La dénutrition au CHU d'Angers : Analyse du codage de 2010 à 2012

La dénutrition est très fréquente chez les patients hospitalisés. Elle résulte d'un déséquilibre entre les apports et les besoins de l'organisme, engendrant une perte de masse tissulaire et des altérations fonctionnelles qui entrainent ou aggravent un grand nombre de pathologies. Son dépistage et sa prise en charge ont démontré leur efficacité et sont une priorité de santé publique. L'analyse du PMSI au CHU d'Angers de 2010 à 2012 .montre que le taux de prévalence du codage de la dénutrition n'est pas un bon indicateur du taux réel de dénutrition hospitalière, probablement en raison d un manque de dépistage mais aussi d'une sous déclaration relative. Le taux de codage semble peu influencé par le degré d'activité des diététiciens, sauf dans certains services où l échange entre médecins et diététicien est renforcé. Il existe d autre part grande hétérogénéité de taux de prévalence du codage de la dénutrition selon les services, reflétant probablement une disparité et une insuffisance de prise en compte des problématiques nutritionnelles.Malnutrition is common in hospitalized patients. It results from an imbalance between contributions and needs of the body, causing a loss of tissue mass and functional alterations that result or aggravate many illnesses. Its detection and treatment have proven effective and are a public health priority. PMSI analysis in the CHU of Angers from 2010 to 2012 shows that the prevalence of malnutrition coding is not a good indicator of the actual rate of hospital malnutrition, probably due to a lack of screening but also an underreporting. The coding rate seems little influenced by the degree of activity dieticians, except in certain services where the relationship between doctors and dietician is strengthened. Otherwise there are great heterogeneity of prevalence of malnutrition coding according to services, probably reflecting a disparity and a lack of consideration of nutritional issues.ANGERS-BU Médecine-Pharmacie (490072105) / SudocSudocFranceF

Propionyl-L-carnitine corrects metabolic and cardiovascular alterations in diet-induced obese mice and improves liver respiratory chain activity

Aims: Obesity is a primary contributor to acquired insulin resistance leading to the development of type 2 diabetes and cardiovascular alterations. The carnitine derivate, propionyl-L-carnitine (PLC), plays a key role in energy control. Our aim was to evaluate metabolic and cardiovascular effects of PLC in diet-induced obese mice. Methods: C57BL/6 mice were fed a high-fat diet for 9 weeks and then divided into two groups, receiving either free- (vehicle-HF) or PLC-supplemented water (200 mg/kg/day) during 4 additional weeks. Standard diet-fed animals were used as lean controls (vehicle-ST). Body weight and food intake were monitored. Glucose and insulin tolerance tests were assessed, as well as the HOMAIR, the serum lipid profile, the hepatic and muscular mitochondrial activity and the tissue nitric oxide (NO) liberation. Systolic blood pressure, cardiac and endothelial functions were also evaluated. Results: Vehicle-HF displayed a greater increase of body weight compared to vehicle-ST that was completely reversed by PLC treatment without affecting food intake. PLC improved the insulin-resistant state and reversed the increased total cholesterol but not the increase in free fatty acid, triglyceride and HDL/LDL ratio induced by high-fat diet. Vehicle-HF exhibited a reduced cardiac output/body weight ratio, endothelial dysfunction and tissue decrease of NO production, all of them being improved by PLC treatment. Finally, the decrease of hepatic mitochondrial activity by high-fat diet was reversed by PLC. Conclusions: Oral administration of PLC improves the insulin-resistant state developed by obese animals and decreases the cardiovascular risk associated to this metabolic alteration probably via correction of mitochondrial function

Yearly Incidence of Stroke and Bleeding in Atrial Fibrillation with Concomitant Hyperthyroidism: A National Discharge Database Study

Background: Hyperthyroidism is associated with atrial fibrillation (AF), and the latter is a major risk factor for stroke. Aim: We aimed to investigate the yearly incidence of stroke and bleeding in AF patients with and without concomitant hyperthyroidism from the French National Hospital Discharge Database. Methods: Admissions with AF between January 2010 and December 2019 were retrospectively identified and retrieved from the French national database. Incidence rates of ischaemic stroke and bleeding were compared in AF patients with and without concomitant hyperthyroidism. The associations of risk factors with ischaemic stroke were assessed by Cox regression. Results: Overall 2,421,087 AF patients, among whom 32,400 had concomitant hyperthyroidism were included in the study. During the follow-up (mean: 2.0 years, standard deviation SD: 2.2 years), the yearly incidence of ischaemic stroke was noted to be 2.6 (95% confidence interval CI: 2.5–2.8) in AF patients with concomitant hyperthyroidism, and 2.3 (95%CI: 2.3–2.4) in non-thyroid AF patients. Hyperthyroidism was noted as an independent risk factor for ischaemic stroke (adjusted hazard ratio aHR: 1.133, 95%CI: 1.080–1.189) overall, particularly within the first year of hyperthyroidism diagnosis (aHR 1.203, 95%CI 1.120–1.291), however, the association became non-significant in subsequent years (aHR 1.047, 95%CI 0.980–1.118). Major bleeding incidence was lower in the hyperthyroid AF group in comparison to the non-thyroid AF group (incidence ratio: 5.1 vs. 5.4%/year, p < 0.001). The predictive value of CHA(2)DS(2)VASc and HAS-BLED scores for ischaemic stroke and bleeding events, respectively, did not differ significantly between AF patients with or without concomitant hyperthyroidism. Conclusions: Hyperthyroidism seems to be an independent risk factor of ischaemic stroke in AF patients, particularly within the first year of hyperthyroidism diagnosis

Microparticles from patients with metabolic syndrome induce vascular hypo-reactivity via Fas/Fas-ligand pathway in mice

Peer reviewedPublisher PD

Gene Expression in Skeletal Muscle Biopsies from People with Type 2 Diabetes and Relatives: Differential Regulation of Insulin Signaling Pathways

BACKGROUND:Gene expression alterations have previously been associated with type 2 diabetes, however whether these changes are primary causes or secondary effects of type 2 diabetes is not known. As healthy first degree relatives of people with type 2 diabetes have an increased risk of developing type 2 diabetes, they provide a good model in the search for primary causes of the disease. METHODS/PRINCIPAL FINDINGS:We determined gene expression profiles in skeletal muscle biopsies from Caucasian males with type 2 diabetes, healthy first degree relatives, and healthy controls. Gene expression was measured using Affymetrix Human Genome U133 Plus 2.0 Arrays covering the entire human genome. These arrays have not previously been used for this type of study. We show for the first time that genes involved in insulin signaling are significantly upregulated in first degree relatives and significantly downregulated in people with type 2 diabetes. On the individual gene level, 11 genes showed altered expression levels in first degree relatives compared to controls, among others KIF1B and GDF8 (myostatin). LDHB was found to have a decreased expression in both groups compared to controls. CONCLUSIONS/SIGNIFICANCE:We hypothesize that increased expression of insulin signaling molecules in first degree relatives of people with type 2 diabetes, work in concert with increased levels of insulin as a compensatory mechanism, counter-acting otherwise reduced insulin signaling activity, protecting these individuals from severe insulin resistance. This compensation is lost in people with type 2 diabetes where expression of insulin signaling molecules is reduced

Evolution sur 6 ans des séjours hospitaliers d'un service de médecine post-urgence

LYON1-BU Santé (693882101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Régulation par l'insuline du transport du glucose dans l'adipocyte

L'insuline augmente le transport du glucose dans l'adipocyte par la translocation à la membrane plasmatique d'un transporteur du glucose, Glut4, appartenant à un groupe de vésicules spécialisées. A l'état de base, ces vésicules sont séquestrées en position peri-nucléaire par le réseau de microtubules. L'insuline stimule fortement la translocation des vésicules contenant Glut4 à la membrane plasmatique en utilisant une double voie de signalisation : la voie dépendante de la phosphatidylinositol 3-kinase et la voie dépendante de la TC-10-kinase. La PKB est une sérine-thréonine kinase indispensable à l'action de l'insuline sur Glut4. Notre hypothe se est que la PKB, en plus de son activation par l'insuline en position membranaire, joue également un rôle au niveau même des vésicules Glut4. En utilisant des techniques d'imagerie cellulaire avec la Green Fluorescent Protein, nous montrons que l'expression de forme négative de PKB au niveau des vésicules Glut4 inhibe leur translocation en réponse à l'insuline. L'expression d'un mutant constitutionnellement actif n'a aucun effet par lui-même mais n'altère pas la translocation induite par l'insuline. In vivo, nous observons dans le tissu adipeux de sujets diabétiques insulinorésistants, une diminution de l'expression du gène codant pour Glut4 à l'état de base, associé à un défaut de stimulation de son expression en réponse à l'insuline. Notre travail montre que le transport du glucose dans l'adipocyte est un processus finement régulé par l'insuline et que la PKB possède un rôle fondamental dans cette régulation. Les sujets présentant une résistance à l'action de l'insuline ont également une baisse d'expression de Glut4 dans le tissu adipeux dont les conséquences sur le métabolisme adipocytaire restent à déterminer.LYON1-BU.Sciences (692662101) / SudocSudocFranceF

Impact du FGF21, une hormone du métabolisme énergétique, sur la reproduction

International audienceObesity or insulin resistance are the major non-infectious diseases that continue to progress worldwide. They promote diabetes and cardiovascular diseases, but also lead to a decrease in fertility in both sexes. FGF21, discovered in the 2000s, is a hormone closely linked to the energy status and has the ability to decrease insulin resistance. Its action through the FGFR1c, 3c & 4 receptors modulates tissues involved in energy-related metabolism but also the brain and the gonads. Recent data favor a role of FGF21 in female and male fertility, but raise the question about the role of FGF21 on reproductive function. In this review, we have scanned the different FGF21 actions on the reproductive axis, suggesting a potential therapeutic role in case of infertility.L’obésité et l’insulinorésistance sont les principales maladies non infectieuses qui progressent le plus dans le monde. Elles favorisent l’hypertension, les maladies cardio-vasculaires, mais conduisent aussi à une chute de la fertilité dans les deux sexes. Le FGF21, découvert dans les années 2000, est lié au statut énergétique de l’organisme et améliore l’insulinorésistance. Via ses récepteurs (FGFR1c, 3c,et 4), il agit sur le foie et au niveau d'organes régulant le métabolisme glucido-lipidique, mais aussi sur le cerveau et les gonades. Des données récentes sont ainsi en faveur d’un rôle régulateur de FGF21 sur la fertilité, tant féminine que masculine. Mais quel rôle FGF21 peut-il jouer dans la reproduction ? Dans cette revue, nous avons examiné les différentes activités que présente cette hormone sur la reproduction, ouvrant la voie à une éventuelle utilisation thérapeutique en cas d’infertilité