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2. Immune Cell Toll-like Receptor 4 Mediates the Development of Obesity- and Endotoxemia-Associated Adipose Tissue Fibrosis

Author

Vila, Isabelle K., Badin, Pierre-Marie, Marques, Marie-Adeline, Monbrun, Laurent, Lefort, Corinne, Mir, Lucile, Louche, Katie, Bourlier, Virginie, Roussel, Balbine, Gui, Philippe, Grober, Jacques, Štich, Vladimír, Rossmeislová, Lenka, Zakaroff-Girard, Alexia, Bouloumié, Anne, Viguerie, Nathalie, Moro, Cedric, Tavernier, Geneviève, and Langin, Dominique

Published
2014
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5. Natriuretic peptides enhance the oxidative capacity of human skeletal muscle

Author

Engeli, Stefan, Birkenfeld, Andreas L., Badin, Pierre-Marie, Bourlier, Virginie, Louche, Katie, Viguerie, Nathalie, Thalamas, Claire, Montastier, Emilie, Larrouy, Dominique, Harant, Isabelle, Glisezinski, Isabelle de, Lieske, Stefanie, Reinke, Julia, Beckmann, Bibiana, Langin, Dominique, Jordan, Jens, and Moro, Cedric

Subjects
Physiological aspects, Research, Oxidative stress -- Physiological aspects, Skeletal muscle -- Physiological aspects, Exercise physiology -- Research, Natriuretic peptides -- Physiological aspects, Exercise -- Physiological aspects, Muscles -- Physiological aspects
Abstract

Introduction The cardiac hormones, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), play a major role in the regulation of fluid homeostasis and cardiac physiology (1). Natriuretic peptide-mediated (NP-mediated) [...], Cardiac natriuretic peptides (NP) are major activators of human fat cell lipolysis and have recently been shown to control brown fat thermogenesis. Here, we investigated the physiological role of NP on the oxidative metabolism of human skeletal muscle. NP receptor type A (NPRA) gene expression was positively correlated to mRNA levels of PPAR γ coactivator-1 α (PGC1A) and several oxidative phosphorylation (OXPHOS) genes in human skeletal muscle. Further, the expression of NPRA, PGC1A, and OXPHOS genes was coordinately upregulated in response to aerobic exercise training in human skeletal muscle. In human myotubes, NP induced PGC-1 α and mitochondrial OXPHOS gene expression in a cyclic GMP-dependent manner. NP treatment increased OXPHOS protein expression, fat oxidation, and maximal respiration independent of substantial changes in mitochondrial proliferation and mass. Treatment of myotubes with NP recapitulated the effect of exercise training on muscle fat oxidative capacity in vivo. Collectively, these data show that activation of NP signaling in human skeletal muscle enhances mitochondrial oxidative metabolism and fat oxidation. We propose that NP could contribute to exercise training-induced improvement in skeletal muscle fat oxidative capacity in humans.

Published
2012
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13. L'invalidation génétique des protéines 4E-BP1/2 chez la souris induit l'insulino-résistance et une lipotoxicité au niveau musculaire

Author

Le Bacquer, Olivier, Combe, Kristell, Salles, Jérôme, Giraudet, Christophe, Patrac, Véronique, Montaurier, Christophe, Berry, Alexandre, Pion, Angélique, Rossignon, F, Domingues Faria, Carla, Guillet, Christelle, Boirie, Yves, Louche, Katie, Moro, Cédric, Walrand, Stephane, Unité de Nutrition Humaine (UNH), Université d'Auvergne - Clermont-Ferrand I (UdA)-Clermont Université-Institut National de la Recherche Agronomique (INRA), Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche en Nutrition Humaine (CRNH). Clermont-Ferrand, FRA., Société Francophone Nutrition Clinique et Métabolisme (SFNEP). FRA., Société Française de Nutrition (SFN). FRA., Institut National de la Recherche Agronomique (INRA)-Université d'Auvergne - Clermont-Ferrand I (UdA)-Clermont Université, Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), and ProdInra, Migration

Subjects
[SDV.AEN] Life Sciences [q-bio]/Food and Nutrition, régime hyperlipidique, Alimentation et Nutrition, Food and Nutrition, désordre métabolique, souris, métabolisme des lipides, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, ComputingMilieux_MISCELLANEOUS, patient obèse
Abstract

Flash Posters : Axe 1; National audience; mTOR (mammalian Target of rapamycin) est un noeud métabolique qui en réponse aux nutriments et facteurs de croissance régule de nombreux processus cellulaires. Une suractivation de mTOR est souvent observée dans les tissus de patients obèses ou les modèles animaux d’obésité et associée à l’insulinorésistance. Cependant, le rôle précis des différentes cibles de mTOR dans l’installation des désordres métaboliques est encore peu exploré. Chez la souris, la délétion des protéines 4EBP1 et 4EBP2 (cibles de mTOR) au niveau du corps entier provoque une sensibilité accrue à l’induction de l’obésité en favorisant l’adipogenèse et l’insulino-résistance. L’objectif de cette étude était de déterminer chez la souris l’impact de la délétion de 4EBP1 et 4EBP2 sur la lipotoxicité musculaire en réponse à un régime riche en graisses. Des souris sauvages (WT) et invalidées pour les protéines 4EBP1 et 2 (4EBP1/2 Double KO, DKO) ont reçu un régime standard (STD. 3,79kcal/g de régime) ou riche en graisses (HFD. 4,60kcal/g) pendant 20 semaines. A la fin de ce régime des tests ITT et ipGTT ont été réalisés pour mesurer le degré d’insulinorésistance et de tolérance au glucose. Les contenus intramusculaires en lipides, céramides et sphingomyélines ont été mesurés par chromatographie gazeuse et HPLC-MS afin de caractériser les atteintes lipidiques musculaires. L’expression des gènes impliqués dans le transport des acides gras, le métabolisme des lipides et la bêta-oxydation a été mesurée dans le muscle par PCR quantitative. L’expression d’ATGL a été mesurée par western blot et l’activité ATGL mesurée. Les résultats ont été analysés par ANOVA à 2 voies. Le régime HFD induit une prise de poids chez les souris WT et DKO, avec une prise de masse musculaire plus importante chez les souris DKO (p

Published
2016

14. Central chronic apelin infusion decreases energy expenditure and thermogenesis in mice

Author

UCL - SSS/LDRI - Louvain Drug Research Institute, Drougard, Anne, Fournel, Audren, Marlin, Alysson, Meunier, Etienne, Abot, Anne, Bautzova, Tereza, Duparc, Thibaut, Louche, Katie, Batut, Aurelie, Lucas, Alexandre, Le-Gonidec, Sophie, Lesage, Jean, Fioramonti, Xavier, Moro, Cedric, Valet, Philippe, Cani, Patrice D., Knauf, Claude, UCL - SSS/LDRI - Louvain Drug Research Institute, Drougard, Anne, Fournel, Audren, Marlin, Alysson, Meunier, Etienne, Abot, Anne, Bautzova, Tereza, Duparc, Thibaut, Louche, Katie, Batut, Aurelie, Lucas, Alexandre, Le-Gonidec, Sophie, Lesage, Jean, Fioramonti, Xavier, Moro, Cedric, Valet, Philippe, Cani, Patrice D., and Knauf, Claude

Abstract

Apelin is a bioactive peptide involved in the control of energy metabolism. In the hypothalamus, chronic exposure to high levels of apelin is associated with an increase in hepatic glucose production, and then contributes to the onset of type 2 diabetes. However, the molecular mechanisms behind deleterious effects of chronic apelin in the brain and consequences on energy expenditure and thermogenesis are currently unknown. We aimed to evaluate the effects of chronic intracerebroventricular (icv) infusion of apelin in normal mice on hypothalamic inflammatory gene expression, energy expenditure, thermogenesis and brown adipose tissue functions. We have shown that chronic icv infusion of apelin increases the expression of pro-inflammatory factors in the hypothalamus associated with an increase in plasma interleukin-1 beta. In parallel, mice infused with icv apelin exhibit a significant lower energy expenditure coupled to a decrease in PGC1alpha, PRDM16 and UCP1 expression in brown adipose tissue which could explain the alteration of thermogenesis in these mice. These data provide compelling evidence that central apelin contributes to the development of type 2 diabetes by altering energy expenditure, thermogenesis and fat browning.

Published
2016

15. Perilipin 5 fine-tunes lipid oxidation to metabolic demand and protects against lipotoxicity in skeletal muscle

Author

Laurens, Claire, primary, Bourlier, Virginie, additional, Mairal, Aline, additional, Louche, Katie, additional, Badin, Pierre-Marie, additional, Mouisel, Etienne, additional, Montagner, Alexandra, additional, Marette, André, additional, Tremblay, Angelo, additional, Weisnagel, John S., additional, Guillou, Hervé, additional, Langin, Dominique, additional, Joanisse, Denis R., additional, and Moro, Cedric, additional

Published
2016
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16. Transient Receptor Potential Canonical 3 (TRPC3) Channels Are Required for Hypothalamic Glucose Detection and Energy Homeostasis

Author

Chrétien, Chloé, primary, Fenech, Claire, additional, Liénard, Fabienne, additional, Grall, Sylvie, additional, Chevalier, Charlène, additional, Chaudy, Sylvie, additional, Brenachot, Xavier, additional, Berges, Raymond, additional, Louche, Katie, additional, Stark, Romana, additional, Nédélec, Emmanuelle, additional, Laderrière, Amélie, additional, Andrews, Zane B., additional, Benani, Alexandre, additional, Flockerzi, Veit, additional, Gascuel, Jean, additional, Hartmann, Jana, additional, Moro, Cédric, additional, Birnbaumer, Lutz, additional, Leloup, Corinne, additional, Pénicaud, Luc, additional, and Fioramonti, Xavier, additional

Published
2016
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17. Central chronic apelin infusion decreases energy expenditure and thermogenesis in mice

Author

Drougard, Anne, primary, Fournel, Audren, additional, Marlin, Alysson, additional, Meunier, Etienne, additional, Abot, Anne, additional, Bautzova, Tereza, additional, Duparc, Thibaut, additional, Louche, Katie, additional, Batut, Aurelie, additional, Lucas, Alexandre, additional, Le-Gonidec, Sophie, additional, Lesage, Jean, additional, Fioramonti, Xavier, additional, Moro, Cedric, additional, Valet, Philippe, additional, Cani, Patrice D., additional, and Knauf, Claude, additional

Published
2016
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19. Partial Inhibition of Adipose Tissue Lipolysis Improves Glucose Metabolism and Insulin Sensitivity Without Alteration of Fat Mass

Author

Girousse, Amandine, Tavernier, Genevieve, Valle, Carine, Moro, Cedric, Mejhert, Niklas, Dinel, Anne-Laure, Houssier, Marianne, Roussel, Balbine, Besse-Patin, Aurele, Combes, Marion, Mir, Lucile, Monbrun, Laurent, Bezaire, Veronic, Prunet-Marcassus, Benedicte, Waget, Aurelie, Vila, Isabelle, Caspar-Bauguil, Sylvie, Louche, Katie, Marques, Marie-Adeline, Mairal, Aline, Renoud, Marie-Laure, Galitzky, Jean, Holm, Cecilia, Mouisel, Etienne, Thalamas, Claire, Viguerie, Nathalie, Sulpice, Thierry, Burcelin, Remy, Arner, Peter, Langin, Dominique, Girousse, Amandine, Tavernier, Genevieve, Valle, Carine, Moro, Cedric, Mejhert, Niklas, Dinel, Anne-Laure, Houssier, Marianne, Roussel, Balbine, Besse-Patin, Aurele, Combes, Marion, Mir, Lucile, Monbrun, Laurent, Bezaire, Veronic, Prunet-Marcassus, Benedicte, Waget, Aurelie, Vila, Isabelle, Caspar-Bauguil, Sylvie, Louche, Katie, Marques, Marie-Adeline, Mairal, Aline, Renoud, Marie-Laure, Galitzky, Jean, Holm, Cecilia, Mouisel, Etienne, Thalamas, Claire, Viguerie, Nathalie, Sulpice, Thierry, Burcelin, Remy, Arner, Peter, and Langin, Dominique

Abstract

When energy is needed, white adipose tissue (WAT) provides fatty acids (FAs) for use in peripheral tissues via stimulation of fat cell lipolysis. FAs have been postulated to play a critical role in the development of obesity-induced insulin resistance, a major risk factor for diabetes and cardiovascular disease. However, whether and how chronic inhibition of fat mobilization from WAT modulates insulin sensitivity remains elusive. Hormone-sensitive lipase (HSL) participates in the breakdown of WAT triacylglycerol into FAs. HSL haploinsufficiency and treatment with a HSL inhibitor resulted in improvement of insulin tolerance without impact on body weight, fat mass, and WAT inflammation in high-fat-diet-fed mice. In vivo palmitate turnover analysis revealed that blunted lipolytic capacity is associated with diminution in FA uptake and storage in peripheral tissues of obese HSL haploinsufficient mice. The reduction in FA turnover was accompanied by an improvement of glucose metabolism with a shift in respiratory quotient, increase of glucose uptake in WAT and skeletal muscle, and enhancement of de novo lipogenesis and insulin signalling in liver. In human adipocytes, HSL gene silencing led to improved insulin-stimulated glucose uptake, resulting in increased de novo lipogenesis and activation of cognate gene expression. In clinical studies, WAT lipolytic rate was positively and negatively correlated with indexes of insulin resistance and WAT de novo lipogenesis gene expression, respectively. In obese individuals, chronic inhibition of lipolysis resulted in induction of WAT de novo lipogenesis gene expression. Thus, reduction in WAT lipolysis reshapes FA fluxes without increase of fat mass and improves glucose metabolism through cell-autonomous induction of fat cell de novo lipogenesis, which contributes to improved insulin sensitivity.

Published
2013

20. Transient Receptor Potential Canonical 3 (TRPC3) Channels Are Required for Hypothalamic Glucose Detection and Energy Homeostasis.

Author

Chrétien, Chloé, Fenech, Claire, Liénard, Fabienne, Grall, Sylvie, Chevalier, Charlène, Chaudy, Sylvie, Brenachot, Xavier, Berges, Raymond, Louche, Katie, Stark, Romana, Nédélec, Emmanuelle, Laderrière, Amélie, Andrews, Zane B., Benani, Alexandre, Flockerzi, Veit, Gascuel, Jean, Hartmann, Jana, Moro, Cédric, Birnbaumer, Lutz, and Leloup, Corinne

Subjects
HYPOTHALAMUS, GLUCOSE, HOMEOSTASIS, NEURONS, TRP channels, GLUCOSE metabolism, ANIMAL experimentation, BODY weight, CARRIER proteins, ENERGY metabolism, FASTING, GLUCOSE tolerance tests, INGESTION, INSULIN, MICE, POLYMERASE chain reaction, RATS, WESTERN immunoblotting
Abstract

The mediobasal hypothalamus (MBH) contains neurons capable of directly detecting metabolic signals such as glucose to control energy homeostasis. Among them, glucose-excited (GE) neurons increase their electrical activity when glucose rises. In view of previous work, we hypothesized that transient receptor potential canonical type 3 (TRPC3) channels are involved in hypothalamic glucose detection and the control of energy homeostasis. To investigate the role of TRPC3, we used constitutive and conditional TRPC3-deficient mouse models. Hypothalamic glucose detection was studied in vivo by measuring food intake and insulin secretion in response to increased brain glucose level. The role of TRPC3 in GE neuron response to glucose was studied by using in vitro calcium imaging on freshly dissociated MBH neurons. We found that whole-body and MBH TRPC3-deficient mice have increased body weight and food intake. The anorectic effect of intracerebroventricular glucose and the insulin secretory response to intracarotid glucose injection are blunted in TRPC3-deficient mice. TRPC3 loss of function or pharmacological inhibition blunts calcium responses to glucose in MBH neurons in vitro. Together, the results demonstrate that TRPC3 channels are required for the response to glucose of MBH GE neurons and the central effect of glucose on insulin secretion and food intake. [ABSTRACT FROM AUTHOR]

Published
2017
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21. Partial Inhibition of Adipose Tissue Lipolysis Improves Glucose Metabolism and Insulin Sensitivity Without Alteration of Fat Mass

Author

Girousse, Amandine, primary, Tavernier, Geneviève, additional, Valle, Carine, additional, Moro, Cedric, additional, Mejhert, Niklas, additional, Dinel, Anne-Laure, additional, Houssier, Marianne, additional, Roussel, Balbine, additional, Besse-Patin, Aurèle, additional, Combes, Marion, additional, Mir, Lucile, additional, Monbrun, Laurent, additional, Bézaire, Véronic, additional, Prunet-Marcassus, Bénédicte, additional, Waget, Aurélie, additional, Vila, Isabelle, additional, Caspar-Bauguil, Sylvie, additional, Louche, Katie, additional, Marques, Marie-Adeline, additional, Mairal, Aline, additional, Renoud, Marie-Laure, additional, Galitzky, Jean, additional, Holm, Cecilia, additional, Mouisel, Etienne, additional, Thalamas, Claire, additional, Viguerie, Nathalie, additional, Sulpice, Thierry, additional, Burcelin, Rémy, additional, Arner, Peter, additional, and Langin, Dominique, additional

Published
2013
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