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Background and Aims: We have recently identified six adipokines that are oversecreted by omental adipose tissue in obesity: 3 chemokines [Growth-Related Oncogen factor (GRO), Regulated upon Activation Normal T cells Expressed and Secreted (RANTES), Macrophage Inflammatory Protein-1ß (MIP-1ß)], 1 interleukin (IL-7), 1 tissue inhibitor of metalloproteinases (TIMP-1) and 1 growth factor (thrombopoietin, TPO). Enhanced expression of these adipokines in adipocytes did correlate with several features of the metabolic syndrome. The aim of the present study was to examine whether the abnormal hormonal milieu and/or the chronic inflammation state that prevail in obesity could contribute to such dysregulation of adipokine production. We thus examined the effects of some hormones (insulin, glucocorticoids and catecholamines) and the proinflammatory cytokine, TNFα on these adipokines in cultured human omental adipocytes. Because of the potent changes induced by TNF, we more particularly focused on its effects. Results: Treatment of omental adipocytes with hormones induced only a modest increase in some adipokines. By contrast, the addition of TNFα to the medium induced strong changes in the expression of all the adipokines. These changes occurred in a dose-dependent fashion and a ~600 fold increase was observed for some of them (i.e. RANTES). Because TNFα appears to be a main regulator, we characterize in some detail its effects on mature adipocytes from lean and obese subjects. We first confirmed that TNF secretion was higher in stromal-vascular cells (SVC; that contain macrophages) than in adipocytes and enhanced in obesity. We next cultured mature adipocytes in the presence of medium previously conditioned by SVC and obtained a pattern of adipokine expression similar to that induced by TNF. Obese adipocytes exhibited much stronger changes in adipokines in response to TNF than lean adipocytes. Eventually, these changes were fully prevented by TNF-neutralizing antibodies. Conclusions: TNF is a key contributor to adipokine dysregulation in omental adipocytes. In obesity, this proinflammatory cytokine, which is mainly oversecreted by SVC acts on enlarged adipocytes, whiwh are hyper-responsive to that inflammatory triggering signal. This ultimately leads to marked adipokine dysregulation, and further worsening of the inflammatory state and of the metabolic syndrome. Précédemment au laboratoire, Maury et al. ont identifié six adipokines qui sont surexprimées dans le TA omental chez les sujets obèses : 3 chémokines [Growth-Related Oncogen factor (GRO), Regulated upon Activation Normal T cells Expressed and Secreted (RANTES), Macrophage Inflammatory Protein-1β (MIP-1β)], une interleukine (IL-7), une protéase de la matrice extracellulaire [Tissue Inhibitor of Metalloproteinases (TIMP-1)] et un facteur hématopoïétique [thrombopoiétine (TPO)]. L’augmentation de l’expression de ces adipokines dans les adipocytes est corrélée avec plusieurs anomalies du syndrome métabolique. Le but de notre étude était d’examiner si les perturbations hormonales et/ou l’état inflammatoire chronique présents dans l’obésité avaient pu contribuer à la dérégulation de la production d’adipokines. Nous avons donc examiné les effets de certaines hormones (insuline, glucocorticoïdes et catécholamines) et d’une cytokine pro-inflammatoire, le TNF-α, sur nos adipokines d’intérêt dans des cultures d’adipocytes omentaux humains. Le TNF-α ayant induit des modifications très importantes, nous nous sommes donc davantage focalisés sur ses effets. Le traitement des adipocytes par les hormones a induit une augmentation modeste uniquement de certaines adipokines. Par contre, le TNF-α a produit des modifications marquées de l’expression de toutes les adipokines étudiées. Ces modifications se sont produites de manière dose-dépendante et une augmentation jusqu’à ~ 600 fois a été observée, par exemple pour RANTES. Nous avons donc caractérisé en détail le rôle du TNF-α sur des adipocytes matures de sujets minces et obèses. Nous avons tout d’abord montré que la sécrétion du TNF-α était plus élevée dans les SVC que dans les adipocytes et qu’elle était augmentée dans l’obésité. Nous avons ensuite cultivé des adipocytes matures en présence de milieux préalablement conditionnés par des SVC et obtenu un profil d’expression des adipokines similaire à celui induit par le TNF-α. Les adipocytes de sujets obèses présentaient une réponse accrue à ces milieux. Toutes ces modifications ont été entièrement prévenues par des anticorps neutralisant l’activité du TNF-α. En conclusion, le TNF-α joue un rôle-clef dans la dérégulation des adipokines dans les adipocytes omentaux chez le sujet obèse. Dans l’obésité, cette cytokine pro-inflammatoire, principalement sécrétée en excès par les SVC, agit sur les adipocytes hypertrophiés qui y répondent de manière excessive. Cette double perturbation (excès de production et d’action du TNF-α) conduit à une dérégulation de toutes les adipokines, à une aggravation de l’état inflammatoire et du SM.

Tumor Necrosis Factor-alpha --- Adipokines --- Obesity

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Central visceral obesity is strongly associated with chronic disorders such as type 2 diabetes, cardiovascular disease and cancer. Adipokines are involved in the pathogenesis of these obesity-linked disorders. However, adipokines secreted by visceral adipose tissue (VAT) are still poorly characterised.
We have searched for novel adipokines secreted by VAT determined whther their secretion was altered in obesity and evaluated the respective contribution of adipocytes vs non-fat (stromal-vascular, SV) cells.
In this context we have identified for the first time 6 adipokines secreted by each cellular fraction of VAT from lean and obese subjects by. These adipokines include 3 chemokines [Growth-Related Oncogen factor (GRO), Regulated upon Activation Normal T cells Expresses and Secreted (RANTES), Macrophage Inflammatory Protein-1β], 1 interleukin (IL-7), 1 tissue inhibitor of metalloproteinases (TIMP-1) and 1 hematopoietic growth factor (thrombopoeitin). Secretion of each adipokine was enhanced in obese subjects with of by pretranslational mechanisms. The higher proportion of macrophages and endothelial cells in VAT of obese subjects may contribute tour findings, as well as changes in intrinsic properties of hypertrophied adipocytes. Accordingly, mRNA concentrations of the majority of these adipokines markedly increased during adipocyte differentiation.
Furthermore we have studied some factors that could change the production of our adipokines : catecholamines (and cAMP), glucocorticoids, insulin and TFNα. We have found that the hormones, normally deregulated in obesity, influenced only moderately the expressions of our adipokines. In contrast, the effects of the TNFα on adipokines were strongly marked. According to these facts we could suggest that the macrophages, the most important source of the TNFα in adipose tissue of obese subjects, may have more impact on the regulation of the adipokines than the hormones studied.
In conclusion, six adipokines were newly identified in VAT. Their expression and secretion were increased in obesity, with a relatively similar contribution of adipocytes and SV cells. Because of their known involvement in cardiovascular disease, cancer or insulin resistance, these adipokines may play a role in obesity-linked adverse health outcomes L’obésité viscérale est un facteur de risque de nombreuses maladies chroniques telles que le diabète de type 2, les maladies cardiovasculaires ou encore certains cancers. Les adipokines sont impliquées dans la pathogénie des co-morbidités de l’obésité. Toutefois, les adipokines secrétées par le tissu adipeux (TA) sont encore très peu étudiées. D’autre part, la contribution des différentes fractions du TA viscéral à cette sécrétion est encore peu connue.
Dans ce cadre, nous avons identifié 6 adipokines, secrétées par le TA viscéral. Ces adipokines comprennent 3 chémokines [Growth-Related Oncogen factor (GRO), Regulated upon Activation Normal T cells Expresses and Secreted (RANTES), Macrophage Inflammatory Protein-1β (MIP-1β)], 1 protéase de la matrice extracellulaire [Tissue Inhibitor of Metalloproteinases (TIMP-1)], 1 facteur hématopoïétique [thrombopoiétine (TPO)] et 1 interleukine (IL-7). La sécrétion de ces adipokines est augmentée chez les sujets obèses par rapport aux minces, et ce à la fois dans les fractions adipocytaire et stomacale vasculaire (FSV) du TA. Nous avons mesuré des variations superposables des ARNm dans les deux fractions : l’augmentation de sécrétion a donc pour origine des mécanismes pré-traductionnels.
Nous avons également mis en évidence une plus grande proportion de macrophages et de cellules endothéliales qui appartiennent à la FSV dans le TA. Ces cellules sont des bonnes sources de cytokines. De concert, elles contribuent à la sécrétion accrue d’adipokines des adipocytes hypertrophiés. En accord avec ces données, l’expression de presque toutes nos adipokines augmente au cours de la différenciation adipocytaire.
Enfin, nous avons étudié certains facteurs (hormones, TNAα) qui peuvent réguler la production de ces adipokines et qui sont susceptibles d’être à l’origine de leur surexpression dans l’obésité. L’effet des hormones est perturbées dans l’obésité (catécholamines, glucocorticoïdes et insuline) est modéré sur l’expression des adipokines. Au contraire, l’effet de TNFα est fortement marqué. Nos données pourraient don suggérer que l’accumulation de macrophages dans le TA des sujets obèse, principale source de TNFα, aurait plus d’impact sur la régulation des adipokines étudiées que les modifications hormonales.
Pour conclure, les 6 adipokines que nous venons d’identifier dans le TA viscéral pourraient stimuler la croissance du TA et également intervenir dans le développement des maladies cardiovasculaires. Elles pourraient aussi favoriser la survenue de la résistance à l’insuline de certaines formes de cancer

Adipose Tissue, White --- Abdominal Fat --- Adipokines --- Obesity --- Adipocytes

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Cardiology and cardiovascular sciences are two rapidly growing areas in medicine, with heart diseases being the number one cause of death worldwide. The last four decades have witnessed many developments in various cardiological sciences, including coronary artery disease, valve disease, heart failure, congenital heart diseases, and cardiovascular imaging, with a number of newly developed concepts, such as cardio-oncology, cardio-renal diseases, and preventive cardiology. This Special Issue (SI) of the Journal of Clinical Medicine, entitled “JCM-Advances in Cardiology”, focuses on recent advances in the cardiological sciences. It published 8 research articles of significant clinical and scientific value.

Medicine --- Pharmacology --- ST segment elevation myocardial infarction --- COVID-19 --- primary percutaneous intervention --- Coptic clergy --- mortality --- cardiovascular risk factors --- prevalence --- major adverse events --- obesity --- ACE2 --- renin–angiotensin system --- extraction --- reimplantation --- pacing --- ICD --- CRT --- dilated cardiomyopathy (DCM) --- LMNA --- lamin A --- lamin C --- next generation sequencing (NGS) --- myocarditis --- arrhythmias --- telemonitoring --- implantable cardioverter defibrillator --- implantable loop recorder --- Holter ECG --- metabolic-dysfunction-associated fatty liver disease (MAFLD) --- hepatic steatosis --- SteatoTest --- adipokines --- adiponectin --- visfatin --- cardiovascular disease --- n/a --- renin-angiotensin system

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The adipokine adiponectin is very concentrated in plasma, and decreased levels of adiponectin are associated with pathological conditions such as obesity, diabetes, cardiovascular diseases, and metabolic syndrome. When produced in its full-length form, adiponectin self-associates to generate multimeric complexes. The full-length form of adiponectin can be cleaved by the globular form of elastase that is produced locally, and the resulting biological effects are exerted in a paracrine or autocrine manner. The different forms of adiponectin bind to specific receptors consisting of two G-protein-independent, seven-transmembrane-spanning receptors, called AdipoR1 and AdipoR2, while T-cadherin has been identified as a potential receptor for high molecular weight complexes of adiponectin. Adiponectin exerts a key role in cellular metabolism, regulating glucose levels as well as fatty acid breakdown. However, its biological effects are heterogeneous, involving multiple target tissues. The Special Issue “Mechanisms of Adiponectin Action” highlights the pleiotropic role of this hormone through 3 research articles and 7 reviews. These papers focus on the recent knowledge regarding adiponectin in different target tissues, both in healthy and in diseased conditions.

acidic and rich in cysteine (SPARC) --- n/a --- regeneration --- fertility --- pig --- endocrine cancer --- NGF? --- reproductive tract --- neuritogenesis --- skeletal muscle --- matricellular proteins --- adiponectin isoforms --- obesity --- atherosclerosis --- hair growth-related factor --- ovarian cancer --- adipose tissue --- AdipoRon --- extracellular signal-regulated kinase (ERK) --- PC12 cells --- endometrial cancer --- AMPK --- metabolism --- adiponectin --- transcriptome --- exercise --- training --- inflammation --- BIAcore --- muscle --- adipokines --- human follicular dermal papilla cell --- estrogen receptor --- endometrium --- adiponectin inducer --- breast cancer --- implantation --- microarray --- Secreted protein --- adipogenesis --- kojyl cinnamate ester derivative --- cell signaling --- lipotoxicity --- cervix cancer --- cancer --- cholesterol efflux --- myopathies --- diabetes

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This Special Issue contributes original research and review articles on the role of new protein, molecular, and genetic markers used for the diagnosis and progression of civilization diseases, as well as biomarkers useful in the monitoring the effects of the implemented treatment.

Medicine --- pharmacogenomics --- NGS variants --- personalized medicine --- FSHR --- personalized drug therapy --- hedgehog-interacting protein --- impaired fasting glucose --- impaired glucose tolerance --- newly diagnosed diabetes --- normal glucose tolerance --- inflammatory bowel disease --- ulcerative colitis --- Crohn’s disease --- extracellular matrix components --- hyaluronan --- inflammatory bowel diseases (IBD) --- Crohn’s disease (CD) --- ulcerative colitis (UC) --- sulfated glycosaminoglycans (sGAG) --- hyaluronan (HA) --- soluble part of syndecan-1 (sCD138) --- microRNA --- cardiovascular disease --- diabetes --- mortality --- antiplatelet therapy --- platelet reactivity --- Let-7e --- miR-126 --- miR-223 --- miR-125a-3p --- CCL11 --- CCL24 --- CCL26 --- CCR3 --- CRC --- adiponectin --- adipokines --- rheumatology --- obesity --- overweight --- case control study --- rheumatoid arthritis --- TNF-α inhibitors --- bone turnover markers --- PINP --- PICP --- NTX-I --- CTX-I --- RANKL/OPG --- ovarian cancer --- interleukin 21 --- interleukin 22 --- lymphocytes --- macrophages --- dendritic cells --- innate lymphoid cells --- breast cancer --- extracellular matrix --- proteins --- tumorigenesis --- tumor microenvironment --- pharmacogenomics --- NGS variants --- personalized medicine --- FSHR --- personalized drug therapy --- hedgehog-interacting protein --- impaired fasting glucose --- impaired glucose tolerance --- newly diagnosed diabetes --- normal glucose tolerance --- inflammatory bowel disease --- ulcerative colitis --- Crohn’s disease --- extracellular matrix components --- hyaluronan --- inflammatory bowel diseases (IBD) --- Crohn’s disease (CD) --- ulcerative colitis (UC) --- sulfated glycosaminoglycans (sGAG) --- hyaluronan (HA) --- soluble part of syndecan-1 (sCD138) --- microRNA --- cardiovascular disease --- diabetes --- mortality --- antiplatelet therapy --- platelet reactivity --- Let-7e --- miR-126 --- miR-223 --- miR-125a-3p --- CCL11 --- CCL24 --- CCL26 --- CCR3 --- CRC --- adiponectin --- adipokines --- rheumatology --- obesity --- overweight --- case control study --- rheumatoid arthritis --- TNF-α inhibitors --- bone turnover markers --- PINP --- PICP --- NTX-I --- CTX-I --- RANKL/OPG --- ovarian cancer --- interleukin 21 --- interleukin 22 --- lymphocytes --- macrophages --- dendritic cells --- innate lymphoid cells --- breast cancer --- extracellular matrix --- proteins --- tumorigenesis --- tumor microenvironment