540692300003

Jatorria

(Docusalut. Repositorio institucional del sistema sanitario público de las Islas Baleares)

Fitxa

Izenburu:: 17β-estradiol ameliorates lipotoxicity-induced hepatic mitochondrial oxidative stress and insulin resistance
Tema:: Estradiol; Oxidative Stress; Liver; Male; Rats, Wistar; Female; Rats; Animals; Non-alcoholic Fatty Liver Disease; Diet, High-Fat; Insulin Resistance; Animales; Ratas; Ratas Wistar; Enfermedad del Hígado Graso no Alcohólico; Femenino; Estrés Oxidativo; Resistencia a la Insulina; Dieta Alta en Grasa; Hígado; Masculino
Deskribapen:: The prevalence and severity of nonalcoholic fatty liver disease (NAFLD) is higher in men and postmenopausal women compared to premenopausal women, suggesting a protective role for ovarian hormones. Diet-induced obesity and fatty acids surplus promote mitochondrial dysfunction in liver, triggering oxidative stress and activation of c-Jun N-terminal kinase (JNK) which has been related to the development of insulin resistance and steatosis, the main hallmarks of NAFLD. Considering that estrogen, in particular 17β-estradiol (E2), have been reported to improve mitochondrial biogenesis and function in liver, our aim was to elucidate the role of E2 in preventing fatty acid-induced insulin resistance in hepatocytes through modulation of mitochondrial function, oxidative stress and JNK activation. An in vivo study was conducted in Wistar rats of both sexes (n = 7) fed control diet and high-fat diet (HFD), and in vitro studies were carried out in HepG2 cells treated with palmitate (PA) and E2 for 24 h. Our HFD-fed male rats showed a prediabetic state characterized by greater systemic and hepatic insulin resistance, as well as higher lipid content in liver, compared to females. JNK activation rose markedly in males in response to HFD feeding, in parallel with mitochondrial dysfunction and oxidative stress. Consistently, in PA-exposed HepG2 cells, E2 treatment prevented JNK activation, insulin resistance and fatty acid accumulation. Altogether, our data highlights the importance of E2 as a mitigating factor of fatty acid-insulin resistance in hepatocytes through downregulation of JNK activation, by means of mitochondrial function improvement.
Idioma:: English
Harreman:: https://doi.org/10.1016/j.freeradbiomed.2020.02.016
Autor/Productor:: Galmes-Pascual, Bel M.; Martínez-Cignoni, Melanie Raquel; Morán-Costoya, Andrea; Bauza-Thorbrügge, Marco; Sbert-Roig, Miquel; Valle, Adamo; Proenza, Ana Maria; Lladó, Isabel; Gianotti, Magdalena
Argitaratzaile:: Elsevier
Eskubideak:: Attribution-NonCommercial-NoDerivatives 4.0 Internacional; http://creativecommons.org/licenses/by-nc-nd/4.0/; open access
Data:: 2023-01-09T13:39:10Z; 2020-04
Tipo de recurso:: research article

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