Asthma and obesity are serious medical and social world problems, and their combined course is characterized by a decrease in the quality of life, an increase in the frequency and duration of hospitalization. The present review summarizes the current views on the mechanisms of formation of asthma phenotype combined with obesity, role of leptin and adiponectin imbalance in the development of systemic inflammation in obesity in the pathophysiology of asthma, its interrelations with metabolic syndrome. We present data that shows that syndrome is closely related not only to the debut of asthma, but also to a decrease in its control. Along with obesity, the role of other components of metabolic syndrome, in particular insulin resistance, as a predictor of asthma development is considered. Insulin resistance may be the most likely factor in the relationship between asthma and obesity, independent of other components of the metabolic syndrome. Insulin resistance associated with obesity can lead to disruption of nitric oxide synthesis. We reveal common mechanism of metabolic disorders of nitric oxide and arginine in metabolic syndrome and asthma and show that insulin resistance treatment can be therapeutically useful in patients with asthma in combination with obesity.
Bronchial asthma (BA) and obesity are one of the major modern problem, requiring the development of an effective therapeutic strategy. The frequent combination of these diseases in one patient indicates the general pathophysiological mechanisms and future study for targeted drug exposure are needed. The endocannabinoid system is involved in a variety of physiological and pathological processes and can be considered as a general mechanism and a potential therapeutic target in asthma and obesity, the receptors of the system are expressed in many central and peripheral tissues. This signal system modulates the functions of the autonomic nervous system, immune system and microcirculation, plays an important role in the regulation of energy balance, metabolism of carbohydrates and lipids. The main research aimed at studying the functioning of this system was focused on neurology and psychiatry, while numerous scientific data demonstrate the importance of the participation of this system in the pathogenesis of other diseases. In particular, this system is involved in the mechanisms of obesity. The role of the endocannabinoid system in the pathogenesis of asthma is actively studied. The wide prevalence of the endocannabinoid signaling system and its regulatory role in the body opens up prospects for therapeutic effects in the treatment of asthma and obesity, as well as the possible phenotype of asthma, combined with obesity. The review is devoted to modern ideas about endocannabinoids, their receptors, mechanisms of action and their role in the pathophysiology of asthma and obesity. The therapeutic prospects and difficulties associated with the use of endocannabinoids and phytocannabinoids in medicine are discussed.
Obesity is a complex and relevant global medical and social problem. The adipose tissue is not only a place of deposition of energy substrates but also a source of secretion of pro-inflammatory and anti-inflammatory mediators involved in the development of the chronic latent systemic inflammatory process in the organism with obesity. The metabolic signal in obesity contributes to the polarization of macrophages in the M1 direction and triggers the Th1 immune response, causing the development of adipose tissue inflammation. A chronic inflammatory condition plays a key role in the pathophysiology of obesity-induced insulin resistance. Toll-like receptors (TLRs) may be a possible pathophysiological link in the development of insulin resistance in inflammation. At the same time, inflammation-induced lipolysis is necessary for the release of energy resources during the development of the infectious process. Thus, low-grade inflammation is important to protect against adipocyte dysfunction. These results suggest that pro-inflammatory signaling is not exclusively pathogenic in obesity. In this regard, the study of inflammatory signaling pathways involved in the modulation of chronic inflammation of adipose tissue is particularly relevant. This review summarizes current views on the structure, function of TLRs and their involvement in the pathogenesis of chronic inflammation in obesity. The possibility of using TLRs as a therapeutic target in this pathology is discussed. Obviously, further study of inflammatory signaling pathways involving TLRs initiating the development of chronic inflammation of adipose tissue will allow the development of new and effective therapeutic strategies for obesity and its metabolic complications.
The combined course of bronchial asthma (BA) and obesity is one of the urgent medical and social problems that requires a comprehensive and careful study in connection with a decrease in the quality of life of such patients, an increase in the frequency, duration of hospitalization and a high economic burden for the state as a whole. The relationship between BA and obesity is now confirmed by numerous studies, at the same time, despite the variability of the proposed mechanisms of pathogenetic effects of obesity on asthma, metabolic aspects of the relationship of these diseases need further study. Adipose tissue hormones are responsible for the energy homeostasis of the body therefore, excessive accumulation of adipose tissue is accompanied by the development of an imbalance in metabolic processes in various organs and tissues. Due to the emergence of new scientific data on the role and function of adipokines in the body, metabolic effects of adipokines are considered in the focus of their pathophysiological association with obesity and asthma. This literary review highlights the current understanding of the role of metabolic effects of the most studied adipokines (resistin, retinol-binding protein, leptin and adiponectin) in the development of obesity and BA. Gender and age-dependent features of adipokine levels in BA and obesity are described. Data on the confirmed role of adiponectin and leptin in the progression of BA combined with obesity are presented. It has been shown that the role of resistin and retinol-binding protein in the development of BA combined with obesity has not been studied. It is demonstrated that further study of metabolic activity of adipokines in BA is an actual and perspective direction of researches which will allow to develop new diagnostic and therapeutic strategies in patients with BA with obesity.
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