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Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease that involves a pathological inflammatory response against articular cartilage in multiple joints throughout the body. It is a complex disorder associated with comorbidities such as depression, lymphoma, osteoporosis, and cardiovascular disease (CVD), which significantly deteriorate patients’ quality of life and prognosis. This has ignited a large initiative to elucidate the physiopathology of RA, aiming to identify new therapeutic targets and approaches in its multidisciplinary management. Recently, various lipid bioactive products have been proposed to have an essential role in this process, including eicosanoids, specialized pro-resolving mediators, phospholipids/sphingolipids, and endocannabinoids. Dietary interventions using omega-3 polyunsaturated fatty acids or treatment with synthetic endocannabinoid agonists have been shown to significantly ameliorate RA symptoms. Indeed, the modulation of lipid metabolism may be crucial in the pathophysiology and treatment of autoimmune diseases.

Adipose tissue (AT) biology is linked to cardiovascular health since obesity is associated with cardiovascular disease (CVD) and positively correlated with excessive visceral fat accumulation. AT signaling to myocardial cells through soluble factors known as adipokines, cardiokines, branched-chain amino acids and small molecules like microRNAs, undoubtedly influence myocardial cells and AT function via the endocrine-paracrine mechanisms of action. Unfortunately, abnormal total and visceral adiposity can alter this harmonious signaling network, resulting in tissue hypoxia and monocyte/macrophage adipose infiltration occurring alongside expanded intra-abdominal and epicardial fat depots seen in the human obese phenotype. These processes promote an abnormal adipocyte proteomic reprogramming, whereby these cells become a source of abnormal signals, affecting vascular and myocardial tissues, leading to meta-inflammation, atrial fibrillation, coronary artery disease, heart hypertrophy, heart failure and myocardial infarction. This review first discusses the pathophysiology and consequences of adipose tissue expansion, particularly their association with meta-inflammation and microbiota dysbiosis. We also explore the precise mechanisms involved in metabolic reprogramming in AT that represent plausible causative factors for CVD. Finally, we clarify how lifestyle changes could promote improvement in myocardiocyte function in the context of changes in AT proteomics and a better gut microbiome profile to develop effective, non-pharmacologic approaches to CVD.

Lifestyle modifications such as energy restriction and increased physical activity are highly effective in the management of obesity. However, adherence to these therapeutic approaches is poor. On the other hand, synthetic drugs used for obesity control are plagued by adverse effects. Despite these failures, adipose tissue is still an attractive therapeutic target for novel molecules, and thus, the characterisation of new and safer anti-obesity drugs is of significant interest. For this reason, in recent years, phenolic constituents of diverse plants have drawn much attention due to their health-promoting properties, opening new research lines related to brown adipose tissue activation and white adipose tissue (WAT) browning. The goal is to increase energy expenditure levels through thermogenic activity activation by multiple factors, like polyphenols. The suggested mechanisms by which polyphenols can modulate thermogenesis include Nor-epinephrine/Catechol-O-Methyl-Transferase (NE/COMT) inhibition, PPARγ co-activator alpha (PGC-1α)-dependent pathways activation, and mitochondrial biogenesis, among others. Although polyphenols such as quercetin, catechins, chrysin, luteolin, curcumin, resveratrol, gallic acid, and lignans have shown a positive effect on Non-Shivering Thermogenesis and WAT browning, most of them have only been active in murine models or in vitro systems, and their reproducibility in humans has to be proved. Probably in the future, an approach that includes these compounds as part of the nutritional regimen in conjunction with physical exercise, pharmacological and surgical therapy, would allow modulating a pathophysiological mechanism that is still elusive.

Introduction: Obesity is a complex, multifactorial, and mostly preventable disease affecting, along with overweight, more than a third of today’s world population. Variations in the nucleotide sequence of both metabolic and appetite control genes have been counted among these non-modifiable factors and are associated with BMI, lipidic profile, and abdominal circumference alterations. Methods: An analytical, non-experimental, and transversal research was done with the purpose to assess the presence of A54T polymorphism in the FABP gene in a sub-sample from the Maracaibo City Metabolic Syndrome Prevalence Study. Results: 154 individuals eight subjects were carriers of the A54Tpolymorphism, namely, a genotypic frequency of 5.19 %, with a sex distribution of 50 % for women (n=4) and 50 % (n=4) for men. In respect of alleles similarity degree, 75 % (n=6) were homozygous, and 25 % (n=2) were heterozygous. Obesity diagnosis throughout BMI was only present in 12.50 % (n=1) of the A54T carriers. Conversely, 25 % (n=2) of the carriers were overweighed; 50 % (n=4) were presented as normal-weight people; and only 12.50 % (n=1), in one underweighted person. Conclusion: As in many other studies, we do not find an association between Ala54Thr polymorphism and obesity. This result reinforces the fact of the multifactorial character of these diseases and a carrier state of this polymorphism is not necessarily to experience a higher obesity risk, at least, in our environment. La obesidad es una enfermedad compleja, multifactorial y en su mayor parte prevenible que afecta, a más de un tercio de la población mundial actual. Las variaciones en la secuencia de nucleótidos de los genes de control del metabolismo y del apetito se consideran hasta ahora como factores no modificables y se asocian con alteraciones del IMC, del perfil lipídico y de la circunferencia abdominal. Métodos: Se realizó una investigación analítica, no experimental y transversal con el propósito de evaluar la presencia del polimorfismo A54T en el gen FABP en una submuestra del Estudio de Prevalencia del Síndrome Metabólico de la Ciudad de Maracaibo. Resultados: De los 154 individuos de la submuestra ocho sujetos fueron portadores del polimorfismo A54T, es decir, una frecuencia genotípica de 5,19 %, con una distribución por sexo de 50 % para las mujeres (n=4) y 50 % (n=4) para los hombres. Con respecto al grado de similitud de los alelos, el 75 % (n=6) eran homocigotos y el 25 % (n=2) heterocigotos. El diagnóstico de obesidad a lo largo del IMC sólo estuvo presente en el 12,50 % (n=1) de los portadores de A54T. Por el contrario, el 25 % (n=2) de los portadores tenían sobrepeso; el 50 % (n=4) se presentaron como personas de peso normal; y sólo el 12,50 % (n=1) en la categoría de peso insuficiente. Conclusión: No se encontró una asociación entre el polimorfismo de Ala54Thr y la obesidad. Este resultado refuerza el carácter multifactorial de estas enfermedades y que un estado portador de este polimorfismo no es causa necesaria para padecer obesidad, al menos, en nuestro medio.

Non-alcoholic fatty liver disease (NAFLD) is considered the most common liver disorder, affecting around 25% of the population worldwide. It is a complex disease spectrum, closely linked with other conditions such as obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome, which may increase liver-related mortality. In light of this, numerous efforts have been carried out in recent years in order to clarify its pathogenesis and create new prevention strategies. Currently, the essential role of environmental pollutants in NAFLD development is recognized. Particularly, endocrine-disrupting chemicals (EDCs) have a notable influence. EDCs can be classified as natural (phytoestrogens, genistein, and coumestrol) or synthetic, and the latter ones can be further subdivided into industrial (dioxins, polychlorinated biphenyls, and alkylphenols), agricultural (pesticides, insecticides, herbicides, and fungicides), residential (phthalates, polybrominated biphenyls, and bisphenol A), and pharmaceutical (parabens). Several experimental models have proposed a mechanism involving this group of substances with the disruption of hepatic metabolism, which promotes NAFLD. These include an imbalance between lipid influx/efflux in the liver, mitochondrial dysfunction, liver inflammation, and epigenetic reprogramming. It can be concluded that exposure to EDCs might play a crucial role in NAFLD initiation and evolution. However, further investigations supporting these effects in humans are required.