Usages du vélo et rapports aux espaces publics des enfants : permanence de la division par sexe dans un dispositif d’apprentissage dans un quartier populaire à Strasbourg

Cadre de la recherche : Dans les quartiers prioritaires de la Politique de la Ville en France, les activités physiques, qu’elles soient effectuées dans un cadre de déplacement ou de loisirs, restent en retrait par rapport au territoire français dans son ensemble. Si de multiples travaux analysent les activités physiques et sportives chez les jeunes, voire les adultes, les pratiques des enfants demeurent un point aveugle. Les enfances pauvres méritent pourtant un regard spécifique, particulièrement leurs rapports à l’espace public. Dans cette optique, la littérature scientifique insiste sur les mobilités indépendantes et sur les contraintes familiales, notamment chez les filles. Objectifs : Il s’agit d’interroger les rapports sexués aux espaces publics dans les quartiers populaires à partir des usages du vélo d’enfants de 9 et 10 ans. Méthodologie : Une équipe de sociologues et de géographes a suivi six classes de CM1 dans trois écoles primaires d’un quartier prioritaire de la Politique de la Ville à Strasbourg. Ces enfants ont bénéficié, pour deux d’entre elles, d’une formation spécifique, d’une part, par des éducateurs sportifs municipaux, et, d’autre part, par des formateurs en sécurité routière. La troisième école fait office de groupe témoin. Des questionnaires ad hoc ont été transmis dans chaque école, avant et après les cycles d’apprentissage du vélo, pour étudier l’évolution de leur niveau technique, de leurs usages du vélo dans le quartier et dans la ville, de leurs relations familiales et amicales nouées autour du vélo. Résultats : Les résultats mettent en avant une différenciation sexuée, nette et persistante, en termes de contrôle du vélo, d’aisance technique dans et hors du quartier et surtout de poids de socialisations distinctes au risque et des contraintes familiales liées à la division par sexe. Conclusion : Dès lors persistent, pour les enfants de ce quartier, des usages singuliers de l’espace public à vélo, liés principalement aux configurations relationnelles sexuées dans les familles populaires. Contribution : Cette étude amène à questionner les méthodes d’apprentissage du vélo pour identifier les précautions à prendre pour favoriser les usages du vélo des garçons et des filles dans l’espace public. Il est alors conseiller de mobiliser les familles pour favoriser le vélo pour tous, particulièrement dans les quartiers socialement défavorisés

Proteolysis inhibition by hibernating bear serum leads to increased protein content in human muscle cells

Muscle atrophy is one of the main characteristics of human ageing and physical inactivity, with resulting adverse health outcomes. To date, there are still no efficient therapeutic strategies for its prevention and/or treatment. However, during hibernation, bears exhibit a unique ability for preserving muscle in conditions where muscle atrophy would be expected in humans. Therefore, our objective was to determine whether there are components of bear serum which can control protein balance in human muscles. In this study, we exposed cultured human differentiated muscle cells to bear serum collected during winter and summer periods, and measured the impact on cell protein content and turnover. In addition, we explored the signalling pathways that control rates of protein synthesis and degradation. We show that the protein turnover of human myotubes is reduced when incubated with winter bear serum, with a dramatic inhibition of proteolysis involving both proteasomal and lysosomal systems, and resulting in an increase in muscle cell protein content. By modulating intracellular signalling pathways and inducing a protein sparing phenotype in human muscle cells, winter bear serum therefore holds potential for developing new tools to fight human muscle atrophy and related metabolic disorders

Le Sentiment d’Injustice Subie : Réactions Comportementales

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Fibroblast growth factor 19 as a countermeasure to muscle and locomotion dysfunctions in experimental cerebral palsy

International audienceBACKGROUND: Cerebral palsy (CP) associates cerebral function damages with strong locomotor defects and premature sarcopenia. We previously showed that fibroblast growth factor 19 (FGF19) exerts hypertrophic effects on skeletal muscle and improves muscle mass and strength in mouse models with muscle atrophy. Facing the lack of therapeutics to treat locomotor dysfunctions in CP, we investigated whether FGF19 treatment could have beneficial effects in an experimental rat model of CP. METHODS: Cerebral palsy was induced in male Wistar rat pups by perinatal anoxia immediately after birth and by sensorimotor restriction of hind paws maintained until Day 28. Daily subcutaneous injections with recombinant human FGF19 (0.1 mg/kg bw) were performed from Days 22 to 28. Locomotor activity and muscle strength were assessed before and after FGF19 treatment. At Day 29, motor coordination on rotarod and various musculoskeletal parameters (weight of tibia bone and of soleus and extensor digitorum longus (EDL) muscles; area of skeletal muscle fibres) were evaluated. In addition, expression of specific genes linked to human CP was measured in rat skeletal muscles. RESULTS: Compared to controls, CP rats had reduced locomotion activity (-37.8% of distance travelled, P \textless 0.05), motor coordination (-88.9% latency of falls on rotarod, P \textless 0.05) and muscle strength (-25.1%, P \textless 0.05). These defects were associated with reduction in soleus (-51.5%, P \textless 0.05) and EDL (-42.5%, P \textless 0.05) weight, smaller area of muscle fibres, and with lower tibia weight (-38%, P \textless 0.05). In muscles from rats submitted to CP, changes in the expression levels of several genes related to muscle development and neuromuscular junctions were similar to those found in wrist muscle of children with CP (increased mRNA levels of Igfbp5, Kcnn3, Gdf8, and MyH4 and decreased expression of Myog, Ucp2 and Lpl). Compared with vehicle-treated CP rats, FGF19 administration improved locomotor activity (+53.2%, P \textless 0.05) and muscle strength (+25.7%, P \textless 0.05), and increased tibia weight (+13.8%, P \textless 0.05) and soleus and EDL muscle weight (+28.6% and +27.3%, respectively, P \textless 0.05). In addition, it reduced a number of very small fibres in both muscles (P \textless 0.05). Finally, gene expression analyses revealed that FGF19 might counteract the immature state of skeletal muscles induced by CP. CONCLUSIONS: These results demonstrate that pharmacological intervention with recombinant FGF19 could restore musculoskeletal and locomotor dysfunction in an experimental CP model, suggesting that FGF19 may represent a potential therapeutic strategy to combat the locomotor disorders associated with CP

Adipose tissue angiogenesis genes are down-regulated by grape polyphenols supplementation during a human overfeeding trial

International audienceThe adaptive response to overfeeding is associated with profound modifications of gene expression in adipose tissue to support lipid storage and weight gain. The objective of this study was to assess in healthy lean men whether a supplementation with polyphenols could interact with these molecular adaptations. Abdominal subcutaneous adipose tissue biopsies were sampled from 42 subjects participating to an overfeeding protocol providing an excess of 50% of their total energy expenditure for 31 days, and who were supplemented with 2 g/day of grape polyphenols or a placebo. Gene expression profiling was performed by RNA sequencing. Overfeeding led to a modification of the expression of 163 and 352 genes in the placebo and polyphenol groups, respectively. The GO functions of these genes were mostly involved in lipid metabolism, followed by genes involved in adipose tissue remodeling and expansion. In response to overfeeding, 812 genes were differentially regulated between groups. Among them, a set of 41 genes were related to angiogenesis and were down-regulated in the polyphenol group. Immunohistochemistry targeting PECAM1, as endothelial cell marker, confirmed reduced angiogenesis in this group. Finally, quercetin and isorhamnetin, two polyphenol species enriched in the plasma of the volunteers submitted to the polyphenols, were found to inhibit human umbilical vein endothelial cells migration in vitro. Polyphenol supplementation do not prevent the regulation of genes related to lipid metabolism in human adipose tissue during overfeeding, but impact the angiogenesis pathways. This may potentially contribute to a protection against adipose tissue expansion during dynamic phase of weight gain

18th Euro Fed Lipid Congress and Expo

International audienceDietary synthetic emulsifiers have recently been shown to promote metabolic syndrome and alter the gut microbiota. The effects of natural emulsifiers, such as vegetable lecithin, remain poorly described. Our objective was to evaluate, in mice, the impact of soy and rapeseed lecithin (SL and RL), both rich in essential α-linolenic acid (ALA), on HFD-induced adiposity, inflammation and the gut microbiota. For 13 weeks, male Swiss mice (n=72) were fed a Chow diet, a HFD devoid of ALA, or different ALA-enriched HFD (identical ALA content: 4.7%) containing 0% lecithin (HF-0L), a nutritional dose (10%) of SL or RL (HF-10SL, HF-10RL) or a supplemental dose of RL (20%; HF-20RL). Biometric parameters and the epididymal adipose tissue (EAT) were analysed; hepatic lipid composition was determined by GC-FID, gene expression by RT-qPCR, and faecal microbiota composition by 16S sequencing. In all groups fed ALA-rich diets, the proportion of ALA in both liver triacylglycerols and phospholipids was increased, but the vectorisation of ALA as lecithin did not further increase its hepatic bioavailability, compared to an oil (HF-0L). The incorporation of 10% SL, but not RL, in ALA-enriched HFD significantly increased weight gain (p<0.001) and adiposity (p<0.001) vs Chow. Both HFD and HF-10SL induced increased expression of genes of macrophage infiltration in the EAT (ex. Tnfα, Cd11c) vs Chow (p<0.05), while HF-0L and RL induced levels of such inflammatory markers in-between Chow and HFD. Finally, HF-10RL reduced HFD-induced loss of α-diversity of the gut microbiota and altered the abundance of several bacterial groups, such as Desulfovibrionaceae. All in all, the addition of lecithins to HFD did not exacerbate HFD-inflammation and RL increased gut bacterial diversity. This study hence illustrates the importance of considering certain natural emulsifiers, notably rapeseed lecithin, as alternatives to synthetic emulsifiers of known detrimental effects

Endoplasmic reticulum-mitochondria miscommunication is an early and causal trigger of hepatic insulin resistance and steatosis

International audienceBACKGROUND & AIMS: Hepatic insulin resistance in obesity and type 2 diabetes was recently associated with endoplasmic reticulum (ER)-mitochondria miscommunication. These contact sites (mitochondria-associated membranes: MAMs) are highly dynamic and involved in many functions. Up to now, it is not clear if MAM miscommunication could have a causal role in hepatic insulin resistance and steatosis. We therefore aimed to determine whether and how organelle miscommunication plays a role in the onset and progression of hepatic metabolic impairment. METHODS: We analyzed hepatic ER-mitochondria interactions and calcium exchange in diet-induced obese mice in a time-dependent and reversible manner, and investigated causality in hepatic metabolic alterations by expressing a specific organelle spacer or linker in mouse liver, using adenovirus. RESULTS: Disruption of ER-mitochondria interactions and calcium exchange is an early event preceding hepatic insulin resistance and steatosis in diet-induced obese mice. Interestingly, an 8-week reversal diet concomitantly reversed hepatic organelle miscommunication and insulin resistance in obese mice. Mechanistically, disrupting structural and functional ER-mitochondria interactions through the hepatic overexpression of the organelle spacer FATE1 was sufficient to impair hepatic insulin action and glucose homeostasis. In addition, FATE1-mediated organelle miscommunication disrupted lipid-related mitochondrial oxidative metabolism and induced hepatic steatosis. Conversely, reinforcement of ER-mitochondria interactions through hepatic expression of a synthetic linker prevented diet-induced glucose intolerance after 4 weeks' overnutrition. Importantly, ER-mitochondria miscommunication was confirmed in the liver of obese patients with type-2 diabetes, and correlated with glycemia, HbA1c and HOMA-IR index. CONCLUSIONS: ER-mitochondria miscommunication is an early causal trigger of hepatic insulin resistance and steatosis, and can be reversed by switching to a healthy diet. Thus, targeting MAMs could contribute to restoring metabolic homeostasis. LAY SUMMARY: The literature suggests that interactions between endoplasmic reticulum (ER) and mitochondria could play a dual role in hepatic insulin resistance and steatosis during chronic obesity. The present study reappraised time-dependent regulation of hepatic ER-mitochondria interactions and calcium exchange in diet-induced obese mice and their causal role in hepatic insulin resistance and steatosis. We show that organelle miscommunication is an early causal trigger of hepatic insulin resistance and steatosis, and can be improved by nutritional strategies