BecA-ILRI Hub capacity building program: Empowering African scientists and institutions to solve Africa’s agricultural challenges

<p>Bars show medians, *p<0.05, **p<0.01 Dunn's tests vs. controls. # p<0.05 two-tails, Mann-Whitney -test vs. controls.</p

Increased Immune Complexes of Hypocretin Autoantibodies in Narcolepsy

International audienceBACKGROUND: Hypocretin peptides participate in the regulation of sleep-wake cycle while deficiency in hypocretin signaling and loss of hypocretin neurons are causative for narcolepsy-cataplexy. However, the mechanism responsible for alteration of the hypocretin system in narcolepsy-cataplexy and its relevance to other central hypersomnias remain unknown. Here we studied whether central hypersomnias can be associated with autoantibodies reacting with hypocretin-1 peptide present as immune complexes. METHODOLOGY: Serum levels of free and dissociated (total) autoantibodies reacting with hypocretin-1 peptide were measured by enzyme-linked immunosorbent assay and analyzed with regard to clinical parameters in 82 subjects with narcolepsy-cataplexy, narcolepsy without cataplexy or idiopathic hypersomnia and were compared to 25 healthy controls. PRINCIPAL FINDINGS: Serum levels of total but not free IgG autoantibodies against hypocretin-1 were increased in narcolepsy-cataplexy. Increased levels of complexed IgG autoantibodies against hypocretin-1 were found in all patients groups with a further increase in narcolepsy-cataplexy. Levels of total IgM hypocretin-1 autoantibodies were also elevated in all groups of patients. Increased levels of anti-idiotypic IgM autoantibodies reacting with hypocretin-1 IgG autoantibodies affinity purified from sera of subjects with narcolepsy-cataplexy were found in all three groups of patients. Disease duration correlated negatively with serum levels of hypocretin-1 IgG and IgM autoantibodies and with anti-idiotypic IgM autoantibodies. CONCLUSION: Central hypersomnias and particularly narcolepsy-cataplexy are characterized by higher serum levels of autoantibodies directed against hypocretin-1 which are present as immune complexes most likely with anti-idiotypic autoantibodies suggesting their relevance to the mechanism of sleep-wake cycle regulation

Facteurs de la faim et de la satiété dans la régulation du plaisir alimentaire

Se nourrir est un comportement instinctif récompensé par une sensation de plaisir pendant l’obtention et l’ingestion d’aliments, correspondant respectivement aux phases de préparation et de consommation au cours d’un comportement motivé. La perception de cet état émotionnel, avec des sensations alternatives de faim et de satiété, entraîne le comportement alimentaire. Étant donné que les altérations de ce comportement, incluant l’hyperphagie ou l’anorexie, peuvent conduire respectivement à l’obésité et à la cachexie, comprendre les mécanismes neurochimiques de la régulation du plaisir de manger peut aider à développer de nouvelles thérapies pour ces maladies. Le système dopaminergique (DA) des projections mésolimbiques joue un rôle clé dans la récompense comportementale en général et est également impliqué dans la régulation du plaisir associé`a la nourriture dans le cerveau, au niveau du noyau accumbens (NAc) et de l’aire hypothalamique latérale (LHA). Cela suggère que ce système DA peut être sélectivement activé par des facteurs spécifiques à différents types de comportements motivés, dont les hormones liées à la faim et à la satiété. Et, en effet, l’administration centrale soit de ghréline orexigène, soit d’α-MSH, anorexigène, augmente la libération de DA dans le NAc. Toutefois, on sait également que la DA, injectée dans la LHA historiquement connue comme un « centre de la faim », inhibe la prise de nourriture, ce qui indique l’implication fonctionnelle de la DA dans la régulation à la fois de l’appétit et du plaisir de manger. Bien que le NAc et la LHA contiennent tous deux des neurones qui expriment les récepteurs de la mélanocortine, seule la LHA reçoit les terminaisons des neurones producteurs d’α-MSH, issues du noyau arqué de l’hypothalamus, principal relais vers le cerveau des signaux périphériques de la faim et de la satiété. Une étude récente a montré que l’α-MSH de la LHA promeut la satiété et inhibe le plaisir tout en stimulant la libération de DA dans cette aire pendant les phases de préparation et de consommation lors de la prise de nourriture. Cela suggère que la signalisation par l’α-MSH au système DA, modifiée dans la LHA, pourrait être impliquée dans la physiopathologie de l’obésité et de l’anorexie. Les mécanismes sous-jacents éventuels sont discutés

Gut Microbiota–Brain Axis in Regulation of Feeding Behavior

The survival of microorganisms inhabiting the intestinal tract depends on the nutrients provided by the host, with the latter obtaining them through food intake. It is hence not surprising that the co-evolution of gut bacteria and their hosts, including humans, shaped intrinsic interactions between their respective metabolisms with an impact on host feeding behavior. Understanding molecular pathways underlying such interactions may aid in the development of new therapeutic approaches for several pathological conditions accompanied by altered feeding behavior. A Special Issue titled “Gut Microbiota–Brain Axis in Regulation of Feeding Behavior” contributes to this topic of research, with eight papers covering its various aspects such as autoprobiotics, metabolic diseases and anorexia

Proteome Modifications of Gut Microbiota in Mice with Activity-Based Anorexia and Starvation: Role in ATP Production

OBJECTIVE: Activity-based anorexia (ABA) in rodents is a behavioral model of anorexia nervosa, characterized by negative energy balance, hyperactivity, and dysbiosis of gut microbiota. Gut bacteria are known to produce energy substrates including adenosine triphosphate (ATP) and acetate. The aim of this study was to determine whether ABA alters the proteome of gut microbiota relevant to ATP and acetate production. METHODS: The ABA was developed in male mice and compared with food-restricted and ad libitum-fed conditions. Proteomic analysis of feces was performed using the two-dimentional gel electrophoresis and mass spectrometry. The in vitro ATP-producing capacity of proteins extracted from feces was assayed. RESULTS: Increased levels of the phosphoglycerate kinase, an ATP-producing glycolytic enzyme, was detected in feces of food-restricted mice and this enzyme was further increased in the ABA group. Starvation also upregulated several other proteins synthetized by order Clostridiales including Clostridiaceae and Lachnospiraceae families. No significant differences in the in vitro ATP-producing capacity by bacterial proteins from ABA, food-restricted, and ad libitum-fed control mice were found. However, plasma levels of acetate strongly tended to be increased in the activity groups including ABA mice. CONCLUSION: The data revealed that starvation in food-restricted and ABA mice induced proteome modification in gut bacteria favoring ATP production mainly by the order Clostridiales. However, this did not result in increased total ATP-production capacity by gut microbiota. These changes can be interpreted as an adaptation of specific gut bacteria to the host malnutrition beneficial for host survival