Abstract
Obesity, one of the most severe public health problems of the 21st century, is a common metabolic syndrome due to excess body fat. The incidence and severity of obesity-related asthma have undergone a dramatic increase. Because obesity-related asthma is poorly controlled using conventional therapies, alternative and complementary therapies are urgently needed. Lipid metabolism may be abnormal in obesity-related asthma, and immune modulation therapies need to be investigated. Herein, we describe the immune regulators of lipid metabolism in obesity as well as the interplay of obesity and asthma. These lay the foundations for targeted therapies in terms of direct and indirect immune regulators of lipid metabolism, which ultimately help provide effective control of obesity-related asthma with a feasible treatment strategy.
Highlights
Obesity is defined as an excess of body fat, and it is one of the main public health challenges worldwide
SREBP1a might modulate the innate immune responses of macrophages, whereas SREBP2 is associated with cell phagocytosis and autophagy, indicating the significant role of Sterol regulatory element-binding proteins (SREBPs) in the onset and development of chronic inflammatory diseases such as obesity [18,19,20]. These findings suggest that targeting SREBPs may be clinically feasible and promising in the treatment of obesity
Recent studies showed that another Dipeptidyl peptidase-4 (DPP-4) inhibitor, anagliptin, could significantly decrease the expression level of SREBP2 messenger ribonucleic acid, which significantly decreased the plasma total cholesterol and triglyceride levels in anagliptintreated mice
Summary
Obesity is defined as an excess of body fat, and it is one of the main public health challenges worldwide. It increases the risk for certain diseases and disorders, including type 2 diabetes, hypertension, chronic kidney disease, cardiovascular diseases, certain types of cancer, and depression [1]. Asthma is a chronic inflammatory disease characterized by variable symptoms of wheezing, shortness of breath, chest tightness, and/or cough and by variable expiratory airflow limitation. We detail the roles of immune responses in lipid metabolism and the pathogenesis of obesity-related asthma. We propose various potential targeted therapies according to distinct cellular types and proteins involved in the regulation of lipid metabolism in obesity-related asthma
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