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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

New Approach in The Treatment of T2DM and Metabolic Syndrome (Focus on a Novel Insulin Sensitizer).

Peroxisome Proliferator-Activate Receptors (PPARs) are transcription factors belonging to the nuclear receptor superfamily. The three PPARs (a, b/d, and g) are distributed differently in the different organs. PPARa is most common in the liver, but also found in kidney, gut, skeletal muscle and adipose tissue, while PPARb/d, is fairly ubiquitous; it may be found in body tissues and brain (for myelination process and lipid metabolism in the brain). PPARg has 3 isoforms, such as PPARg 1, PPARg 2, and PPARg 3. The syndrome-X was firstly coined by Reaven in 1988 and then to be provided in 1999 by the name : the metabolic syndrome-X.1 This metabolic syndrome represents a "Cluster" of metabolic disorders and cardiovascular risk factors which has been collected and summarized by the author and such a cluster includes: insulin resistance/hyperinsulinemia, central obesity, glucose intolerance/DM, atherogenic dyslipidemia (hTG, iHDL-cholesterol,hApo-B, hsmall dense LDL), hypertension, prothrombotic state (hPAI-1, hF-VII, hfibrinogen, hvWF, hadhesion molecules), endothelial dysfunction, hyperuricemia, and increased hsC-RP and cytokines. The metabolic syndrome-X may lead to the development of T2DM and coronary heart disease (CHD); insulin resistance plays pivotal roles in the progression of such a syndrome and cardiovascular diseases. Improvement of Insulin Resistance, therefore, is most likely to reduce the high cardiovascular event rate in T2DM. It has been generally accepted that Insulin Resistance (detected by HOMA-R) and Acute Insulin Response = AIR (by HOMA-B) are both usually present in T2DM. The Thiazolidinedions (TZDs) are Insulin Sensitizers (e.g Rosiglitazone = ROS, Pioglitazone = PIO) introduced into clinical practice in 1997; clinical evidence data showed that TZDs improved both HOMA-R, and HOMA-B. PPARg can be activated by TZDs and it appears to be fundamental to the pathophysiology of diabetes mellitus i.e hGLUT-4, hglucokinase, iPEPCK, hGLUT-4, and decreases production by fat cell of several mediators that may cause insulin resistance, such as TNFa and resistin. PPARg also mediates increased production of Adiponectin and the insulin signaling intermediate PI3K, and both actions lead to increase insulin sensitivity. A "dual PPARg -PPARa agonists" (e.g PIO, but ROS poorly activate PPARa) might lower glucose and modulate lipids. Thus, PIO, as a stronger "dual PPARg -PPARa agonists", shows an important therapeutic pathway in diabetes mellitus and cardiovascular diseases, even in metabolic syndrome. Current evidence suggests a close relationship between activation of PPARg and restoration of insulin sensitivity by reductions in TNFa and FFAs, and the enhancement of insulin stimulation of PI3-K Pathway and also upward arrow adiponectin & downward arrow resistin.[1]

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