Carlos BOCOS

Dr. Carlos BOCOS

Facultad Farmacia, Universidad San Pablo-CEU, Madrid
orcid

Research Focus & Metrics

Academic Career Length

35Years (1992-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 June 1995 in The Journal of Steroid Biochemistry and Molecular Biology
Verified
Journal Article
Closed access
CBCarlos BOCOS
Carlos BOCOS
MGMartin Göttlicher
Martin Göttlicher
KGKaty Gearing
Katy Gearing
CBCarol Banner
Carol Banner
EEEva Enmark
Eva Enmark
JGJan-Åke Gustaffson
Jan-Åke Gustaffson

1 September 1998 in Molecular Pharmacology
Verified
Journal Article
Closed access
JCJ. Christopher Corton
J. Christopher Corton
LFLi-Qun Fan
Li-Qun Fan
SBSherri Brown
Sherri Brown
SASteven P. Anderson
Steven P. Anderson
CBCarlos BOCOS
Carlos BOCOS
JGJan-Åke Gustafsson
Jan-Åke Gustafsson
In this study, we show that peroxisome proliferator chemical (PPC) exposure leads to alterations in the expression of genes in rat liver regulated by the sex-specific growth hormone secretory pattern and induced during inflammation. Expression of the male-specificcytochrome P450 (P450) 2C11 and α2 urinary globulin (α2u) genes and the female-specificP450 2C12 gene was down-regulated by some PPC. Expression ofP450 2C13, also under control by the sex-specific growth hormone secretory pattern, was not altered by PPC treatment, indicating that regulation of CYP2C family members does not involve perturbation of the growth hormone secretory pattern. In contrast to the increases in expression observed when inflammation was induced in male rats, two positive acute-phase response genes, α1-acid glycoprotein and β-fibrinogen, were decreased by PPC exposure. The down-regulation of the P450 2C11 by WY-14,643 could be reproduced in cultured rat hepatocytes, indicating the down-regulation is a direct effect. Experiments in wild-type mice and mice that lacked a functional peroxisome proliferator-activated receptor-α gene showed that down-regulation by WY of α1-acid glycoprotein,β-fibrinogen, and a mouse homologue of α2uwas dependent on peroxisome proliferator-activated receptor-α expression. Our results demonstrate that PPC exposure leads to down-regulation of diverse liver-specific genes, includingCYP2C family members important in hormonal homeostasis and acute-phase response genes important in inflammatory responses.

1 October 2013 in The Journal of Nutritional Biochemistry
Verified
Journal Article
Closed access
LRLourdes Rodríguez
Lourdes Rodríguez
MPMaribel Panadero
Maribel Panadero
NRNúria Roglans
Núria Roglans
POPaola Otero
Paola Otero
JÁJuan J. Álvarez-Millán
Juan J. Álvarez-Millán
CBCarlos BOCOS
Carlos BOCOS

1 January 2015 in Journal of Nutrition and Metabolism
Verified
Journal Article
Open access
PDF file
LRLourdes Rodríguez
Lourdes Rodríguez
POPaola Otero
Paola Otero
MPMaribel Panadero
Maribel Panadero
SRSilvia Rodrigo
Silvia Rodrigo
JÁJuan J. Álvarez-Millán
Juan J. Álvarez-Millán
CBCarlos BOCOS
Carlos BOCOS
Objective. Fructose intake from added sugars correlates with the epidemic rise in metabolic syndrome and cardiovascular diseases. However, consumption of beverages containing fructose is allowed during gestation. Recently, we found that an intake of fructose (10% wt/vol) throughout gestation produces an impaired fetal leptin signalling. Therefore, we have investigated whether maternal fructose intake produces subsequent changes in their progeny.Methods. Blood samples from fed and 24 h fasted female and male 90-day-old rats born from fructose-fed, glucose-fed, or control mothers were used.Results. After fasting, HOMA-IR and ISI (estimates of insulin sensitivity) were worse in male descendents from fructose-fed mothers in comparison to the other two groups, and these findings were also accompanied by a higher leptinemia. Interestingly, plasma AOPP and uricemia (oxidative stress markers) were augmented in male rats from fructose-fed mothers compared to the animals from control or glucose-fed mothers. In contrast, female rats did not show any differences in leptinemia between the three groups. Further, insulin sensitivity was significantly improved in fasted female rats from carbohydrate-fed mothers. In addition, plasma AOPP levels tended to be diminished in female rats from carbohydrate-fed mothers.Conclusion. Maternal fructose intake induces insulin resistance, hyperleptinemia, and plasma oxidative stress in male, but not female, progeny.

1 February 1997 in Biochimie
Verified
Journal Article
Closed access
JCJ.C. Corton
J.C. Corton
CBCarlos BOCOS
Carlos BOCOS
EME.S. Moreno
E.S. Moreno
AMA. Merritt
A. Merritt
RCR.C. Cattley
R.C. Cattley
JGJ.-Å. Gustafsson
J.-Å. Gustafsson

26 March 2015 in European Journal of Nutrition
Verified
Journal Article
Closed access
PDF file
LRLourdes Rodríguez
Lourdes Rodríguez
MPMaribel Panadero
Maribel Panadero
NRNúria Roglans
Núria Roglans
POPaola Otero
Paola Otero
SRSilvia Rodrigo
Silvia Rodrigo
CBCarlos BOCOS
Carlos BOCOS