Leptin and its receptor gene polymorphism as a target for pharmacotherapy in T2DM and COPD

Abstract

Combined pathology is a real problem for rational pharmacotherapy due to multiple organ damage. The need to affect simultaneously several pathogenesis processes leads to polypharmacy that can appear to be less effective, toxic and unacceptable in some time. For comorbid patients with long - term ongoing type 2 diabetes mellitus (T2DM), the problem of drug interactions is as relevant as the selection of optimal hypoglycemic therapy. This review aims to identify opportunities to optimize drug therapy in comorbid pathology to increase the effectiveness of pharmacotherapy, improve the prognosis and outcomes of concomitant diseases, and slow the progression of one or a combination of diseases. One of the ways to individualize pharmacotherapy is to identify polymorphic genes that can account not only to the predisposition to the disease, but also to the formation of a pharmacological response, thus determining the effectiveness of drug therapy. A peptide hormone leptin along with its receptors in various tissues could be the milestone of unifying pathology that contributes both to the development of diseases - chronic obstructive pulmonary disease (COPD) and T2DM. This modality potentially forms the pharmacological response to prescribed drug therapy of such. Gene polymorphism determines the development of pathologies such as leptin and insulin resistance. These deteriorations are in turn likely to be the targets of many oral antidiabetic drugs. The review suggests potential associations and directions for research in the field of pharmacogenetics of drugs used for the treatment of comorbid patients. The duly identified mutations involved in the general pathogenesis of type 2 diabetes and COPD will account to the approach toward tailored medicine and contribute to proper control of both diseases.