M BRUNO FEVE

Pourquoi vous devez consulter ce praticien

7 raisons identifiées

Plateau technique de référence

Assistance publique – Hôpitaux de Paris (APHP) — équipements et expertise pointus pour les cas complexes

Auteur de référence en rhumatologie

50 articles scientifiques publiés — un praticien à la pointe de la recherche

Encadrant universitaire

Forme la prochaine génération de rhumatologues (5 thèses dirigées)

En plein centre-ville

PARIS (75006) — accessible depuis tout le bassin urbain

Expérience confirmée

34 ans d'exercice en rhumatologie — recul clinique solide

Disponibilité géographique

2 lieux d'exercice — choisissez celui qui vous arrange

Délais de RDV courts dans la région

336.2 rhumatos / 100 000 hab. — département bien doté

Rhumatologue

📍 PARIS (75)HospitalierRPPS 10001577468

EnseignementExpérience confirmée

34ans d'exercice (thèse 1992)

📊 Reconnaissance scientifique : 49/100📝 328 articles publiés🇫🇷 Publications académiques françaises (8)🎓 5 thèses dirigées

✨ Profil synthétique

IA · 19/05/2026

M. Bruno Feve est un rhumatologue hospitalier à Paris, avec une production scientifique importante (h-index de 49 et 328 publications). Ses recherches portent principalement sur les maladies métaboliques, l'inflammation et la régulation hormonale. Il a dirigé plusieurs thèses dans le domaine de la physiologie, physiopathologie et thérapeutique.

Expertises présumées

Maladies métaboliques
Inflammation
Régulation hormonale
Corticothérapie
Pathologies rhumatismales avec composante métabolique
Fatigue et santé mentale
Biomarqueurs en rhumatologie

Synthèse automatique à partir des sources publiques (HAL, OpenAlex, theses.fr, ClinicalTrials.gov, FAI²R, ANS). Pas une évaluation clinique. Le médecin peut corriger via son compte.

Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.

Top publications · les plus citées

Molecular Mechanisms of Glucocorticoid-Induced Insulin Resistance

International journal of molecular sciences · 2021

📚 175 citations🎯 RCR 14.74Top 1% NIH🔓 Open Access📄 PDF gratuit ↗

Lire l'abstract Crossref ↓

Glucocorticoids (GCs) are steroids secreted by the adrenal cortex under the hypothalamic-pituitary-adrenal axis control, one of the major neuro-endocrine systems of the organism. These hormones are involved in tissue repair, immune stability, and metabolic processes, such as the regulation of carbohydrate, lipid, and protein metabolism. Globally, GCs are presented as ‘flight and fight’ hormones and, in that purpose, they are catabolic hormones required to mobilize storage to provide energy for the organism. If acute GC secretion allows fast metabolic adaptations to respond to danger, stress, or metabolic imbalance, long-term GC exposure arising from treatment or Cushing’s syndrome, progressively leads to insulin resistance and, in fine, cardiometabolic disorders. In this review, we briefly summarize the pharmacological actions of GC and metabolic dysregulations observed in patients exposed to an excess of GCs. Next, we describe in detail the molecular mechanisms underlying GC-induced insulin resistance in adipose tissue, liver, muscle, and to a lesser extent in gut, bone, and brain, mainly identified by numerous studies performed in animal models. Finally, we present the paradoxical effects of GCs on beta cell mass and insulin secretion by the pancreas with a specific focus on the direct and indirect (through insulin-sensitive organs) effects of GCs. Overall, a better knowledge of the specific action of GCs on several organs and their molecular targets may help foster the understanding of GCs’ side effects and design new drugs that possess therapeutic benefits without metabolic adverse effects.

Metformin alleviates stress-induced cellular senescence of aging human adipose stromal cells and the ensuing adipocyte dysfunction

eLife · 2021

📚 73 citations🎯 RCR 4.76Top 8% NIH🔓 Open Access

Lire l'abstract Crossref ↓

Aging is associated with central fat redistribution and insulin resistance. To identify age-related adipose features, we evaluated the senescence and adipogenic potential of adipose-derived stromal cells (ASCs) from abdominal subcutaneous fat obtained from healthy normal-weight young (<25 years) or older women (>60 years). Increased cell passages of young-donor ASCs (in vitro aging) resulted in senescence but not oxidative stress. ASC-derived adipocytes presented impaired adipogenesis but no early mitochondrial dysfunction. Conversely, aged-donor ASCs at early passages displayed oxidative stress and mild senescence. ASC-derived adipocytes exhibited oxidative stress, and early mitochondrial dysfunction but adipogenesis was preserved. In vitro aging of aged-donor ASCs resulted in further increased senescence, mitochondrial dysfunction, oxidative stress, and severe adipocyte dysfunction. When in vitro aged young-donor ASCs were treated with metformin, no alteration was alleviated. Conversely, metformin treatment of aged-donor ASCs decreased oxidative stress and mitochondrial dysfunction resulting in decreased senescence. Metformin’s prevention of oxidative stress and of the resulting senescence improved the cells’ adipogenic capacity and insulin sensitivity. This effect was mediated by the activation of AMP-activated protein kinase as revealed by its specific inhibition and activation. Overall, aging ASC-derived adipocytes presented impaired adipogenesis and insulin sensitivity. Targeting stress-induced senescence of ASCs with metformin may improve age-related adipose tissue dysfunction.

Molecular and Cellular Bases of Lipodystrophy Syndromes

Frontiers in endocrinology · 2021

📚 62 citations🎯 RCR 5.47Top 7% NIH🔓 Open Access📄 PDF gratuit ↗

Lire l'abstract Crossref ↓

Lipodystrophy syndromes are rare diseases originating from a generalized or partial loss of adipose tissue. Adipose tissue dysfunction results from heterogeneous genetic or acquired causes, but leads to similar metabolic complications with insulin resistance, diabetes, hypertriglyceridemia, nonalcoholic fatty liver disease, dysfunctions of the gonadotropic axis and endocrine defects of adipose tissue with leptin and adiponectin deficiency. Diagnosis, based on clinical and metabolic investigations, and on genetic analyses, is of major importance to adapt medical care and genetic counseling. Molecular and cellular bases of these syndromes involve, among others, altered adipocyte differentiation, structure and/or regulation of the adipocyte lipid droplet, and/or premature cellular senescence. Lipodystrophy syndromes frequently present as systemic diseases with multi-tissue involvement. After an update on the main molecular bases and clinical forms of lipodystrophy, we will focus on topics that have recently emerged in the field. We will discuss the links between lipodystrophy and premature ageing and/or immuno-inflammatory aggressions of adipose tissue, as well as the relationships between lipomatosis and lipodystrophy. Finally, the indications of substitutive therapy with metreleptin, an analog of leptin, which is approved in Europe and USA, will be discussed.

Cookies & analyse de trafic

M BRUNO FEVE

Pourquoi vous devez consulter ce praticien

Thèses universitaires

Direction de thèses

Activité de recherche & publications

Publications académiques en France

Lieux de consultation(2)

Tarifs & secteur de conventionnement

Prendre rendez-vous & contact

Top publications · les plus citées

Publications scientifiques (50) — classées par pathologie

Transversal38

Génétique5

Corticothérapie2

Microbiote2

Santé mentale / fatigue2

AINS1

Biomarqueurs / Auto-Ac1

Épidémiologie & registres1

Revue / méta-analyse1

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