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1. Safety and efficacy of avalglucosidase alfa versus alglucosidase alfa in patients with late-onset Pompe disease (COMET): a phase 3, randomised, multicentre trial

Author

Behin, Anthony, Boentert, Matthias, Carvalho, Gerson, Chahin, Nizar, Charrow, Joel, Deegan, Patrick, Durmus Tekce, Hacer, Duval, Fanny, Genge, Angela, Gutmann, Ludwig, Henderson, Robert D, Hennermann, Julia B, Hiwot, Tarekegn, Hughes, Derralynn, Karaa, Amel, Karam, Chafic, Kautzky-Willer, Alexandra, Komaki, Hirofumi, Laforet, Pascal, Longo, Nicola, Malinova, Vera, Maré, Ricardo, Maxit, Clarisa, Mengel, Eugen, Moggio, Maurizio Gualtiero, Molnár, Mária Judit, Mongini, Tiziana Enrica, Nadaj-Pakleza, Aleksandra, Nascimento Osorio, Andres, Noury, Jean-Baptiste, Oliveira, Acary Souza Bulle, Parman, Yesim, Pena, Loren, Remiche, Gauthier, Sciacco, Monica, Shieh, Perry B, Smith, Cheryl, Stulnig, Thomas, Taithe, Frederic, Tard, Céline, Tarnopolsky, Mark, Vorgerd, Matthias, Whitley, Chester, Young, Peter, Alonso-Pérez, Jorge, Altemus, Patricia, Aubé-Nathier, Anne-Catherine, Avelar, Jennifer B, Bailey, Carrie, Bekircan-Kurt, Can Ebru, Billy, Jenny, Boschi, Silvia, Brown, Kathryn E, Carrera Garcia, Laura, Chase, Lauren, Cirne, Hamilton, Danjoux, Loïc, Davion, Jean-Baptiste, DeArmey, Stephanie, Fedotova, Ekaterina, Gandolfo, Eve, Grosz, Zoltan, Guellec, Dewi, Guettsches, Anne-Katrin, Guglieri, Michela, Hatcher, Erin, Helms, Sina, Hufgard-Leitner, Miriam, Klyushnikov, Sergey A., Langton, Jacqui, Linková, Lenka, Mavroudakis, Nicolas, Mazurová, Stella, Mori, Madoka, Müller-Miny, Louisa, Musumeci, Olimpia, Nance, Christopher S, Natera-de Benito, Daniel, Neel, Robert, Niizawa, Gabriela A, Noll, Lauren, Ortega, Erik, Pasnoor, Mamatha, Pautot, Vivien, Potulska-Chromik, Anna, Pugliese, Alessia, Questienne, Claire, Ramos Lopes, Margarida, Reyes-Leiva, David, Riedl, Michaela, Rugiero, Marcelo Francisco, Salort-Campana, Emmanuelle, Sgobbi Souza, Paulo Victor, Sole, Guilhem, Solera, Luca, Souto Lopes, Suzara, Specht, Sabine, Statland, Jeffrey, Swenson, Andrea, Tan, Chong Yew, Tizon, Sónia, van der Beek, N A M E, van Kooten, Harmke A., Wencel, Marie, Wenninger, Stephan, Zagnoli, Fabien, Diaz-Manera, Jordi, Kishnani, Priya S, Kushlaf, Hani, Ladha, Shafeeq, Mozaffar, Tahseen, Straub, Volker, Toscano, Antonio, van der Ploeg, Ans T, Berger, Kenneth I, Clemens, Paula R, Chien, Yin-Hsiu, Day, John W, Illarioshkin, Sergey, Roberts, Mark, Attarian, Shahram, Borges, Joao Lindolfo, Bouhour, Francoise, Choi, Young Chul, Erdem-Ozdamar, Sevim, Goker-Alpan, Ozlem, Kostera-Pruszczyk, Anna, Haack, Kristina An, Hug, Christopher, Huynh-Ba, Olivier, Johnson, Judith, Thibault, Nathan, Zhou, Tianyue, Dimachkie, Mazen M, and Schoser, Benedikt

Published
2021
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2. The management and clinical outcomes of pregnancies in women with urea cycle disorders: A review of the literature and results of an international survey.

Author

Stepien, Karolina M., Langendonk, Janneke G., Dao, Myriam, Gomes, Daniel Costa, Douillard, Claire, Filipsson, Karin, Glamuzina, Emma, Haverkamp, Jorien A., Langeveld, Mirjam, Lehman, Anna, de Lonlay, Pascale, Lund, Allan M., Oscarson, Mikael, Peltenburg, N. Chantal, Ramadža, Danijela Petković, Ramachandran, Radha, Reismann, Peter, Shtylla, Alboren, Tchan, Michel, and Tan, Chong Yew

Abstract

An increasing number of women with urea cycle disorders (UCDs) are reaching child‐bearing age and becoming pregnant. Improved diagnostics and increased awareness of inherited metabolic diseases has also led to more previously undetected women being diagnosed with a UCD during or shortly after pregnancy. Pregnancy increases the risk of acute metabolic decompensation with hyperammonemia—which can occur in any trimester, and/or the postpartum period, and may lead to encephalopathy, psychosis, coma, and even death, if not diagnosed promptly and treated appropriately. There are also (theoretical) concerns that a maternal UCD, or its treatment, may cause potential risks for the unborn child. Currently evidence on management and outcome of pregnancies in UCDs is limited to case reports and there are no clear guidelines. In order to inform management and investigate outcomes of pregnancies in women with a UCD, we performed a retrospective review of published cases and analyzed data collected from an international online survey. We conclude that, although risk during the intra‐ and postpartum period exists, multidisciplinary management by an experienced team and a prospective plan usually result in successful pregnancy, labor, delivery, and postpartum period. No deaths were reported in mothers managed accordingly. With the exception of male neonates with Ornithine Transcarbamylase deficiency, the clinical outcome of children born to mothers with UCDs appears positive, although follow‐up is limited. The outcome for women presenting with a first acute metabolic decompensation during pregnancy or postpartum is less favorable. Deaths were associated with diagnostic delay/late management of hyperammonemia in previously undiagnosed women. [ABSTRACT FROM AUTHOR]

Published
2024
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3. The management and clinical outcomes of pregnancies in women with urea cycle disorders: A review of the literature and results of an international survey

Author

Stepien, Karolina M., primary, Langendonk, Janneke G., additional, Dao, Myriam, additional, Gomes, Daniel Costa, additional, Douillard, Claire, additional, Filipsson, Karin, additional, Glamuzina, Emma, additional, Haverkamp, Jorien A., additional, Langeveld, Mirjam, additional, Lehman, Anna, additional, de Lonlay, Pascale, additional, Lund, Allan M., additional, Oscarson, Mikael, additional, Peltenburg, N. Chantal, additional, Ramadža, Danijela Petković, additional, Ramachandran, Radha, additional, Reismann, Peter, additional, Shtylla, Alboren, additional, Tchan, Michel, additional, Tan, Chong Yew, additional, Wilson, Callum, additional, Woodall, Alison, additional, Murphy, Elaine, additional, and Wagenmakers, Margreet A. E. M., additional

Published
2023
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6. Regulation of mitochondrial morphology and function by stearoylation of TFR1

Author

Senyilmaz, Deniz, Virtue, Sam, Xu, Xiaojun, Tan, Chong Yew, Griffin, Julian L., Miller, Aubry K., Vidal-Puig, Antonio, and Teleman, Aurelio A.

Subjects
Genetic aspects, Health aspects, Cell receptors -- Health aspects -- Genetic aspects, Mitochondria -- Health aspects -- Genetic aspects, Stearic acid -- Health aspects, Genetic regulation -- Health aspects
Abstract

To study the function of very long chain fatty acids, we analysed Drosophila lacking Elovl6 (refs 6, 7), the enzyme elongating C16 fatty acids to C18. Sequence analysis identified noa [...], Mitochondria are involved in a variety of cellular functions, including ATP production, amino acid and lipid biogenesis and breakdown, signalling and apoptosis (1-3). Mitochondrial dysfunction has been linked to neurodegenerative diseases, cancer and ageing (4). Although transcriptional mechanisms that regulate mitochondrial abundance are known (5), comparatively little is known about how mitochondrial function is regulated. Here we identify the metabolite stearic acid (C18:0) and human transferrin receptor 1 (TFR1; also known as TFRC) as mitochondrial regulators. We elucidate a signalling pathway whereby C18:0 stearoylates TFR1, thereby inhibiting its activation of JNK signalling. This leads to reduced ubiquitination of mitofusin via HUWE1, thereby promoting mitochondrial fusion and function. We find that animal cells are poised to respond to both increases and decreases in C18:0 levels, with increased C18:0 dietary intake boosting mitochondrial fusion in vivo. Intriguingly, dietary C18:0 supplementation can counteract the mitochondrial dysfunction caused by genetic defects such as loss of the Parkinson's disease genes Pink or Parkin in Drosophila. This work identifies the metabolite C18:0 as a signalling molecule regulating mitochondrial function in response to diet.

Published
2015

8. Safety and efficacy of avalglucosidase alfa versus alglucosidase alfa in patients with late-onset Pompe disease (COMET): a phase 3, randomised, multicentre trial

Author

Diaz-Manera, Jordi, primary, Kishnani, Priya S, additional, Kushlaf, Hani, additional, Ladha, Shafeeq, additional, Mozaffar, Tahseen, additional, Straub, Volker, additional, Toscano, Antonio, additional, van der Ploeg, Ans T, additional, Berger, Kenneth I, additional, Clemens, Paula R, additional, Chien, Yin-Hsiu, additional, Day, John W, additional, Illarioshkin, Sergey, additional, Roberts, Mark, additional, Attarian, Shahram, additional, Borges, Joao Lindolfo, additional, Bouhour, Francoise, additional, Choi, Young Chul, additional, Erdem-Ozdamar, Sevim, additional, Goker-Alpan, Ozlem, additional, Kostera-Pruszczyk, Anna, additional, Haack, Kristina An, additional, Hug, Christopher, additional, Huynh-Ba, Olivier, additional, Johnson, Judith, additional, Thibault, Nathan, additional, Zhou, Tianyue, additional, Dimachkie, Mazen M, additional, Schoser, Benedikt, additional, Behin, Anthony, additional, Boentert, Matthias, additional, Carvalho, Gerson, additional, Chahin, Nizar, additional, Charrow, Joel, additional, Deegan, Patrick, additional, Durmus Tekce, Hacer, additional, Duval, Fanny, additional, Genge, Angela, additional, Gutmann, Ludwig, additional, Henderson, Robert D, additional, Hennermann, Julia B, additional, Hiwot, Tarekegn, additional, Hughes, Derralynn, additional, Karaa, Amel, additional, Karam, Chafic, additional, Kautzky-Willer, Alexandra, additional, Komaki, Hirofumi, additional, Laforet, Pascal, additional, Longo, Nicola, additional, Malinova, Vera, additional, Maré, Ricardo, additional, Maxit, Clarisa, additional, Mengel, Eugen, additional, Moggio, Maurizio Gualtiero, additional, Molnár, Mária Judit, additional, Mongini, Tiziana Enrica, additional, Nadaj-Pakleza, Aleksandra, additional, Nascimento Osorio, Andres, additional, Noury, Jean-Baptiste, additional, Oliveira, Acary Souza Bulle, additional, Parman, Yesim, additional, Pena, Loren, additional, Remiche, Gauthier, additional, Sciacco, Monica, additional, Shieh, Perry B, additional, Smith, Cheryl, additional, Stulnig, Thomas, additional, Taithe, Frederic, additional, Tard, Céline, additional, Tarnopolsky, Mark, additional, Vorgerd, Matthias, additional, Whitley, Chester, additional, Young, Peter, additional, Alonso-Pérez, Jorge, additional, Altemus, Patricia, additional, Aubé-Nathier, Anne-Catherine, additional, Avelar, Jennifer B, additional, Bailey, Carrie, additional, Bekircan-Kurt, Can Ebru, additional, Billy, Jenny, additional, Boschi, Silvia, additional, Brown, Kathryn E, additional, Carrera Garcia, Laura, additional, Chase, Lauren, additional, Cirne, Hamilton, additional, Danjoux, Loïc, additional, Davion, Jean-Baptiste, additional, DeArmey, Stephanie, additional, Fedotova, Ekaterina, additional, Gandolfo, Eve, additional, Grosz, Zoltan, additional, Guellec, Dewi, additional, Guettsches, Anne-Katrin, additional, Guglieri, Michela, additional, Hatcher, Erin, additional, Helms, Sina, additional, Hufgard-Leitner, Miriam, additional, Klyushnikov, Sergey A., additional, Langton, Jacqui, additional, Linková, Lenka, additional, Mavroudakis, Nicolas, additional, Mazurová, Stella, additional, Mori, Madoka, additional, Müller-Miny, Louisa, additional, Musumeci, Olimpia, additional, Nance, Christopher S, additional, Natera-de Benito, Daniel, additional, Neel, Robert, additional, Niizawa, Gabriela A, additional, Noll, Lauren, additional, Ortega, Erik, additional, Pasnoor, Mamatha, additional, Pautot, Vivien, additional, Potulska-Chromik, Anna, additional, Pugliese, Alessia, additional, Questienne, Claire, additional, Ramos Lopes, Margarida, additional, Reyes-Leiva, David, additional, Riedl, Michaela, additional, Rugiero, Marcelo Francisco, additional, Salort-Campana, Emmanuelle, additional, Sgobbi Souza, Paulo Victor, additional, Sole, Guilhem, additional, Solera, Luca, additional, Souto Lopes, Suzara, additional, Specht, Sabine, additional, Statland, Jeffrey, additional, Swenson, Andrea, additional, Tan, Chong Yew, additional, Tizon, Sónia, additional, van der Beek, N A M E, additional, van Kooten, Harmke A., additional, Wencel, Marie, additional, Wenninger, Stephan, additional, and Zagnoli, Fabien, additional

Published
2021
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10. In-Depth Phenotyping for Clinical Stratification of Gaucher Disease

Author

D'Amore, Simona, primary, Page, Kathleen, additional, Donald, Aimée, additional, Taiyari, Khadijeh, additional, Tom, Brian, additional, Deegan, Patrick Brian, additional, Tan, Chong Yew, additional, Poole, Kenneth, additional, Jones, Simon Allan, additional, Mehta, Atul, additional, Hughes, Derralynn, additional, Sharma, Reena, additional, Lachmann, Robin Henry, additional, Chakrapani, Aunpam, additional, Geberhiwot, Tarekegn, additional, Santra, Saikat, additional, and Cox, Timothy Martin, additional

Published
2021
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11. Adaptive Changes of the Insig1/SREBP1/SCD1 Set Point Help Adipose Tissue to Cope With Increased Storage Demands of Obesity

Author

Carobbio, Stefania, Hagen, Rachel M., Lelliott, Christopher J., Slawik, Marc, Medina-Gomez, Gema, Tan, Chong-Yew, Sicard, Audrey, Atherton, Helen J., Barbarroja, Nuria, Bjursell, Mikael, Bohlooly-Y, Mohammad, Virtue, Sam, Tuthill, Antoinette, Lefai, Etienne, Laville, Martine, Wu, Tingting, Considine, Robert V., Vidal, Hubert, Langin, Dominique, Oresic, Matej, Tinahones, Francisco J., Fernandez-Real, Jose Manuel, Griffin, Julian L., Sethi, Jaswinder K., López, Miguel, and Vidal-Puig, Antonio

Published
2013
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17. No metabolic effects of mustard allyl-isothiocyanate compared with placebo in men

Author

Universitat Politècnica de València. Departamento de Estadística e Investigación Operativa Aplicadas y Calidad - Departament d'Estadística i Investigació Operativa Aplicades i Qualitat, National Institute for Health Research, Reino Unido, British Retail Consortium, European Commission, Wellcome Trust, Medical Research Council, Reino Unido, British Heart Foundation, Biotechnology and Biological Sciences Research Council, Reino Unido, Langeveld, Mirjam, Tan, Chong Yew, Soeters, Maarten R., Virtue, Samuel, Watson, Laura P. E., Murgatroyd, Peter R., Ambler, Graeme K., Vidal Puig, Santiago, Chatterjee, Krishna V., Vidal-Puig, Antonio, Universitat Politècnica de València. Departamento de Estadística e Investigación Operativa Aplicadas y Calidad - Departament d'Estadística i Investigació Operativa Aplicades i Qualitat, National Institute for Health Research, Reino Unido, British Retail Consortium, European Commission, Wellcome Trust, Medical Research Council, Reino Unido, British Heart Foundation, Biotechnology and Biological Sciences Research Council, Reino Unido, Langeveld, Mirjam, Tan, Chong Yew, Soeters, Maarten R., Virtue, Samuel, Watson, Laura P. E., Murgatroyd, Peter R., Ambler, Graeme K., Vidal Puig, Santiago, Chatterjee, Krishna V., and Vidal-Puig, Antonio

Abstract

[EN] Background: Induction of nonshivering thermogenesis can be used to influence energy balance to prevent or even treat obesity. The pungent component of mustard, allyl-isothiocyanate (AITC), activates the extreme cold receptor transient receptor potential channel, subfamily A, member 1 and may thus induce energy expenditure and metabolic changes. Objective: The objective of our study was to evaluate the potential of mustard AITC to induce thermogenesis (primary outcome) and alter body temperature, cold and hunger sensations, plasma metabolic parameters, and energy intake (secondary outcomes). Design: Energy expenditure in mice was measured after subcutaneous injection with vehicle, 1 mg norepinephrine/kg, or 5 mg AITC/kg. In our human crossover study, 11 healthy subjects were studied under temperature-controlled conditions after an overnight fast. After ingestion of 10 g of capsulated mustard or uncapsulated mustard or a capsulated placebo mixture, measurements of energy expenditure, substrate oxidation, core temperature, cold and hunger scores, and plasma parameters were repeated every 30 min during a 150-min period. Subjects were randomly selected for the placebo and capsulated mustard intervention; 9 of 11 subjects received the uncapsulated mustard as the final intervention because this could not be blinded. After the experiments, energy intake was measured with the universal eating monitor in a test meal. Results: In mice, AITC administration induced a 32% increase in energy expenditure compared with vehicle (17.5 +/- 4.9 J . min(-1) . mouse(-1) compared with 12.5 +/- 1.2 J . min(-1) . mouse(-1), P = 0.03). Of the 11 randomly selected participants, 1 was excluded because of intercurrent illness after the first visit and 1 withdrew after the second visit. Energy expenditure did not increase after ingestion of capsulated or uncapsulated mustard compared with placebo. No differences in substrate oxidation, core temperature, cold and hunger scores, or plasma para

Published
2017

20. Lipocalin prostaglandin D synthase and PPARγ2 coordinate to regulate carbohydrate and lipid metabolism in vivo

Author

Virtue, Sam, Masoodi, Mojgan, Velagapudi, Vidya, Tan, Chong Yew, Dale, Martin, Suorti, Tapani, Slawik, Marc, Blount, Margaret, Burling, Keith, Campbell, Mark, Eguchi, Naomi, Medina-Gomez, Gema, Sethi, Jaswinder K, Oresic, Matej, Urade, Yoshihiro, Griffin, Julian L, Vidal-Puig, Antonio, Virtue, Sam, Masoodi, Mojgan, Velagapudi, Vidya, Tan, Chong Yew, Dale, Martin, Suorti, Tapani, Slawik, Marc, Blount, Margaret, Burling, Keith, Campbell, Mark, Eguchi, Naomi, Medina-Gomez, Gema, Sethi, Jaswinder K, Oresic, Matej, Urade, Yoshihiro, Griffin, Julian L, and Vidal-Puig, Antonio

Abstract

Mice lacking Peroxisome Proliferator-Activated Receptor γ2 (PPARγ2) have unexpectedly normal glucose tolerance and mild insulin resistance. Mice lacking PPARγ2 were found to have elevated levels of Lipocalin prostaglandin D synthase (L-PGDS) expression in BAT and subcutaneous white adipose tissue (WAT). To determine if induction of L-PGDS was compensating for a lack of PPARγ2, we crossed L-PGDS KO mice to PPARγ2 KO mice to generate Double Knock Out mice (DKO). Using DKO mice we demonstrated a requirement of L-PGDS for maintenance of subcutaneous WAT (scWAT) function. In scWAT, DKO mice had reduced expression of thermogenic genes, the de novo lipogenic program and the lipases ATGL and HSL. Despite the reduction in markers of lipolysis in scWAT, DKO mice had a normal metabolic rate and elevated serum FFA levels compared to L-PGDS KO alone. Analysis of intra-abdominal white adipose tissue (epididymal WAT) showed elevated expression of mRNA and protein markers of lipolysis in DKO mice, suggesting that DKO mice may become more reliant on intra-abdominal WAT to supply lipid for oxidation. This switch in depot utilisation from subcutaneous to epididymal white adipose tissue was associated with a worsening of whole organism metabolic function, with DKO mice being glucose intolerant, and having elevated serum triglyceride levels compared to any other genotype. Overall, L-PGDS and PPARγ2 coordinate to regulate carbohydrate and lipid metabolism., Funding agencies:Diabetes UK EU HEPADIP FP6 (Hepatic and Adipose Tissue and Functions in the Metabolic Syndrome) The Medical Research Council Centre for Obesity Related Disorders Medical Research Council

Published
2012
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21. Association of lipidome remodeling in the adipocyte membrane with acquired obesity in humans

Author

Pietiläinen, Kirsi H, Róg, Tomasz, Seppänen-Laakso, Tuulikki, Virtue, Sam, Gopalacharyulu, Peddinti, Tang, Jing, Rodriguez-Cuenca, Sergio, Maciejewski, Arkadiusz, Naukkarinen, Jussi, Ruskeepää, Anna-Liisa, Niemelä, Perttu S, Yetukuri, Laxman, Tan, Chong Yew, Velagapudi, Vidya, Castillo, Sandra, Nygren, Heli, Hyötyläinen, Tuulia, Rissanen, Aila, Kaprio, Jaakko, Yki-Järvinen, Hannele, Vattulainen, Ilpo, Vidal-Puig, Antonio, Oresic, Matej, Pietiläinen, Kirsi H, Róg, Tomasz, Seppänen-Laakso, Tuulikki, Virtue, Sam, Gopalacharyulu, Peddinti, Tang, Jing, Rodriguez-Cuenca, Sergio, Maciejewski, Arkadiusz, Naukkarinen, Jussi, Ruskeepää, Anna-Liisa, Niemelä, Perttu S, Yetukuri, Laxman, Tan, Chong Yew, Velagapudi, Vidya, Castillo, Sandra, Nygren, Heli, Hyötyläinen, Tuulia, Rissanen, Aila, Kaprio, Jaakko, Yki-Järvinen, Hannele, Vattulainen, Ilpo, Vidal-Puig, Antonio, and Oresic, Matej

Abstract

Identification of early mechanisms that may lead from obesity towards complications such as metabolic syndrome is of great interest. Here we performed lipidomic analyses of adipose tissue in twin pairs discordant for obesity but still metabolically compensated. In parallel we studied more evolved states of obesity by investigating a separated set of individuals considered to be morbidly obese. Despite lower dietary polyunsaturated fatty acid intake, the obese twin individuals had increased proportions of palmitoleic and arachidonic acids in their adipose tissue, including increased levels of ethanolamine plasmalogens containing arachidonic acid. Information gathered from these experimental groups was used for molecular dynamics simulations of lipid bilayers combined with dependency network analysis of combined clinical, lipidomics, and gene expression data. The simulations suggested that the observed lipid remodeling maintains the biophysical properties of lipid membranes, at the price, however, of increasing their vulnerability to inflammation. Conversely, in morbidly obese subjects, the proportion of plasmalogens containing arachidonic acid in the adipose tissue was markedly decreased. We also show by in vitro Elovl6 knockdown that the lipid network regulating the observed remodeling may be amenable to genetic modulation. Together, our novel approach suggests a physiological mechanism by which adaptation of adipocyte membranes to adipose tissue expansion associates with positive energy balance, potentially leading to higher vulnerability to inflammation in acquired obesity. Further studies will be needed to determine the cause of this effect., Funding Agencies:EU HEPADIP Academy of Finland Helsinki University Central Hospital Jalmari and Rauha Ahokas Yrjo Jahnsson Biomedicum Helsinki Novo Nordisk Foundations BBSRC

Published
2011
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22. Integrating post-genomic approaches as a strategy to advance our understanding of health and disease

Author

Tang, Jing, Tan, Chong Yew, Oresic, Matej, Vidal-Puig, Antonio, Tang, Jing, Tan, Chong Yew, Oresic, Matej, and Vidal-Puig, Antonio

Abstract

Following the publication of the complete human genomic sequence, the post-genomic era is driven by the need to extract useful information from genomic data. Genomics, transcriptomics, proteomics, metabolomics, epidemiological data and microbial data provide different angles to our understanding of gene-environment interactions and the determinants of disease and health. Our goal and our challenge are to integrate these very different types of data and perspectives of disease into a global model suitable for dissecting the mechanisms of disease and for predicting novel therapeutic strategies. This review aims to highlight the need for and problems with complex data integration, and proposes a framework for data integration. While there are many obstacles to overcome, biological models based upon multiple datasets will probably become the basis that drives future biomedical research.

Published
2009
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23. Lipocalin Prostaglandin D Synthase and PPARγ2 Coordinate to Regulate Carbohydrate and Lipid Metabolism In Vivo

Author

Virtue, Sam, primary, Masoodi, Mojgan, additional, Velagapudi, Vidya, additional, Tan, Chong Yew, additional, Dale, Martin, additional, Suorti, Tapani, additional, Slawik, Marc, additional, Blount, Margaret, additional, Burling, Keith, additional, Campbell, Mark, additional, Eguchi, Naomi, additional, Medina-Gomez, Gema, additional, Sethi, Jaswinder K., additional, Orešič, Matej, additional, Urade, Yoshihiro, additional, Griffin, Julian L., additional, and Vidal-Puig, Antonio, additional

Published
2012
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24. Association of Lipidome Remodeling in the Adipocyte Membrane with Acquired Obesity in Humans

Author

Pietiläinen, Kirsi H., primary, Róg, Tomasz, additional, Seppänen-Laakso, Tuulikki, additional, Virtue, Sam, additional, Gopalacharyulu, Peddinti, additional, Tang, Jing, additional, Rodriguez-Cuenca, Sergio, additional, Maciejewski, Arkadiusz, additional, Naukkarinen, Jussi, additional, Ruskeepää, Anna-Liisa, additional, Niemelä, Perttu S., additional, Yetukuri, Laxman, additional, Tan, Chong Yew, additional, Velagapudi, Vidya, additional, Castillo, Sandra, additional, Nygren, Heli, additional, Hyötyläinen, Tuulia, additional, Rissanen, Aila, additional, Kaprio, Jaakko, additional, Yki-Järvinen, Hannele, additional, Vattulainen, Ilpo, additional, Vidal-Puig, Antonio, additional, and Orešič, Matej, additional

Published
2011
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27. Association of Lipidome Remodeling in the Adipocyte Membrane with Acquired Obesity in Humans.

Author

Pietiläine, Kirsi H., Ró, Tomasz, Seppänen-Laakso, Tuulikki, Virtue, Sam, Gopalacharyulu, Peddinti, Tang, Jing, Rodriguez-Cuenca, Sergio, Maciejewski, Arkadiusz, Naukkarinen, Jussi, Ruskeepää, Anna-Liisa, Niemelä, Perttu S., Yetukuri, Laxman, Tan, Chong Yew, Velagapudi, Vidya, Castillo, Sandra, Nygren, Heli, Hyötyläinen, Tuulia, Rissanen, Aila, Kaprio, Jaakko, and Yki-Järvinen, Hannele

Subjects
FAT cells, OBESITY, METABOLIC syndrome, LIPID metabolism, UNSATURATED fatty acids in human nutrition, ETHANOLAMINES, ARACHIDONIC acid
Abstract

Identification of early mechanisms that may lead from obesity towards complications such as metabolic syndrome is of great interest. Here we performed lipidomic analyses of adipose tissue in twin pairs discordant for obesity but still metabolically compensated. In parallel we studied more evolved states of obesity by investigating a separated set of individuals considered to be morbidly obese. Despite lower dietary polyunsaturated fatty acid intake, the obese twin individuals had increased proportions of palmitoleic and arachidonic acids in their adipose tissue, including increased levels of ethanolamine plasmalogens containing arachidonic acid. Information gathered from these experimental groups was used for molecular dynamics simulations of lipid bilayers combined with dependency network analysis of combined clinical, lipidomics, and gene expression data. The simulations suggested that the observed lipid remodeling maintains the biophysical properties of lipid membranes, at the price, however, of increasing their vulnerability to inflammation. Conversely, in morbidly obese subjects, the proportion of plasmalogens containing arachidonic acid in the adipose tissue was markedly decreased. We also show by in vitro Elovl6 knockdown that the lipid network regulating the observed remodeling may be amenable to genetic modulation. Together, our novel approach suggests a physiological mechanism by which adaptation of adipocyte membranes to adipose tissue expansion associates with positive energy balance, potentially leading to higher vulnerability to inflammation in acquired obesity. Further studies will be needed to determine the cause of this effect. [ABSTRACT FROM AUTHOR]

Published
2011
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28. Adaptive changes of the Insig1/SREBP1/SCD1 set point help adipose tissue to cope with increased storage demands of obesity

Author

Carobbio, Stefania, Hagen, Rachel M, Lelliott, Christopher J, Slawik, Marc, Medina-Gomez, Gema, Tan, Chong-Yew, Sicard, Audrey, Atherton, Helen J, Barbarroja, Nuria, Bjursell, Mikael, Bohlooly-Y, Mohammad, Virtue, Sam, Tuthill, Antoinette, Lefai, Etienne, Laville, Martine, Wu, Tingting, Considine, Robert V, Vidal, Hubert, Langin, Dominique, Oresic, Matej, Tinahones, Francisco J, Fernandez-Real, Jose Manuel, Griffin, Julian L, Sethi, Jaswinder K, López, Miguel, and Vidal-Puig, Antonio

Subjects
Mice, Knockout, Adipose Tissue, White, Down-Regulation, Membrane Proteins, Lipid Metabolism, Adaptation, Physiological, 3. Good health, Obesity, Morbid, Mice, 3T3-L1 Cells, Animals, Humans, lipids (amino acids, peptides, and proteins), Obesity, RNA, Messenger, Insulin Resistance, Sterol Regulatory Element Binding Protein 1, Stearoyl-CoA Desaturase
Abstract

The epidemic of obesity imposes unprecedented challenges on human adipose tissue (WAT) storage capacity that may benefit from adaptive mechanisms to maintain adipocyte functionality. Here, we demonstrate that changes in the regulatory feedback set point control of Insig1/SREBP1 represent an adaptive response that preserves WAT lipid homeostasis in obese and insulin-resistant states. In our experiments, we show that Insig1 mRNA expression decreases in WAT from mice with obesity-associated insulin resistance and from morbidly obese humans and in in vitro models of adipocyte insulin resistance. Insig1 downregulation is part of an adaptive response that promotes the maintenance of SREBP1 maturation and facilitates lipogenesis and availability of appropriate levels of fatty acid unsaturation, partially compensating the antilipogenic effect associated with insulin resistance. We describe for the first time the existence of this adaptive mechanism in WAT, which involves Insig1/SREBP1 and preserves the degree of lipid unsaturation under conditions of obesity-induced insulin resistance. These adaptive mechanisms contribute to maintain lipid desaturation through preferential SCD1 regulation and facilitate fat storage in WAT, despite on-going metabolic stress.

29. No metabolic effects of mustard allyl-isothiocyanate compared with placebo in men

Author

Langeveld, Mirjam, Tan, Chong Yew, Soeters, Maarten R, Virtue, Samuel, Watson, Laura Pe, Murgatroyd, Peter R, Ambler, Graeme K, Vidal-Puig, Santiago, Chatterjee, Krishna V, and Vidal-Puig, Antonio

Subjects
Adult, Blood Glucose, Male, allyl-isothiocyanate, Adolescent, Hunger, mustard, Body Temperature, Mice, Norepinephrine, Young Adult, Oxygen Consumption, Isothiocyanates, energy expenditure, Animals, Humans, Aged, Cross-Over Studies, Thermogenesis, Middle Aged, 3. Good health, thermogenic food, Female, Energy Intake, Energy Metabolism, Mustard Plant
Abstract

Background: Induction of nonshivering thermogenesis can be used to influence energy balance to prevent or even treat obesity. The pungent component of mustard, allyl-isothiocyanate (AITC), activates the extreme cold receptor transient receptor potential channel, subfamily A, member 1 and may thus induce energy expenditure and metabolic changes.Objective: The objective of our study was to evaluate the potential of mustard AITC to induce thermogenesis (primary outcome) and alter body temperature, cold and hunger sensations, plasma metabolic parameters, and energy intake (secondary outcomes).Design: Energy expenditure in mice was measured after subcutaneous injection with vehicle, 1 mg norepinephrine/kg, or 5 mg AITC/kg. In our human crossover study, 11 healthy subjects were studied under temperature-controlled conditions after an overnight fast. After ingestion of 10 g of capsulated mustard or uncapsulated mustard or a capsulated placebo mixture, measurements of energy expenditure, substrate oxidation, core temperature, cold and hunger scores, and plasma parameters were repeated every 30 min during a 150-min period. Subjects were randomly selected for the placebo and capsulated mustard intervention; 9 of 11 subjects received the uncapsulated mustard as the final intervention because this could not be blinded. After the experiments, energy intake was measured with the universal eating monitor in a test meal.Results: In mice, AITC administration induced a 32% increase in energy expenditure compared with vehicle (17.5 ± 4.9 J · min-1 · mouse-1 compared with 12.5 ± 1.2 J · min-1 · mouse-1, P = 0.03). Of the 11 randomly selected participants, 1 was excluded because of intercurrent illness after the first visit and 1 withdrew after the second visit. Energy expenditure did not increase after ingestion of capsulated or uncapsulated mustard compared with placebo. No differences in substrate oxidation, core temperature, cold and hunger scores, or plasma parameters were found, nor was the energy intake at the end of the experiment different between the 3 conditions.Conclusion: The highest tolerable dose of mustard we were able to use did not elicit a relevant thermogenic response in humans. This trial was registered at www.controlled-trials.com as ISRCTN19147515.

30. Integrating post-genomic approaches as a strategy to advance our understanding of health and disease.

Author

Tang J, Tan CY, Oresic M, and Vidal-Puig A

Abstract

Following the publication of the complete human genomic sequence, the post-genomic era is driven by the need to extract useful information from genomic data. Genomics, transcriptomics, proteomics, metabolomics, epidemiological data and microbial data provide different angles to our understanding of gene-environment interactions and the determinants of disease and health. Our goal and our challenge are to integrate these very different types of data and perspectives of disease into a global model suitable for dissecting the mechanisms of disease and for predicting novel therapeutic strategies. This review aims to highlight the need for and problems with complex data integration, and proposes a framework for data integration. While there are many obstacles to overcome, biological models based upon multiple datasets will probably become the basis that drives future biomedical research.

Published
2009
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