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Article

Effects of Maternal Fructose Intake on Perinatal ER-Stress: A Defective XBP1s Nuclear Translocation Affects the ER-stress Resolution

1
Facultad de Farmacia, Universidad San Pablo-CEU, CEU Universities, Montepríncipe, Boadilla del Monte, 28668 Madrid, Spain
2
Facultad de Farmacia, Universidad de Barcelona, CIBERobn, IBUB, Avda. Joan XXIII 27-31, 08028 Barcelona, Spain
3
CQS Lab, Calle Marie Curie 5, Rivas-Vaciamadrid, 28521 Madrid, Spain
*
Author to whom correspondence should be addressed.
Nutrients 2019, 11(8), 1935; https://doi.org/10.3390/nu11081935
Received: 28 June 2019 / Revised: 13 August 2019 / Accepted: 15 August 2019 / Published: 17 August 2019
Endoplasmic reticulum (ER) homeostasis is crucial to appropriate cell functioning, and when disturbed, a safeguard system called unfolded protein response (UPR) is activated. Fructose consumption modifies ER homeostasis and has been related to metabolic syndrome. However, fructose sweetened beverages intake is allowed during gestation. Therefore, we investigate whether maternal fructose intake affects the ER status and induces UPR. Thus, administrating liquid fructose (10% w/v) to pregnant rats partially activated the ER-stress in maternal and fetal liver and placenta. In fact, a fructose-induced increase in the levels of pIRE1 (phosphorylated inositol requiring enzyme-1) and its downstream effector, X-box binding protein-1 spliced form (XBP1s), was observed. XBP1s is a key transcription factor, however, XBP1s nuclear translocation and the expression of its target genes were reduced in the liver of the carbohydrate-fed mothers, and specifically diminished in the fetal liver and placenta in the fructose-fed mothers. These XBP1s target genes belong to the ER-associated protein degradation (ERAD) system, used to buffer ER-stress and to restore ER-homeostasis. It is known that XBP1s needs to form a complex with diverse proteins to migrate into the nucleus. Since methylglyoxal (MGO) content, a precursor of advanced glycation endproducts (AGE), was augmented in the three tissues in the fructose-fed mothers and has been related to interfere with the functioning of many proteins, the role of MGO in XBP1s migration should not be discarded. In conclusion, maternal fructose intake produces ER-stress, but without XBP1s nuclear migration. Therefore, a complete activation of UPR that would resolve ER-stress is lacking. A state of fructose-induced oxidative stress is probably involved. View Full-Text
Keywords: fructose; pregnancy; ER stress; methylglyoxal; XBP1s fructose; pregnancy; ER stress; methylglyoxal; XBP1s
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MDPI and ACS Style

Rodrigo, S.; Panadero, M.I.; Fauste, E.; Rodríguez, L.; Roglans, N.; Álvarez-Millán, J.J.; Otero, P.; Laguna, J.C.; Bocos, C. Effects of Maternal Fructose Intake on Perinatal ER-Stress: A Defective XBP1s Nuclear Translocation Affects the ER-stress Resolution. Nutrients 2019, 11, 1935. https://doi.org/10.3390/nu11081935

AMA Style

Rodrigo S, Panadero MI, Fauste E, Rodríguez L, Roglans N, Álvarez-Millán JJ, Otero P, Laguna JC, Bocos C. Effects of Maternal Fructose Intake on Perinatal ER-Stress: A Defective XBP1s Nuclear Translocation Affects the ER-stress Resolution. Nutrients. 2019; 11(8):1935. https://doi.org/10.3390/nu11081935

Chicago/Turabian Style

Rodrigo, Silvia, María I. Panadero, Elena Fauste, Lourdes Rodríguez, Núria Roglans, Juan J. Álvarez-Millán, Paola Otero, Juan C. Laguna, and Carlos Bocos. 2019. "Effects of Maternal Fructose Intake on Perinatal ER-Stress: A Defective XBP1s Nuclear Translocation Affects the ER-stress Resolution" Nutrients 11, no. 8: 1935. https://doi.org/10.3390/nu11081935

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