M. Luisa Bonet

Centro de Investigación Biomédica en Red

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Andreu Palou

Universitat de les Illes Balears

100

Joan Ribot

Universitat de les Illes Balears

Catalina Picó

Universitat de les Illes Balears

Jaap Keijer

Wageningen University & Research

Jaume Amengual

American Jewish University

Petar Petrov

Universitat de València

Johannes von Lintig

Case Western Reserve University

Francisca Serra

Universitat de les Illes Balears

Evert M. van Schothorst

Wageningen University & Research

Nuria Granados

Centro de Investigación Biomédica en Red

Cooperative Institutions

Instituto de Salud Carlos III

Centro de Investigación Biomédica en Red

Universitat de les Illes Balears

Spanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition

Health Research Institute of the Balearic Islands

Inserm

Universitat de Barcelona

Universidad de Navarra

Cambridge University Press

Hospital Clínic de Barcelona

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Obesity: molecular bases of a multifactorial problem

European Journal of Nutrition (2000)

Andreu Palou Francisca Serra M. Luisa Bonet Catalina Picó

10.1007/s003940070017

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Citations (99)

SAT0486 Reference Intervals for Bone Turnover Markers in Spanish Premenopausal Women

Annals of the Rheumatic Diseases (2014)

Núria Guañabens Xavier Filella Ana Monegal Carmen Gómez‐Vaquero M. Luisa Bonet

Background

Bone turnover markers (BTMs) are used in clinical practice for assessing patients with osteoporosis and their treatment. In Spain it is necessary to fine-tune the reference intervals, since they were established years ago in a low number of individuals.

Objectives

The aims of this study were to establish robust reference intervals for BTMs in healthy young premenopausal Spanish women and to investigate the factors influencing BTMs.

Methods

185 women aged 35 to 45 yrs. from 13 centres in Catalonia were recruited. Blood and second void urine samples were collected between 8 and 10 a.m. after an overnight fast. Serum PINP and βCTX were measured by two automated methods (Elecsys, Roche^a and IDS-ISYS, Immunodiagnostic Systems^b), bone ALP by ELISA (IDS, Vitro), osteocalcin by IRMA (Cis Bio) and urinary NTX by ELISA (Osteomark, Vitro). PTH and 25OHD levels were measured in all participants, who completed a questionnaire on lifestyle factors. A quantile regression was fit to estimate the 5%, 50% and 95% percentiles for the BMTs, and the Fisher9s exact test and non-parametric tests were used to assess the influence of factors on BTMs.

Results

The median (P5-P95) for BTMs were: Bone ALP 9.3 (6.0-13.8) ng/ml, PINP^a 35.9 (20.8-60.6) ng/ml, PINP^b 35.8 (20.8-64.9) ng/ml, NTX 32.7 (19.3-68.9) nM/mM, CTX^a 0.250 (0.137-0.480) ng/ml, CTX^b 0.246 (0.107-0.541), Osteocalcin 14.0 (8.0-23.0) ng/ml. Oral contraceptive pills (OCPs) were reported in 10.9% of participants, mean BMI was 23 and 60% had 25OHD levels lower than 20 ng/ml. Women on OCPs had lower PINP levels (p=0.007).25OHD levels didn9t influence BTMs, but low BMI was associated with higher levels of almost all BTMs.

Conclusions

In conclusion, robust reference intervals for BTMs in a southern European country are provided.

Acknowledgements

This study was funded by a research grant from de Societat Catalana de Reumatologia.

Disclosure of Interest

None declared

DOI

10.1136/annrheumdis-2014-eular.1755

Bone remodeling

10.1136/annrheumdis-2014-eular.1755

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UCP1 Induction during Recruitment of Brown Adipocytes in White Adipose Tissue Is Dependent on Cyclooxygenase Activity

PLoS ONE (2010)

Lise Madsen Lone Møller Pedersen Haldis Haukaas Lillefosse Even Fjære Ingeborg Brønstad

Background The uncoupling protein 1 (UCP1) is a hallmark of brown adipocytes and pivotal for cold- and diet-induced thermogenesis. Methodology/Principal Findings Here we report that cyclooxygenase (COX) activity and prostaglandin E2 (PGE2) are crucially involved in induction of UCP1 expression in inguinal white adipocytes, but not in classic interscapular brown adipocytes. Cold-induced expression of UCP1 in inguinal white adipocytes was repressed in COX2 knockout (KO) mice and by administration of the COX inhibitor indomethacin in wild-type mice. Indomethacin repressed β-adrenergic induction of UCP1 expression in primary inguinal adipocytes. The use of PGE2 receptor antagonists implicated EP4 as a main PGE2 receptor, and injection of the stable PGE2 analog (EP3/4 agonist) 16,16 dm PGE2 induced UCP1 expression in inguinal white adipose tissue. Inhibition of COX activity attenuated diet-induced UCP1 expression and increased energy efficiency and adipose tissue mass in obesity-resistant mice kept at thermoneutrality. Conclusions/Significance Our findings provide evidence that induction of UCP1 expression in white adipose tissue, but not in classic interscapular brown adipose tissue is dependent on cyclooxygenase activity. Our results indicate that cyclooxygenase-dependent induction of UCP1 expression in white adipose tissues is important for diet-induced thermogenesis providing support for a surprising role of COX activity in the control of energy balance and obesity development.

Thermogenin

10.1371/journal.pone.0011391

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Citations (194)

All-Trans Retinoic Acid Decreases Murine Adipose Retinol Binding Protein 4 Production

Cellular Physiology and Biochemistry (2008)

Josep Mercader Nuria Granados M. Luisa Bonet Andreu Palou

Background/Aims: Adipose-derived retinol binding protein 4 (RBP4) might contribute to the development of insulin resistance, and therefore further knowledge of factors regulating it is of interest. Retinoic acid, the acid form of vitamin A, affects the expression of several adipokines related to insulin sensitivity in mice. Here, we sought to investigate its impact on adipose RBP4 production. Methods: Changes in RBP4 expression were analyzed in adipose tissues and liver of mice treated in vivo with all-trans retinoic acid (ATRA), and in 3T3-L1 adipocytes and adipocytes derived from mouse embryonic fibroblasts exposed to ATRA. Results: ATRA treatment in mice increased insulin sensitivity as assessed by the homeostatic model assessment for insulin resistance, and led to a reduction of RBP4 mRNA and protein levels in adipose tissues, a reduction of RBP4 protein but not RBP4 mRNA levels in the liver, and a marked increase in circulating RBP4 protein levels. In adipocyte cell models, ATRA down-regulated RBP4 mRNA levels in a dose-dependent manner: this effect was reproduced by retinaldehyde and retinoid receptors agonists, and correlated with a reduced accumulation of RBP4 protein in the culture medium. Conclusion: These results reveal a selective effect of ATRA inhibiting RBP4 expression specifically in adipocytes, and reinforce the concept that vitamin A vitamers may affect insulin sensitivity through effects on adipokine production.

Tretinoin

Retinol binding protein

10.1159/000149815

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Citations (51)

Reference intervals for bone turnover markers in Spanish premenopausal women

Bone Abstracts (2014)

Núria Guañabens Xavier Filella Ana Monegal Carmen Gómez‐Vaquero M. Luisa Bonet

Searchable abstracts of presentations at key conferences on calcified tissues ISSN 2052-1219 (online)

Turnover Intention

Bone remodeling

10.1530/boneabs.3.pp237

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Citations (5)

A global perspective on carotenoids: Metabolism, biotechnology, and benefits for nutrition and health

Progress in Lipid Research (2018)

Manuel Rodríguez‐Concepción Javier Ávalos M. Luisa Bonet Albert Boronat Lourdes Gómez‐Gómez

Photoprotection

10.1016/j.plipres.2018.04.004

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Citations (835)

Brown adipose tissue response to cafeteria diet-feeding involves induction of the UCP2 gene and is impaired in female rats as compared to males

Pflügers Archiv - European Journal of Physiology (1999)

Pilar Roca Ana M. Rodríguez Paula Oliver M. Luisa Bonet S. Quevedo

Cafeteria

10.1007/s004240051086

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Citations (57)

Glutathione S Transferase Activity in the Basal Forebrain Cholinergic Population

Neural Plasticity (1992)

Anna Francis Orlando Castellano Jimena García K. de la Guétara M. Luisa Bonet

The role of glutathione S transferase (GST) in the detoxification mechanisms in different

Glutathione S-transferase

Glutathione transferase

Transferase

Basal (medicine)

10.1155/np.1992.194

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Retinoblastoma Protein Knockdown Favors Oxidative Metabolism and Glucose and Fatty Acid Disposal in Muscle Cells

Journal of Cellular Physiology (2015)

Petar Petrov Joan Ribot Isabel C. López‐Mejía Lluís Fajas Andreu Palou

Deficiency in the retinoblastoma protein (Rb) favors leanness and a healthy metabolic profile in mice largely attributed to activation of oxidative metabolism in white and brown adipose tissues. Less is known about Rb modulation of skeletal muscle metabolism. This was studied here by transiently knocking down Rb expression in differentiated C2C12 myotubes using small interfering RNAs. Compared with control cells transfected with non-targeting RNAs, myotubes silenced for Rb (by 80-90%) had increased expression of genes related to fatty acid uptake and oxidation such as Cd36 and Cpt1b (by 61% and 42%, respectively), increased Mitofusin 2 protein content (∼2.5-fold increase), increased mitochondrial to nuclear DNA ratio (by 48%), increased oxygen consumption (by 65%) and decreased intracellular lipid accumulation. Rb silenced myotubes also displayed up-regulated levels of glucose transporter type 4 expression (∼5-fold increase), increased basal glucose uptake, and enhanced insulin-induced Akt phosphorylation. Interestingly, exercise in mice led to increased Rb phosphorylation (inactivation) in skeletal muscle as evidenced by immunohistochemistry analysis. In conclusion, the silencing of Rb enhances mitochondrial oxidative metabolism and fatty acid and glucose disposal in skeletal myotubes, and changes in Rb status may contribute to muscle physiological adaptation to exercise.

GLUT4

10.1002/jcp.25121

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Citations (11)

Up-regulation of muscle uncoupling protein 3 gene expression in mice following high fat diet, dietary vitamin A supplementation and acute retinoic acid-treatment

International Journal of Obesity (2003)

Félix López de Felipe M. Luisa Bonet Joan Ribot Andreu Palou

UCP3

Thermogenin

10.1038/sj.ijo.0802188

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Citations (77)