Metabolic syndrome (MS) is a chronic non‐infective syndrome characterised clinically by a set of vascular risk factors that include insulin resistance, hypertension, abdominal obesity, impaired glucose metabolism, and dyslipidaemia. These risk factors are due to a pro‐inflammatory state, oxidative stress, haemodynamic dysfunction, and ischaemia, which overlap in ‘dysmetabolic’ patients. This review aimed to evaluate the relationship between the traditional components of MS with cardiovascular disease (CVD), inflammation, and oxidative stress. MEDLINE‐PubMed, EMBASE, and Cochrane databases were searched. Chronic low‐grade inflammatory states and metaflammation are often accompanied by metabolic changes directly related to CVD incidence, such as diabetes mellitus, hypertension, and obesity. Moreover, the metaflammation is characterised by an increase in the serum concentration of pro‐inflammatory cytokines, mainly interleukin‐1 β (IL‐1β), IL‐6, and tumour necrosis factor‐α (TNF‐α), originating from the chronically inflamed adipose tissue and associated with oxidative stress. The increase of reactive oxygen species overloads the antioxidant systems causing post‐translational alterations of proteins, lipids, and DNA leading to oxidative stress. Hyperglycaemia contributes to the increase in oxidative stress and the production of advanced glycosylation end products (AGEs) which are related to cellular and molecular dysfunction. Oxidative stress and inflammation are associated with cellular senescence and CVD. CVD should not be seen only as being triggered by classical MS risk factors. Atherosclerosis is a multifactorial pathological process with several triggering and aetiopathogenic mechanisms. Its medium and long‐term repercussions, however, invariably constitute a significant cause of morbidity and mortality. Implementing preventive and therapeutic measures against oxy‐reductive imbalances and metaflammation states has unquestionable potential for favourable clinical outcomes in cardiovascular medicine.

Skeletal muscle is capable of secreting different factors in order to communicate with other tissues. These mediators, the myokines, show potentially far-reaching effects on non-muscle tissues and can provide a molecular interaction between muscle and body physiology. Sarcopenia is a chronic degenerative neuromuscular disease closely related to cardiomyopathy and chronic heart failure, which influences the production and release of myokines. Our objective was to explore the relationship between myokines, sarcopenia, and cardiovascular diseases (CVD). The autocrine, paracrine, and endocrine actions of myokines include regulation of energy expenditure, insulin sensitivity, lipolysis, free fatty acid oxidation, adipocyte browning, glycogenolysis, glycogenesis, and general metabolism. A sedentary lifestyle accelerates the aging process and is a risk factor for developing sarcopenia, metabolic syndrome, and CVD. Increased adipose tissue resulting from the decrease in muscle mass in patients with sarcopenia may also be involved in the pathology of CVD. Myokines are protagonists in the complex condition of sarcopenia, which is associated with adverse clinical outcomes in patients with CVD. The discovery of new pathways and the link between myokines and CVD remain a cornerstone toward multifaceted interventions and perhaps the minimization of the damage resulting from muscle loss induced by factors such as atherosclerosis.

BackgroundThe genus Arachis comprises 80 species and it is subdivided into nine taxonomic sections (Arachis, Caulorrhizae, Erectoides, Extranervosae, Heteranthae, Procumbentes, Rhizomatosae, Trierectoides, and Triseminatae). This genus is naturally confined to South America and most of its species are native to Brazil. In order to provide a better understanding of the evolution of the genus, we reconstructed the phylogeny of 45 species using the variation observed on nucleotide sequences in internal transcribed spacer regions (ITS1 and ITS2) and 5.8 S of nuclear ribosomal DNA.ResultsIntraspecific variation was detected, but in general it was not enough to place accessions of the same species in different clades. Our data support the view that Arachis is a monophyletic group and suggested Heteranthae as the most primitive section of genus Arachis. The results confirmed the circumscriptions of some sections (Caulorrhizae, Extranervosae), but raised questions about others. Sections Erectoides, Trierectoides and Procumbentes were not well defined, while sections Arachis and Rhizomatosae seem to include species that could be moved to different sections. The division of section Arachis into A and B genome species was also observed in the phylogenetic tree and these two groups of species may not have a monophyletic origin. The 2n = 2x = 18 species of section Arachis (A. praecox, A. palustris and A. decora) were all placed in the same clade, indicating they are closely related to each other, and their genomes are more related to B genome than to the A genome. Data also allowed insights on the origin of tetraploid A. glabrata, suggesting rhizome appeared twice within the genus and raising questions about the placement of that species in section Rhizomatosae.ConclusionThe main clades established in this study in general agreed with many other studies that have used other types of evidences and sets of species, being some of them included in our study and some not. Thus, the relationships established can be a useful framework for future systematic reviews of genus Arachis and for the selection of species to pre-breeding programs.

Populations all over the world are increasingly inactive and are consuming increasing quantities of fats and sugars, which is generally linked to industrially processed foods. The consequences have rapidly manifest as an increase in overweight/obesity and in physiological and metabolic changes, such as the Metabolic Syndrome, which is a series of changes in glycemia, lipids and blood pressure. There is evidence of a close relationship between these changes and inflammatory processes, which can also be linked to oxidative stress. These conditions lead to the pathogenesis of vascular abnormalities or intensify metabolic processes that accompany the metabolic syndrome. The objective of this review is to compare the large number of bibliographic references that show correlations between components of the Metabolic Syndrome and increases in the mediators of inflammation. The publications reviewed were located using the Pubmed, Scopus, Lilacs and Scielo databases and the majority of the articles selected were published within the last 5 years.Keywords: metabolic syndrome ; arteriosclerosis; inflammation. ResumoObserva-se, nas populações mundiais, aumento do sedentarismo e aumento do consumo de gorduras e açúcares, sendo estes vinculados normalmente aos alimentos industrializados. A consequência disso rapidamente se manifestou no aumento do sobrepeso/obesidade e na instalação de alterações fisiológicas e metabólicas, como a Síndrome Metabólica, que é representada por alterações na glicemia, nos lipídeos e na pressão arterial. Há evidências de ligação estreita entre estas alterações e os processos inflamatórios, que também podem estar associados ao estresse oxidativo. Estas condições levam à patogênese das alterações vasculares ou intensificam os processos metabólicos que acompanham a Síndrome Metabólica. O objetivo desta revisão foi comparar as inúmeras referências literárias que mostram correlação entre os componentes da Síndrome Metabólica e o aumento dos mediadores de inflamação. Para isso, utilizou-se Pubmed, Scopus, Lilacs e Scielo como base de dados, sendo que os artigos selecionados dataram principalmente dos últimos cinco anos.Palavras-chave: síndrome metabólica; arteriosclerose; inflamação.

Our study aimed to associate IL-1β and IL-1RN polymorphisms with AD disease in comparison with elderly control group from São Paulo - Brazil. We genotyped 199 Alzheimer's disease (AD) patients, 165 elderly control and 122 young control samples, concerning VNTR (IL-1RN) and -511C>T and -31T>C (IL-1β) polymorphisms. Our findings revealed that -511C/-31T/2-repetitions VNTR haplotype had a protective effect for AD when compared to EC (p=0.005), whereas -511C/-31C/1-repetition VNTR haplotype was associated as a risk factor for AD (p=0.021). Taken together, we may suggest that there is a relevant role of IL-1 genes cluster in AD pathogenesis in this Brazilian population.

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This work reports the characterization of 11 polymorphic microsatellite loci in section Caulorrhizae. The primer pairs were designed from Arachis pintoi and showed full transferability to Arachis repens species. These new markers were used to evaluate the genetic diversity in germplasm (accessions and cultivars) of section Caulorrhizae. This new set of markers detected greater gene diversity than morphological and molecular markers such as AFLP (amplified fragment length polymorphism) and RAPD (rapid analysis of polymorphic DNA) previously used in this germplasm.

Non-alcoholic steatohepatitis (NASH) is characterized by steatosis, lobular inflammation, and enlargement of the diameter of hepatocytes (ballooning hepatocytes), with or without fibrosis. It affects 20% of patients with non-alcoholic fatty liver disease (NAFLD). Due to liver dysfunction and the numerous metabolic changes that commonly accompany the condition (obesity, insulin resistance, type 2 diabetes, and metabolic syndrome), the secretion of organokines is modified, which may contribute to the pathogenesis or progression of the disease. In this sense, this study aimed to perform a review of the role of organokines in NASH. Thus, by combining descriptors such as NASH, organokines, oxidative stress, inflammation, insulin resistance, and dyslipidemia, a search was carried out in the EMBASE, MEDLINE-PubMed, and Cochrane databases of articles published in the last ten years. Insulin resistance, inflammation and mitochondrial dysfunction, fructose, and intestinal microbiota were factors identified as participating in the genesis and progression of NASH. Changes in the pattern of organokines secretion (adipokines, myokines, hepatokines, and osteokines) directly or indirectly contribute to aggravating the condition or compromise homeostasis. Thus, further studies involving skeletal muscle, adipose, bone, and liver tissue as endocrine organs are essential to better understand the modulation of organokines involved in the pathogenesis of NASH to advance in the treatment of this disease.