Adipose tissue is also a secretory organ producing active substances called adipokines. Some of them (apelin, resistin, adiponectin, leptin, chemerin, or visfatin) may play a role in the pathogenesis and course of respiratory diseases, e.g. COPD, asthma, pulmonary hypertension, or lung cancer. There are limited and conflicting data on the role of adipokines in asthma. It has been confirmed, however, that visfatin and leptin can be markers of inflammation in COPD. Elevated concentrations of leptin and resistin play a pro-inflammatory role in the development of cancer cachexia. The role of adipokines has also been demonstrated in pulmonary hypertension, and the apelinadiponectin axis disruption may exacerbate pulmonary hypertension.
Type 1 diabetes is based on apoptosis, which leads to b-cell death. Factors triggering apoptosis processes are very diverse and currently not fully explained. The main role is attributed to genetic and environmental factors. Genetic studies have shown that the inherited propensity for type 1 diabetes is multi-genetic. Environmental factors modify the response to their own antigens, but are probably not necessary to start the autoaggression process. The effect of b-cell destruction is confirmed by the appearance of autoantibodies in the blood. The paper presents a review of the available literature regarding the self-destruction of pancreatic b-cells. The aim of the study was to draw attention to the extremely complicated and still unknown etiopathogenesis of type 1 diabetes by reviewing current literature related to the above topic. The goal is to acquire the knowledge necessary to develop and implement causal treatment for diabetes. At the moment, unfortunately, we do not have safe, innovative therapy methods in the field of diabetes prevention. Intensive research on the etiopathogenesis of type 1 diabetes is an extremely important field of medical research.
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