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Institution

University of Nice Sophia Antipolis

EducationNice, France
About: University of Nice Sophia Antipolis is a education organization based out in Nice, France. It is known for research contribution in the topics: Population & Stars. The organization has 10291 authors who have published 19964 publications receiving 680762 citations. The organization is also known as: UNS & University of Nice-Sophia Antipolis.


Papers
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Journal ArticleDOI
TL;DR: The importance of clock‐driven Lpl expression in energy balance is demonstrated and circadian disruption as a potential cause for the metabolic syndrome is highlighted.
Abstract: Mutations of clock genes can lead to diabetes and obesity. REV-ERBα, a nuclear receptor involved in the circadian clockwork, has been shown to control lipid metabolism. To gain insight into the role of REV-ERBα in energy homeostasis in vivo, we explored daily metabolism of carbohydrates and lipids in chow-fed, unfed, or high-fat-fed Rev-erbα−/− mice and their wild-type littermates. Chow-fed Rev-erbα−/− mice displayed increased adiposity (2.5-fold) and mild hyperglycemia (∼10%) without insulin resistance. Indirect calorimetry indicates that chow-fed Rev-erbα−/− mice utilize more fatty acids during daytime. A 24-h nonfeeding period in Rev-erbα−/− animals favors further fatty acid mobilization at the expense of glycogen utilization and gluconeogenesis, without triggering hypoglycemia and hypothermia. High-fat feeding in Rev-erbα−/− mice amplified metabolic disturbances, including expression of lipogenic factors. Lipoprotein lipase (Lpl) gene, critical in lipid utilization/storage, is triggered in liver at ni...

193 citations

Journal ArticleDOI
TL;DR: In this paper, the authors analyzed the quarterly average sale prices of new houses sold in the USA as a whole, in the Northeast, Midwest, South, and West of the USA, in each of the 50 states and the District of Columbia of USA, to determine whether they have grown at a faster-than-exponential rate which they took as the diagnostic of a bubble.
Abstract: Using a methodology developed in previous papers, we analyze the quarterly average sale prices of new houses sold in the USA as a whole, in the Northeast, Midwest, South, and West of the USA, in each of the 50 states and the District of Columbia of the USA, to determine whether they have grown at a faster-than-exponential rate which we take as the diagnostic of a bubble. We find that 22 states (mostly Northeast and West) exhibit clear-cut signatures of a fast-growing bubble. From the analysis of the S&P 500 Home Index, we conclude that the turning point of the bubble will probably occur around mid-2006.

192 citations

Journal ArticleDOI
TL;DR: Alfred P. Sloan Foundation, National Science Foundation, US Department of Energy Office of Science, University of Arizona, Brazilian Participation Group, Brookhaven National Laboratory; University of Cambridge; Carnegie Mellon University; University Of Florida; French Participation Group; German Participation Group and Harvard University; Instituto de Astrofisica de Canarias; Michigan State/Notre Dame/JINA Participation Group as discussed by the authors.
Abstract: Alfred P. Sloan Foundation; National Science Foundation; US Department of Energy Office of Science; University of Arizona; Brazilian Participation Group; Brookhaven National Laboratory; University of Cambridge; Carnegie Mellon University; University of Florida; French Participation Group; German Participation Group; Harvard University; Instituto de Astrofisica de Canarias; Michigan State/Notre Dame/JINA Participation Group; Johns Hopkins University; Lawrence Berkeley National Laboratory; Max Planck Institute for Astrophysics; New Mexico State University; New York University; Ohio State University; Pennsylvania State University; University of Portsmouth; Princeton University; Spanish Participation Group; University of Tokyo; University of Utah; Vanderbilt University; University of Virginia; University of Washington; Yale University; Physics Frontier Center/Joint Institute or Nuclear Astrophysics (JINA) [PHY 14-30152]; Physics Frontier Center/JINA Center for the Evolution of the Elements (JINA-CEE) by the US National Science Foundation; US National Science Foundation; Spanish Ministry of Economy and Competitiveness [AYA2010-16717, AYA2013-42781P]; Spanish Ministry of Economy and Competitiveness (MINECO) [AYA2014-56359-P]; Australian Research Council through DECRA Fellowship [DE140100598]; Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences; Ramon y Cajal fellowship [RYC-2013-14182]; MINECO [AYA-2014-58082-P]

192 citations

Journal ArticleDOI
02 May 2012-PLOS ONE
TL;DR: The results indicate that insulin resistance shares common molecular mechanisms in flies and human and that Drosophila could emerge as a powerful genetic system to study some aspects of this complex syndrome.
Abstract: In multicellular organisms, insulin/IGF signaling (IIS) plays a central role in matching energy needs with uptake and storage, participating in functions as diverse as metabolic homeostasis, growth, reproduction and ageing. In mammals, this pleiotropy of action relies in part on a dichotomy of action of insulin, IGF-I and their respective membrane-bound receptors. In organisms with simpler IIS, this functional separation is questionable. In Drosophila IIS consists of several insulin-like peptides called Dilps, activating a unique membrane receptor and its downstream signaling cascade. During larval development, IIS is involved in metabolic homeostasis and growth. We have used feeding conditions (high sugar diet, HSD) that induce an important change in metabolic homeostasis to monitor possible effects on growth. Unexpectedly we observed that HSD-fed animals exhibited severe growth inhibition as a consequence of peripheral Dilp resistance. Dilp-resistant animals present several metabolic disorders similar to those observed in type II diabetes (T2D) patients. By exploring the molecular mechanisms involved in Drosophila Dilp resistance, we found a major role for the lipocalin Neural Lazarillo (NLaz), a target of JNK signaling. NLaz expression is strongly increased upon HSD and animals heterozygous for an NLaz null mutation are fully protected from HSD-induced Dilp resistance. NLaz is a secreted protein homologous to the Retinol-Binding Protein 4 involved in the onset of T2D in human and mice. These results indicate that insulin resistance shares common molecular mechanisms in flies and human and that Drosophila could emerge as a powerful genetic system to study some aspects of this complex syndrome.

192 citations


Authors

Showing all 10355 results

NameH-indexPapersCitations
Robert J. Lefkowitz214860147995
Johan Auwerx15865395779
Kenneth M. Yamada13944672136
Jean-Luc Starck13365776224
Christophe Benoist13247063181
Jacques Pouysségur12541254656
Michel Lazdunski12556254650
E. A. De Wolf124133383171
Leon O. Chua12282471612
Tomasz Bulik12169886211
James G. Krueger12050546275
Austin Smith11130163156
Peter Fritschel10842772722
Didier Sornette104129544157
François Bondu10044069284
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202310
2022139
2021203
2020264
2019441
2018536