Like 
					catching two fish with one worm, treating two problems with 
					a single drug is efficient, but exceedingly difficult. In 
					particular, for new diabetes medications, in which one drug 
					aims to tackle two major complications of diabetes the 
					excess of both lipids and glucose in the blood the 
					therapeutic benefits, while great, frequently are 
					accompanied by dangerous toxic effects to the heart. Why and 
					how these drugs, known as dual PPARα/γ agonists cause heart 
					dysfunction in diabetes patients has been unclear. 
					Researcher show for the first time that dual PPARα/γ 
					diabetes drugs have a profound toxic effect on the 
					generation and function of mitochondria, the tiny energy 
					factories that power cells. Researcher found that the 
					combined activation of PPARα and PPARγ receptors by a single 
					agonist drug, tesaglitazar, blocked the activity of proteins 
					involved in mitochondrial biogenesis and energy production, 
					including a protein known as SIRT1. The popular diabetes 
					drugs known as thiazolidinediones (TZDs), which include 
					pioglitazone and rosiglitazone (the latter marketed as 
					Avandia), bind to PPARγ receptors. Because these drugs given 
					alone have been questioned for cardiac toxicity, the idea 
					emerged for dual PPARα/γ activation by a single drug the one 
					piece of bait that in theory successfully lures the two fish 
					the combined lipid- and glucose-lowering effects of PPARα/γ 
					coactivation. The researchers then repeated their 
					experiment, this time treating diabetic mice with 
					tesaglitazar in combination with resveratrol, which serves 
					as an activator of SIRT1. Mice treated with the combination 
					of the two drugs had reduced heart toxicity, relative to 
					tesaglitazar-only therapy, and their heart cells exhibited 
					normal mitochondrial function.  |