Marie Boutant

ORCID: 0000-0002-0902-8478
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Adipose Tissue and Metabolism
  • Mitochondrial Function and Pathology
  • Sirtuins and Resveratrol in Medicine
  • Pancreatic function and diabetes
  • ATP Synthase and ATPases Research
  • Biochemical effects in animals
  • Autophagy in Disease and Therapy
  • Hormonal Regulation and Hypertension
  • PARP inhibition in cancer therapy
  • Calcium signaling and nucleotide metabolism
  • Cholesterol and Lipid Metabolism
  • FOXO transcription factor regulation
  • Regulation of Appetite and Obesity
  • Peroxisome Proliferator-Activated Receptors
  • Diabetes Treatment and Management
  • Liver Disease Diagnosis and Treatment
  • RNA modifications and cancer
  • Genetic Neurodegenerative Diseases
  • Lipid metabolism and biosynthesis
  • Muscle metabolism and nutrition
  • Endoplasmic Reticulum Stress and Disease
  • Muscle Physiology and Disorders
  • Nutrition and Health in Aging
  • Diabetes and associated disorders
  • Fuel Cells and Related Materials

Nestlé (Switzerland)
2013-2019

École Polytechnique Fédérale de Lausanne
2013-2019

Institut Cochin
2011-2015

Inserm
2009-2015

Centre de Gestion Scientifique
2012-2015

Délégation Paris 5
2009-2015

Sorbonne Paris Cité
2012-2015

Université Paris Cité
2009-2015

Centre National de la Recherche Scientifique
2009-2013

Abstract NAD + is a vital redox cofactor and substrate required for activity of various enzyme families, including sirtuins poly(ADP-ribose) polymerases. Supplementation with precursors, such as nicotinamide mononucleotide (NMN) or riboside (NR), protects against metabolic disease, neurodegenerative disorders age-related physiological decline in mammals. Here we show that kinase 1 (NRK1) necessary rate-limiting the use exogenous NR NMN synthesis. Using genetic gain- loss-of-function models,...

10.1038/ncomms13103 article EN cc-by Nature Communications 2016-10-11

Mitochondrial fusion and fission events, collectively known as mitochondrial dynamics, act quality control mechanisms to ensure function fine-tune cellular bioenergetics. Defective mitofusin 2 (Mfn2) expression enhanced in skeletal muscle are hallmarks of insulin-resistant states. Interestingly, Mfn2 is highly expressed brown adipose tissue (BAT), yet its role remains unexplored. Using adipose-specific knockout (Mfn2-adKO) mice, we demonstrate that Mfn2, but not Mfn1, deficiency BAT leads a...

10.15252/embj.201694914 article EN cc-by-nc-nd The EMBO Journal 2017-03-27

Sarcopenia is thought to be associated with mitochondrial (Mito) loss. It unclear whether the decrease in Mito content consequent aging per se or decreased physical activity.The objective of study was examine influence fitness on and function assess exercise could improve older adults.Three distinct studies were conducted: 1) a cross-sectional observation comparing large heterogeneous cohort adults; 2) case-control chronically endurance-trained adults sedentary (S) subjects matched for age...

10.1210/jc.2013-3983 article EN The Journal of Clinical Endocrinology & Metabolism 2014-01-17

Abstract Aim Healthy ageing interventions encompass regular exercise to prevent mitochondrial dysfunction, key player in sarcopenia pathogenesis. Mitochondrial biogenesis has been well documented, but remodelling response training is poorly understood. Here we investigated fusion, fission and mitophagy before after an intervention older adults. Methods Skeletal muscle biopsies were collected from 22 healthy sedentary men women 4 months of supervised training. Eight lifelong trained age‐...

10.1111/apha.13179 article EN Acta Physiologica 2018-08-24

SIRT1 has been proposed to be a key signaling node linking changes in energy metabolism transcriptional adaptations. Although overexpression is protective against diverse metabolic complications, especially response high-fat diets, studies aiming understand the etiology of such benefits are scarce. Here, we aimed identify tissues and mechanisms implicated beneficial effects on glucose homeostasis.We have used mouse model moderate overexpression, under control its natural promoter, evaluate...

10.1016/j.molmet.2014.12.008 article EN cc-by-nc-nd Molecular Metabolism 2014-12-20

Mitochondrial function can be influenced by mitochondrial shape and connectivity with other cellular organelles through fusion fission processes. Disturbances in architecture fusion-related genes are observed situations of type 2 diabetes obesity, leading to a highly fissioned network. To directly test the effect reduced on hepatic metabolism, we generated mice liver-specific deletion Mfn1 gene (Mfn1LKO) monitored their energy homeostasis, function, susceptibility diet-induced insulin...

10.2337/db15-1725 article EN Diabetes 2016-09-09

Supplementation with the NAD+ precursor nicotinamide riboside (NR) ameliorates and prevents a broad array of metabolic aging disorders in mice. However, little is known about physiological role endogenous NR metabolism. We have previously shown that kinase 1 (NRK1) rate-limiting essential for NR-induced synthesis hepatic cells. To understand relevance metabolism, we generated whole body liver-specific NRK1 knockout Here, show deficiency leads to decreased gluconeogenic potential impaired...

10.1038/s41467-019-12262-x article EN cc-by Nature Communications 2019-09-20

Caloric restriction (CR) has been shown to prevent the onset of insulin resistance and delay age-related physiological decline in mammalian organisms. SIRT1, a NAD(+)-dependent deacetylase enzyme, suggested mediate adaptive responses CR, leading speculation that SIRT1 activation could be therapeutically used as CR-mimetic strategy. Here, we mouse model moderate overexpression test whether gain function mimic or boost metabolic benefits induced by every-other-day feeding (EODF). Our results...

10.1016/j.celrep.2016.02.007 article EN cc-by-nc-nd Cell Reports 2016-02-26

Background The control of the functional pancreatic β-cell mass serves key homeostatic function releasing right amount insulin to keep blood sugar in normal range. It is not fully understood though how determined. Methodology/Principal Findings Conditional chicken ovalbumin upstream promoter transcription factor II (COUP-TFII)-deficient mice were generated and crossed with expressing Cre under duodenal homeobox 1 (pdx1) gene promoter. Ablation COUP-TFII pancreas resulted glucose intolerance....

10.1371/journal.pone.0030847 article EN cc-by PLoS ONE 2012-01-24

The nuclear receptor Chicken Ovalbumin Upstream Promoter–Transcription Factor II (COUP-TFII) is an important coordinator of glucose homeostasis through its function in different organs such as the endocrine pancreas, adipose tissue, skeletal muscle, and liver. Recently we have demonstrated that COUP-TFII expression hypothalamus restricted to a subpopulation neurons expressing steroidogenic factor 1 transcription factor, known play crucial role homeostasis. To understand functional...

10.1073/pnas.1219262110 article EN Proceedings of the National Academy of Sciences 2013-02-25

Background The Nuclear Receptor 2F2 (NR2F2/COUP-TFII) heterozygous knockout mice display low basal insulinemia and enhanced insulin sensitivity. We previously established that represses NR2F2 gene expression in pancreatic β-cells. cis-regulatory region of the promoter is unknown its influence on metabolism humans poorly understood. present study aimed to identify regulatory regions control transcription evaluate effect variation glucose homeostasis humans. Methodology/Principal Findings...

10.1371/journal.pone.0035810 article EN cc-by PLoS ONE 2012-05-14

Chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) is an orphan nuclear receptor involved in the control of numerous functions various organs (organogenesis, differentiation, metabolic homeostasis, etc.). The aim present work was to characterize regulation and contribution COUP-TFII hepatic fatty acid glucose metabolisms newborn mice. Our data show that postnatal increase mRNA levels enhanced by glucagon (via cAMP) PPARα. To function liver suckling mice, we used a...

10.1152/ajpendo.00433.2014 article EN AJP Endocrinology and Metabolism 2015-03-18
Coming Soon ...