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Liver cirrhosis is associated with impairment of cardiovascular function including alterations of the heart innervation, humoral and nervous dysregulation, changes in systemic circulation and electrophysiological abnormalities. Choline acetyltransferase (ChAT), enzyme forming acetylcholine, tyrosine hydroxylase (TH), and dopamine-[beta]-hydroxylase (DBH), enzymes participating in noradrenaline synthesis, are responsible for the production of classical neurotransmitters, and atrial natriuretic peptide (ANP) is produced by cardiomyocytes. The aim of this study was to evaluate the influence of experimentally induced hepatic dysfunction on the expression of proANP, ChAT, TH, and DBH in the heart. Hepatic dysfunction was induced by application of thioacetamide (TAA) or by ligation of bile duct. Biochemical parameters of hepatic injury and levels of peroxidation in the liver and heart were measured. Liver enzymes measured in the plasma were significantly elevated. Cardiac level of peroxidation was increased in operated but not TAA group animals. In the left atrium of operated rats, the expression of TH and DBH was lower, while expression of ChAT remained unchanged. In TAA group, no significant differences in the expression of the genes compared to controls were observed. Liver injury induced by ligation leads to an imbalance in the intracardiac innervation, which might impair nervous control of the heart. Key words: cirrhotic cardiomyopathy, thioacetamide, bile duct ligation, heart, intracardiac nervous system, catecholamines, lipid peroxidation. La cirrhose est associee a une atteinte de la fonction cardiovasculaire, y compris des modifications de l'innervation du creur, un dereglement hormonal et nerveux, des variations de la circulation generale et des anomalies electrophysiologiques. La choline acetyltransferase (ChAT), un enzyme responsable de la formation de l'acetylcholine, la tyrosine hydroxylase (TH) et la dopamine-[beta]-hydroxylase (DBH), des enzymes participant a la synthese de la noradrenaline, sont responsables de la production de neurotransmetteurs classiques, et le peptide natriuretique auriculaire (ANP) est produit par les cardiomyocytes. Cette etude avait pour but d'evaluer l'influence d'un dysfonctionnement hepatique provoque experimentalement sur l'expression des facteurs proANP, ChAT, TH et DBH dans le creur. Le dysfonctionnement hepatique a ete provoque par l'exposition au thioacetamide (TAA) ou par la ligature du conduit choledoque. Nous avons mesure les parametres biochimiques des lesions hepatiques et les taux de peroxydation dans le foie et le creur. Nous avons mesure une augmentation notable des enzymes hepatiques dans le plasma. Nous avons observe une augmentation des taux de peroxydation cardiaque chez les animaux operes, mais pas dans le groupe TAA. L'expression de la TH et de la DBH etait moins elevee dans l'oreillette gauche des rats operes, alors que l'expression de la ChAT demeurait inchangee. Dans le groupe TAA, nous n'avons observe aucune difference notable dans l'expression des genes comparativement aux temoins. Les lesions hepatiques provoquees par la ligature menent a un desequilibre dans l'innervation intracardiaque, ce qui pourrait avoir un effet negatif sur le controle nerveux du creur. [Traduit par la Redaction] Mots-cles: cardiomyopathie cirrhotique, thioacetamide, ligature du conduit choledoque, creur, systeme nerveux intracardiaque, catecholamines, peroxydation lipidique., Introduction Liver cirrhosis is associated with impairment of cardiovascular function including abnormal hemodynamics and latent heart failure termed 'cirrhotic cardiomyopathy', which is characterized by altered diastolic relaxation, electrophysiological abnormalities, such [...]

Obesogens, as environmental endocrine-disrupting chemicals, are supposed to have had an impact on the prevalence of rising obesity around the world over the last forty years. These chemicals are probably able to contribute not only to the development of obesity and metabolic disturbances in individuals, but also in their progeny, having the capability to epigenetically reprogram genetically inherited set-up points for body weight and body composition control during critical periods of development, such as fetal, early life, and puberty. In individuals, they may act on myriads of neuro-endocrine–immune metabolic regulatory pathways, leading to pathophysiological consequences in adipogenesis, lipogenesis, lipolysis, immunity, the influencing of central appetite and energy expenditure regulations, changes in gut microbiota–intestine functioning, and many other processes. Evidence-based medical data have recently brought much more convincing data about associations of particular chemicals and the probability of the raised risk of developing obesity. Foods are the main source of obesogens. Some obesogens occur naturally in food, but most are environmental chemicals, entering food as a foreign substance, whether in the form of contaminants or additives, and they are used in a large amount in highly processed food. This review article contributes to a better overview of obesogens, their occurrence in foods, and their impact on the human organism. [ABSTRACT FROM AUTHOR]

The contribution of environmental pollutants to the obesity pandemic is still not yet fully recognized. Elucidating possible cellular and molecular mechanisms of their effects is of high importance. Our study aimed to evaluate the effect of chronic, 21-day-long, 2,2-bis (4-chlorophenyl)-1,1-dichlorethylenedichlorodiphenyldichloroethylene (p,p´-DDE) exposure of human adipose-derived mesenchymal stem cells committed to adipogenesis on mitochondrial oxygen consumption on days 4, 10, and 21. In addition, the mitochondrial membrane potential (MMP), the quality of the mitochondrial network, and lipid accumulation in maturing cells were evaluated. Compared to control differentiating adipocytes, exposure to p,p´-DDE at 1 μM concentration significantly increased basal (routine) mitochondrial respiration, ATP-linked oxygen consumption and MMP of intact cells on day 21 of adipogenesis. In contrast, higher pollutant concentration seemed to slow down the gradual increase in ATP-linked oxygen consumption typical for normal adipogenesis. Organochlorine p,p´-DDE did not alter citrate synthase activity. In conclusion, in vitro 1 μM p,p´-DDE corresponding to human exposure is able to increase the mitochondrial respiration per individual mitochondrion at the end of adipocyte maturation. Our data reveal that long-lasting exposure to p,p´-DDE could interfere with the metabolic programming of mature adipocytes. [ABSTRACT FROM AUTHOR]