Čes. slov. farm. 2014, 63(4):152-159 | DOI: 10.36290/csf.2014.031
Metabolic syndrome - dysregulation of adipose tissue endocrine function
- 1 Ústav humánní farmakologie a toxikologie FaF, Veterinární a Farmaceutická Univerzita, Brno, ČR
- 2 Lékařská fakulta MU, Farmakologický ústav, Brno
- 3 Masarykova Univerzita, CEITEC - Středoevropský technologický institut, Brno, ČR
Metabolic syndrome, acondition increasing cardiovascular morbidity, mortality and risk for diabetes mellitus type 2, is currently worldwide reaching epidemic proportions. This complex disorder represents an urgent challenge for new pharmacotherapeutic strategies formulation. Pathophysiological mechanisms underlying metabolic syndrome are not completely understood, nevertheless growing evidence is supporting the hypothesis that multiple metabolic dysregulations do contribute to its development. Apotential target for pharmacological intervention is considered to be dysregulation of adipose tissue endocrine/paracrine function. Specific adipokines, proteins secreted by the adipose tissue, with some pleiotropic effects, have been identified with strong association to regulation of energy metabolism, appetite, insulin signaling, tissue insulin sensitivity and the proinflammatory state related to metabolic syndrome. The aim of this paper is to provide abrief overview of endocrine/paracrine functions of the adipose tissue with regard to metabolic syndrome development and pathophysiology and particular adipokines as potential targets for innovative pharmacotherapeutic approaches.
Keywords: metabolic syndrome; insulin resistance; adipose tissue; adipokines
Grants and funding:
This work was supported by: Project Internal Grant Agency (IGA) VFU Brno (48/2014/FaF), Project Internal Agency for Education (IVA) VFU Brno (2014FaF/3140/071), Project of specific research at the Masaryk University (MUNI/A/0886/2013) and Project "CEITEC - Central European Institute of Technology" (CZ.1.05/1.1.00/02.0068) from European Regional Development Fund.
Received: June 4, 2014; Accepted: July 4, 2014; Published: April 1, 2014 Show citation
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