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263 results on '"Rohner-Jeanrenaud, Françoise"'

4. A Stat6/Pten Axis Links Regulatory T Cells with Adipose Tissue Function

Author

Kälin, Stefanie, Becker, Maike, Ott, Verena B., Serr, Isabelle, Hosp, Fabian, Mollah, Mohammad M.H., Keipert, Susanne, Lamp, Daniel, Rohner-Jeanrenaud, Francoise, Flynn, Victoria K., Scherm, Martin G., Nascimento, Lucas F.R., Gerlach, Katharina, Popp, Vanessa, Dietzen, Sarah, Bopp, Tobias, Krishnamurthy, Purna, Kaplan, Mark H., Serrano, Manuel, Woods, Stephen C., Tripal, Philipp, Palmisano, Ralf, Jastroch, Martin, Blüher, Matthias, Wolfrum, Christian, Weigmann, Benno, Ziegler, Anette-Gabriele, Mann, Matthias, Tschöp, Matthias H., and Daniel, Carolin

Published
2017
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7. Central Melanin-Concentrating Hormone Influences Liver and Adipose Metabolism Via Specific Hypothalamic Nuclei and Efferent Autonomic/JNK1 Pathways

Author

Imbernon, Monica, Beiroa, Daniel, Vázquez, María J., Morgan, Donald A., Veyrat–Durebex, Christelle, Porteiro, Begoña, Díaz–Arteaga, Adenis, Senra, Ana, Busquets, Silvia, Velásquez, Douglas A., Al–Massadi, Omar, Varela, Luis, Gándara, Marina, López–Soriano, Francisco–Javier, Gallego, Rosalía, Seoane, Luisa M., Argiles, Josep M., López, Miguel, Davis, Roger J., Sabio, Guadalupe, Rohner–Jeanrenaud, Françoise, Rahmouni, Kamal, Dieguez, Carlos, and Nogueiras, Ruben

Published
2013
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20. The central melanocortin system directly controls peripheral lipid metabolism

Author

Nogueiras, Ruben, Wiedmer, Petra, Perez-Tilve, Diego, Veyrat-Durebex, Christelle, Keogh, Julia M., Sutton, Gregory M., Pfluger, Paul T., Castaneda, Tamara R., Neschen, Susanne, Hofmann, Susanna M., Howles, Philip N., Morgan, Donald A., Benoit, Stephen C., Szanto, Ildiko, Schrott, Brigitte, Schürmann, Annette, Joost, Hans-Georg, Hammond, Craig, Hui, David Y., Woods, Stephen C., Rahmouni, Kamal, Butler, Andrew A., Farooqi, I. Sadaf, OʼRahilly, Stephen, Rohner-Jeanrenaud, Françoise, and Tschöp, Matthias H.

Published
2007

21. Ghrelin action in the brain controls adipocyte metabolism

Author

Theander-Carrillo, Claudia, Wiedmer, Petra, Cettour-Rose, Philippe, Nogueiras, Ruben, Perez-Tilve, Diego, Pfluger, Paul, Castaneda, Tamara R., Muzzin, Patrick, Schürmann, Annette, Szanto, Ildiko, Tschöp, Matthias H., and Rohner-Jeanrenaud, Françoise

Published
2006

33. Oxytocin Administration Alleviates Acute but Not Chronic Leptin Resistance of Diet-Induced Obese Mice

Author

Labyb, Mehdi, Chrétien, Chloé, Caillon, Aurélie, Rohner-Jeanrenaud, Françoise, and Altirriba, Jordi

Subjects
Male, endocrine system, obesity, food intake, Brief Report, Body Weight, digestive, oral, and skin physiology, Mice, Obese, Diet, High-Fat, leptin, Mice, Inbred C57BL, lcsh:Chemistry, Eating, Mice, lcsh:Biology (General), lcsh:QD1-999, oxytocin, Animals, lcsh:QH301-705.5, hormones, hormone substitutes, and hormone antagonists
Abstract

Whereas leptin administration only has a negligible effect on the treatment of obesity, it has been demonstrated that its action can be improved by co-administration of leptin and one of its sensitizers. Considering that oxytocin treatment decreases body weight in obese animals and humans, we investigated the effects of oxytocin and leptin cotreatment. First, lean and diet-induced obese (DIO) mice were treated with oxytocin for 2 weeks and we measured the acute leptin response. Second, DIO mice were treated for 2 weeks with saline, oxytocin (50 μg/day), leptin (20 or 40 µg/day) or oxytocin plus leptin. Oxytocin pre-treatment restored a normal acute leptin response, decreasing food intake and body weight gain. Chronic continuous administration of oxytocin or leptin at 40 µg/day decreased body weight in the presence (leptin) or in the absence (oxytocin) of cumulative differences in food intake. Saline or leptin treatment at 20 µg/day had no impact on body weight. Oxytocin and leptin cotreatments had no additional effects compared with single treatments. These results point to the fact that chronic oxytocin treatment improves the acute, but not the chronic leptin response, suggesting that this treatment could be used to improve the short-term satiety effect of leptin.

Published
2018

34. Erratum to: Evidence against a direct role of klotho in insulin resistance

Author

Lorenzi, Olivier, Veyrat-Durebex, Christelle, Wollheim, Claes, Villemin, Pascal, Rohner-Jeanrenaud, Françoise, Zanchi, Anne, Vischer, Ulrich, Lorenzi, Olivier, Veyrat-Durebex, Christelle, Wollheim, Claes, Villemin, Pascal, Rohner-Jeanrenaud, Françoise, Zanchi, Anne, and Vischer, Ulrich

Published
2018

38. Preserving of postnatal leptin signaling in obesity-resistant lou/c rats following a perinatal high-fat diet

Author

Poher, Anne-Laure, Arsenijevic, Denis, Asrih, Mohamed, Dulloo, Abdul G., Jornayvaz, François R., Rohner-Jeanrenaud, Françoise, Veyrat-Durebex, Christelle, Poher, Anne-Laure, Arsenijevic, Denis, Asrih, Mohamed, Dulloo, Abdul G., Jornayvaz, François R., Rohner-Jeanrenaud, Françoise, and Veyrat-Durebex, Christelle

Abstract

Physiological processes at adulthood, such as energy metabolism and insulin sensitivity may originate before or weeks after birth. These underlie the concept of fetal and/or neonatal programming of adult diseases, which is particularly relevant in the case of obesity and type 2 diabetes. The aim of this study was to determine the impact of a perinatal high fat diet on energy metabolism and on leptin as well as insulin sensitivity, early in life and at adulthood in two strains of rats presenting different susceptibilities to diet-induced obesity. The impact of a perinatal high fat diet on glucose tolerance and diet-induced obesity was also assessed. The development of glucose intolerance and of increased fat mass was confirmed in the obesity-prone Wistar rat, even after 28 days of age. By contrast, in obesity-resistant Lou/C rats, an improved early leptin signaling may be responsible for the lack of deleterious effect of the perinatal high fat diet on glucose tolerance and increased adiposity in response to high fat diet at adulthood. Altogether, this study shows that, even if during the perinatal period adaptation to the environment appears to be genetically determined, adaptive mechanisms to nutritional challenges occurring at adulthood can still be observed in rodents.

Published
2017

40. Brown adipose tissue activity as a target for the treatment of obesity/insulin resistance

Author

Poher, Anne-Laure, Altirriba Gutierrez, Jorge, Veyrat-Durebex, Christelle, and Rohner-Jeanrenaud, Françoise

Subjects
ddc:612
Abstract

Presence of brown adipose tissue (BAT), characterized by the expression of the thermogenic uncoupling protein 1 (UCP1), has recently been described in adult humans. UCP1 is expressed in classical brown adipocytes, as well as in "beige cells" in white adipose tissue (WAT). The thermogenic activity of BAT is mainly controlled by the sympathetic nervous system. Endocrine factors, such as fibroblast growth factor 21 (FGF21) and bone morphogenic protein factor-9 (BMP-9), predominantly produced in the liver, were shown to lead to activation of BAT thermogenesis, as well as to "browning" of WAT. This was also observed in response to irisin, a hormone secreted by skeletal muscles. Different approaches were used to delineate the impact of UCP1 on insulin sensitivity. When studied under thermoneutral conditions, UCP1 knockout mice exhibited markedly increased metabolic efficiency due to impaired thermogenesis. The impact of UCP1 deletion on insulin sensitivity in these mice was not reported. Conversely, several studies in both rodents and humans have shown that BAT activation (by cold exposure, β3-agonist treatment, transplantation and others) improves glucose tolerance and insulin sensitivity. Interestingly, similar results were obtained by adipose tissue-specific overexpression of PR-domain-containing 16 (PRDM16) or BMP4 in mice. The mediators of such beneficial effects seem to include FGF21, interleukin-6, BMP8B and prostaglandin D2 synthase. Interestingly, some of these molecules can be secreted by BAT itself, indicating the occurrence of autocrine effects. Stimulation of BAT activity and/or recruitment of UCP1-positive cells are therefore relevant targets for the treatment of obesity/type 2 diabetes in humans.

Published
2015

41. Effets métaboliques de l'ocytocine et ses applications potentielles pour le traitement de l'obésité

Author

Altirriba Gutierrez, Jorge, Pataky, Zoltan, Golay, Alain, and Rohner-Jeanrenaud, Françoise

Subjects
Obesity/drug therapy, Animals, Humans, Metabolism/drug effects, Oxytocin/pharmacology/therapeutic use, ddc:612, ddc:613
Abstract

Oxytocin is a hormone known for a long time, mainly used in the field of gynecology. Apart from these well-defined effects, the role of oxytocin in controlling the stress response or behavior and the regulation of glucose/lipid metabolism seems to be very interesting, especially in obese patients. Several clinical studies are currently underway to assess the impact of oxytocin in the treatment of obesity. Taking these new data into consideration, the use of this hormone for weight loss in obese patients or as a complementary treatment in diabetic patients seems to be promising.

Published
2015

42. Adipokines at the crossroad between obesity and cardiovascular disease

Author

Molica, Filippo, Morel, Sandrine, Kwak, Brenda, Rohner-Jeanrenaud, Françoise, and Steffens, Sabine

Subjects
ddc:616, ddc:616.07
Abstract

Obesity, and especially excessive visceral adipose tissue accumulation, is considered as a low-grade inflammatory state that is responsible for adipocyte dysfunction and associated metabolic disorders. Adipose tissue displays endocrine functions by releasing pro- or anti-inflammatory bioactive molecules named adipokines. An altered expression of these molecules, provoked by obesity or adipocyte dysregulation, contributes to major metabolic diseases such as insulin resistance and type 2 diabetes mellitus that are important risk factors for cardiovascular disease. However, obesity is also characterised by the expansion of perivascular adipose tissue that acts locally via diffusion of adipokines into the vascular wall. Local inflammation within blood vessels induced by adipokines contributes to the onset of endothelial dysfunction, atherosclerosis and thrombosis, but also to vascular remodelling and hypertension. A fast expansion of obesity is expected in the near future, which will rapidly increase the incidence of these cardiovascular diseases. The focus of this review is to summarise the link between metabolic and cardiovascular disease and discuss current treatment approaches, limitations and future perspectives for more targeted therapies.

Published
2015

45. Leptin as a Potential Regulator of FGF21

Author

Asrih, Mohamed, primary, Veyrat-Durebex, Christelle, additional, Poher, Anne-Laure, additional, Lyautey, Jacqueline, additional, Rohner-Jeanrenaud, Françoise, additional, and Jornayvaz, François R., additional

Published
2016
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47. A role for adipose tissue de novo lipogenesis in glucose homeostasis during catch-up growth: a Randle cycle favoring fat storage

Author

Marcelino Helena, Veyrat-Durebex Christelle, Summermatter Serge, Sarafian Delphine, Miles-Chan Jennifer, Arsenijevic Denis, Zani Fabio, Montani Jean-Pierre, Seydoux Josiane, Solinas Giovanni, Rohner-Jeanrenaud Françoise, and Dulloo Abdul G

Subjects
Male, Lipogenesis, Hypertrophy, Hyperphagia, Diet, High-Fat, ddc:616.8, Rats, Rats, Sprague-Dawley, Glucose, Metabolism, Adipose Tissue, Hyperinsulinism, Adipocytes, Animals, Homeostasis, Hypoglycemic Agents, Insulin, Refeeding Syndrome, ddc:612, Signal Transduction
Abstract

Catch-up growth, a risk factor for type 2 diabetes, is characterized by hyperinsulinemia and accelerated body fat recovery. Using a rat model of semistarvation-refeeding that exhibits catch-up fat, we previously reported that during refeeding on a low-fat diet, glucose tolerance is normal but insulin-dependent glucose utilization is decreased in skeletal muscle and increased in adipose tissue, where de novo lipogenic capacity is concomitantly enhanced. Here we report that isocaloric refeeding on a high-fat (HF) diet blunts the enhanced in vivo insulin-dependent glucose utilization for de novo lipogenesis (DNL) in adipose tissue. These are shown to be early events of catch-up growth that are independent of hyperphagia and precede the development of overt adipocyte hypertrophy, adipose tissue inflammation, or defective insulin signaling. These results suggest a role for enhanced DNL as a glucose sink in regulating glycemia during catch-up growth, which is blunted by exposure to an HF diet, thereby contributing, together with skeletal muscle insulin resistance, to the development of glucose intolerance. Our findings are presented as an extension of the Randle cycle hypothesis, whereby the suppression of DNL constitutes a mechanism by which dietary lipids antagonize glucose utilization for storage as triglycerides in adipose tissue, thereby impairing glucose homeostasis during catch-up growth.

Published
2012

49. Uroguanylin Action in the Brain Reduces Weight Gain in Obese Mice via Different Efferent Autonomic Pathways

Author

Folgueira, Cintia, primary, Beiroa, Daniel, additional, Callon, Aurelie, additional, Al-Massadi, Omar, additional, Barja-Fernandez, Silvia, additional, Senra, Ana, additional, Fernø, Johan, additional, López, Miguel, additional, Dieguez, Carlos, additional, Casanueva, Felipe F., additional, Rohner-Jeanrenaud, Françoise, additional, Seoane, Luisa M., additional, and Nogueiras, Ruben, additional

Published
2015
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50. The K+channel TASK1 modulates β‐adrenergic response in brown adipose tissue through the mineralocorticoid receptor pathway

Author

Pisani, Didier F., primary, Beranger, Guillaume E., additional, Corinus, Alain, additional, Giroud, Maude, additional, Ghandour, Rayane A., additional, Altirriba, Jordi, additional, Chambard, Jean‐Claude, additional, Mazure, Nathalie M., additional, Bendahhou, Saïd, additional, Duranton, Christophe, additional, Michiels, Jean‐François, additional, Frontini, Andrea, additional, Rohner‐Jeanrenaud, Françoise, additional, Cinti, Saverio, additional, Christian, Mark, additional, Barhanin, Jacques, additional, and Amri, Ez‐Zoubir, additional

Published
2015
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