Chapters authored
Role of Heat Shock Proteins in Skeletal Muscle
Part of the book: Skeletal Muscle
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.
Part of the book: Muscle Cell and Tissue
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.
Part of the book: Diabetes and Its Complications
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.
Part of the book: Reactive Oxygen Species