CELEBRANDO 20 ANOS DA REVISTA CONTEXTO & SAÚDE

Nesta edição, publicada no último trimestre de 2021, a Revista Contexto & Saúde (RCS) comemora seus 20 anos de divulgação científica com 31 artigos publicados em uma edição extra. Temos a satisfação de celebrar a data, oportunizando a publicação dos artigos de autores de 11 diferentes estados brasileiros, divulgando o conhecimento produzido em 35 instituições de ensino. Assim, mantendo a RCS ativa e em evolução, comemoramos o aniversário da revista com a certeza do reconhecimento em abrangência nacional, e iniciando uma caminhada na internacionalização, mas fundamentalmente agradecendo aos autores e revisores que atuaram nestas duas décadas em prol da educação e da divulgação científica, assim como agradecemos e equipe técnica da editora Unijuí pelo empenho e dedicação nos processos editoriais. Destacamos também, o intenso trabalho dos professores da Unijuí, pesquisadores do Programa de Pós-Graduação em Atenção Integral à Saúde, pela atuação como editores das seções (áreas) da RCS, sendo responsável pelo fluxo avaliativo responsável de mais de 300 artigos submetidos por ano

Oxidative Stress in Type 2 Diabetes and The Impact of Exercise: from mitochondria to glucose management in skeletal muscle

Oxidative stress is the result of reactive oxygen species (ROS) overproduction and/or a decline in antioxidant defense mechanisms. Oxidative stress can be marked by deleterious effects on DNA, proteins, and lipids structure, changing cell homeostasis, and contributing to the development of metabolic diseases as type two diabetes (T2D), characterized mainly by insulin resistance in several tissues, as skeletal muscle.  The T2D development and its complications are related to mitochondrial dysfunction and oxidative stress, as well as pro-inflammatory state and metabolic unbalance. Acute exercise represents a necessary type of challenge to whole-body homeostasis. Therefore, regular exercise (sum of acute exercise challenges) promotes antioxidant, anti-inflammatory, and metabolic adaptations induced by each stress induced by the exercise session, evoking a hormesis effect (from mitochondria to many tissues) that is beneficial for T2D prevention and treatment. Despite of a considerable research information in the field, the characterization of the sources and pathways of ROS generation in T2D and during exercise still a matter for investigation. Therefore, the multifaceted effects of oxidative stress in T2D and the link of exercise in T2D are discussed in this review

Fine Particulate Matter (PM2.5) Air Pollution and Type 2 Diabetes Mellitus (T2DM): When Experimental Data Explains Epidemiological Facts

Epidemiologic and experimental studies suggest that environmental exposures to air pollutants can increase prevalence of metabolic and cardiorespiratory diseases. Among the risk factors, many studies have shown that air pollution, especially by fine particulate matter (PM2.5), can lead to the development of type 2 diabetes mellitus (T2DM) or make diabetics more susceptible to other health complications. This chapter aimed to discuss the pathophysiologic mechanisms evolved in susceptibility to cardiorespiratory PM2.5 effects in T2DM subjects, as well as the enhancing effect of PM2.5 exposure on development of T2DM. We discussed the pathophysiologic mechanisms of PM2.5 exposure and T2DM based on pro−/anti-inflammatory balance, metabolic regulation, redox status, and heat shock response, reinforcing the complex nature of T2DM etiology and highlighting the PM2.5 air pollution as a critical health problem

Lifestyle and Aging Effects in the Development of Insulin Resistance — Activating the Muscle as Strategy Against Insulin Resistance by Modulating Cytokines and HSP70

This chapter discusses about subclinical processes related to insulin resistance development that worsen the muscle metabolic functions, generated by factors such as lifestyle (bad quality food intake and sedentary behavior) and aging. Also discussed are the effects of regular physical exercise as a strategy to prevent the metabolic impairment in organisms, approaching since muscle subclinical molecular processes to the whole body’s integrative physiology. Insulin resistance development includes modification in the pattern of inflammatory cytokines, heat shock proteins, tissue- specific defects in insulin action and signaling, oxidative stress and ectopic lipid deposition. The exercise is a known modulator of all parameters listed above and has important role in the regulation of “immune-metabolic” homeostasis from the muscle to the whole body. This chapter aims to present a new molecular approach related to the control of metabolism and encourage scientists and students to propose new strategies against insulin resistance and diabetes type 2 developments

Are heat shock proteins an important link between type 2 diabetes and Alzheimer disease?

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. Type 2 diabetes (T2D) and Alzheimer’s disease (AD) are growing in prevalence worldwide. The development of T2D increases the risk of AD disease, while AD patients can show glucose imbalance due to an increased insulin resistance. T2D and AD share similar pathological features and underlying mechanisms, including the deposition of amyloidogenic peptides in pancreatic islets (i.e., islet amyloid polypeptide; IAPP) and brain (β-Amyloid; Aβ). Both IAPP and Aβ can undergo misfolding and aggregation and accumulate in the extracellular space of their respective tissues of origin. As a main response to protein misfolding, there is evidence of the role of heat shock proteins (HSPs) in moderating T2D and AD. HSPs play a pivotal role in cell homeostasis by providing cytoprotection during acute and chronic metabolic stresses. In T2D and AD, intracellular HSP (iHSP) levels are reduced, potentially due to the ability of the cell to export HSPs to the extracellular space (eHSP). The increase in eHSPs can contribute to oxidative damage and is associated with various pro-inflammatory pathways in T2D and AD. Here, we review the role of HSP in moderating T2D and AD, as well as propose that these chaperone proteins are an important link in the relationship between T2D and AD

Suppressed anti-inflammatory heat shock response in high-risk COVID-19 patients : lessons from basic research (inclusive bats), light on conceivable therapies

The major risk factors to fatal outcome in COVID-19 patients, i.e., elderliness and pre-existing metabolic and cardiovascular diseases (CVD), share in common the characteristic of being chronic degenerative diseases of inflammatory nature associated with defective heat shock response (HSR). The molecular components of the HSR, the principal metabolic pathway leading to the physiological resolution of inflammation, is an anti-inflammatory biochemical pathway that involves molecular chaperones of the heat shock protein (HSP) family during homeostasis-threatening stressful situations (e.g., thermal, oxidative and metabolic stresses). The entry of SARS coronaviruses in target cells, on the other hand, aggravates the already-jeopardized HSR of this specific group of patients. In addition, cellular counterattack against virus involves interferon (IFN)-mediated inflammatory responses. Therefore, individuals with impaired HSR cannot resolve virus-induced inflammatory burst physiologically, being susceptible to exacerbated forms of inflammation, which leads to a fatal “cytokine storm”. Interestingly, some species of bats that are natural reservoirs of zoonotic viruses, including SARS-CoV-2, possess an IFN-based antiviral inflammatory response perpetually activated but do not show any sign of disease or cytokine storm. This is possible because bats present a constitutive HSR that is by far (hundreds of times) more intense and rapid than that of human, being associated with a high core temperature. Similarly in humans, fever is a physiological inducer of HSR while antipyretics, which block the initial phase of inflammation, impair the resolution phase of inflammation through the HSR. These findings offer a rationale for the reevaluation of patient care and fever reduction in SARS, including COVID-19

Environmental Particulate Air Pollution Exposure and the Oxidative Stress Responses: A Brief Review of the Impact on the Organism and Animal Models of Research

Particulate matter (PM) is a mixture of solid particles and liquid droplets found in the air, and it is one of the most harmful air pollutants. When inhaled, it affects the pulmonary system, cardiovascular systems, and other tissues. The size, composition, and deposition of PM, mainly related to fine and ultrafine particulate matter, are factors that determine the harmful effects of exposure to particles. Among the main effects is the inducer of ROS production, and consequently oxidative tissue damage in target organs and other responses, mediated by inflammatory cytokines and cellular stress response. The main pathway through which particles are potent mediators of oxidative stress is the damage caused to DNA and lipid molecules, whereas the pro-inflammatory response involves an immune response against PM, which in turn, it is related to cell stress responses observed by heat shock proteins (HSPs) expression and release. Thus, the ability of an organism to respond to PM inhalation requires anti-oxidative, anti-inflammatory, and cellular stress defenses that can be impaired in susceptible subjects as people with chronic diseases as diabetes and obesity. In this chapter, we discuss the mechanistic aspects of PM effects on health and present some animal research models in particle inhalation studies

Effects of Physical Activity on The Inflammatory Process Related to Insulin Resistance and Obesity

Atherosclerosis, the pathophysiological substrate for cardiovascular disease (CVD), is the final stage of an inflammatory cascade. During the process, endothelial dysfunction ensues and the inflammatory state is perpetuated. A number of traditional risk factors, as obesity and insulin resistance/type 2 diabetes, are characterized by a proinflammatory state as well, with increased levels of cytokines, interleukins, vasoactive peptides and enhanced expression of specific cellular receptors. The anti-inflammatory properties of physical exercise and its positive effects as a strategy for obesity and insulin resistance have already been shown in terms of cardiovascular protection and survival

Diet and Inflammation: Effects of Macronutrients and Dietary Patterns

Cardiovascular disease (CVD) has already been demonstrated to be related to a chronic and complex inflammatory process, in which the loss of endothelial protective properties - the so-called endothelial dysfunction - plays a central role. A number of different approaches, both pharmacological and non-pharmacological, have been tested with inconclusive results so far. One field of special interest is the impact of the different macronutrients and dietary patterns in the inflammatory response that, ultimately, leads to endothelial dysfunction and increased cardio-metabolic risk. Although apparently simple, interventions regarding dietary habits have complex implications and involve a number of covariates that may interfere in the final results. To date, results about the protective effects of diet - in general - regarding cardio-metabolic risk remain to be fully proven