Peroxisome proliferator-activated receptors are expressed in many tissues, including adipocytes, hepatocytes, muscles and endothelial cells; however, the affinity depends on the isoform of PPAR, and different distribution and expression profiles, which ultimately lead to different clinical outcomes. Because they play an important role in lipid and glucose homeostasis, they are called lipid and insulin sensors. Their actions are limited to specific tissue types and thus, reveal a characteristic influence on target cells. PPARα mainly influences fatty acid metabolism and its activation lowers lipid levels, while PPARγ is mostly involved in the regulation of the adipogenesis, energy balance, and lipid biosynthesis. PPARβ/δ participates in fatty acid oxidation, mostly in skeletal and cardiac muscles, but it also regulates blood glucose and cholesterol levels. Many natural and synthetic ligands influence the expression of these receptors. Synthetic ligands are widely used in the treatment of dyslipidemia (e.g. fibrates - PPARα activators) or in diabetes mellitus (e.g. thiazolidinediones - PPARγ agonists). New generation drugs - PPARα/γ dual agonists - reveal hypolipemic, hypotensive, antiatherogenic, anti-inflammatory and anticoagulant action while the overexpression of PPARβ/δ prevents the development of obesity and reduces lipid accumulation in cardiac cells, even during a high-fat diet. Precise data on the expression and function of natural PPAR agonists on glucose and lipid metabolism are still missing, mostly because the same ligand influences several receptors and a number of reports have provided conflicting results. To date, we know that PPARs have the capability to accommodate and bind a variety of natural and synthetic lipophilic acids, such as essential fatty acids, eicosanoids, phytanic acid and palmitoylethanolamide. A current understanding of the effects of PPARs, their molecular mechanisms and the role of these receptors in nutrition and therapeutic treatment are delineated in this paper.
The presence of antinuclear antibodies (ANA) is mainly associated with connective tissue diseases (CTD). In addition, their presence is found in healthy people. These antibodies are more common in women and the elderly. Some drugs and xenobiotics are also important for the development of autoimmunity and ANA synthesis. Moreover, the deficiency of vitamin D in the body of patients correlates with occurrence of these antibodies. Unlike the healthy group, a positive ANA count was observed in patients with atopic dermatitis (AD) and in people with immune disorders. Antinuclear antibodies in low counts are also found in the course of chronic bacterial or viral infection and in patients with hematological malignancies. Also the possibility of false positive results, which may be caused by the choice of method used to determine antibodies, should be borne in mind. Taking into account all these factors, it is concluded that the ANA result itself has no diagnostic value.
Systemic sclerosis (SSc) is an autoimmune connective tissue disorder of unknown etiology. This disease is characterized by a large variety of clinical patterns, which include the fibrosis of skin and visceral organs causing a variety of clinical manifestations. Genetic and environmental factors participate in the etiology of this disease; however, recently many studies underline the oxidative background influencing the course and complications of this disease. Reactive oxygen species (ROS) synthesized in SSc can mediate extra- and intracellular oxidative processes affecting endothelial cells and fibroblasts. The estimation of prooxidative markers in the pathogenesis of SSc can enable the identification of useful markers for disease activity and, thus, may help in planning appropriate therapy focusing on the fibrotic or vascular pattern. Recently, many attempts have been made to find antioxidative molecules (nutritional and pharmacological) reducing the prooxidant state in a variety of cells—mainly in endothelium and proliferating fibroblasts. This paper presents both the background of oxidative stress processes in systemic sclerosis mediated by different mechanisms and the evidence suggesting which of the dietary and pharmacological antioxidants can be used as therapeutic targets for this disease.
Major advances in the understanding and treatment of GPA over recent decades have contributed to the notable decline in morbidity and mortality of patients. The ultimate goal is an improved prognosis through outcome measures which assesses the disease control with minimal adverse effects of intensive immunosuppressive regimens, an integral part of the clinical approach to improve the quality of life of GPA patients.
Nutritional habits and physical activity influence the health status of young adults. In this study, we engaged a group of 151 students from a medical university (90 female and 61 male subjects). Anthropometric parameters, dietary habits (a 7-day dietary recall), and level of physical activity were measured. It was found that the daily food rations of female (F) and male (M) students were improperly balanced and characterized by high amount of total and animal protein, phosphorus, vitamin A, cholesterol, and insufficient intake of carbohydrates, dietary fiber, and vitamin C. Female subjects consumed low amounts of total fat and calcium. The intake of protein (total and animal), fat, phosphorus, and cholesterol correlated with higher body mass. The physical activity of the students was found to be higher than the average physical activity of the European Union populations, and a general tendency of lowering level of physical activity with age was observed. Students with the highest level of physical activity (MET > 1500) consumed lower amounts of simple carbohydrates (galactose and saccharose) when compared to students with lower physical activity (MET < 600, p < 0.05). Therefore, this study concluded that the dietary habits should be modified to prevent the development of diet-dependent diseases. Various forms of physical activity should be proposed to students and they should be encouraged to participate in high level of physical activity so as to promote good health status.
The aim of this study was to assess the nutritional status and dietary habits among female adolescents. Four hundred seventy nine subjects aged from 17 to 18 years, from secondary schools of the Great Poland Region participated in the study. Anthropometric parameter measurements included those of body height and mass, skinfold thickness and circumferences of waist, hip and arm. The measurements served to calculate the percentage of fat mass and arm muscle area. Nutritional questionnaires were used to estimate the frequency and intake of selected food products. Mean values of body height and mass were approximately in the 50 th percentile. However, 13.7% of females were underweight, 7.7% were overweight and 1.2% were obese. Cluster analysis resulted in 3 clusters, of which the second one showed the most detrimental nutritional habits. This cluster was characterised by the lowest intake of dairy products, fruits and vegetables, fish, meat and also by frequent long breaks between meals (longer than 5 hours). Improper nutritional behavior is a frequent finding in female adolescents, in Poland. Nevertheless, overweight and obesity are not more common than in other countries. Studies in this area should be continued and extended.
Research in the past two decades has revolutionized our understanding of depressive illnesses. Proinflammatory cytokines have become a point of interest in the interconnecting areas of neuropsychiatric and autoimmune diseases. The cytokine hypothesis of depression suggests that pro‐inflammatory cytokines play a primary role in the mediation of the pathophysiological characteristics of major depression, in which an inflammatory process may be induced by external and internal stressors, such as psychological and inflammatory diseases, respectively. The higher prevalence of depression, particularly in patients with chronic autoimmune connective tissue disorders (CTD), suggests that depression may present a dysfunctional adaptation of cytokine‐induced sickness, which could manifest in times of an exacerbated activation of the innate immune system. Inflammation is thought to contribute to the development of clinical depression through its ability to induce sickness behaviors corresponding to the neurovegetative features of depression, through the dysregulation of the hypothalamic–pituitary–adrenal axis, alterations in neurotransmitter synthesis and reuptake, and through its involvement in the neuroprogression pathways. This review explores the complex interrelationships in which inflammatory responses alter neuroendocrine and neuropsychological regulation contributing to depressive symptoms in CTD. The prevalence and characteristics of depression, and its correlation to the levels of inflammatory cytokines and disease activity among different CTD will be reviewed.
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