Peroxisome Proliferator-Activated Receptor (PPAR) has drawn increased attention as a drug discovery target by regulating glucose and lipid metabolism [3] . PPAR, and its subtypes PPARa and PPARc, belong to the superfamily of nuclear receptors that function as transcription factors activated by several ligands. PPARs played a vitally important role in treating obesity, atherogenic dyslipidemia, hypertension, and insulin resistance as main therapeutic targets [4] . The primary function of PPARa is to act as regulator responding to transport and degradation of free fatty acids as well as reverse cholesterol transport by peroxisomal and beta-oxidation pathways [5] . A class of lipid-lowering drugs, such as fenofibrate and gemfibrozil, specially activate PPARa [6, 7, 8] . PPARc played a significant role in transcriptionally regulating lots of physiological pathways, including adipocyte differentiation and glucose homeostasis [9] . Thiazolidinediones (TZDs) are a class of the antidiabetic drugs, which act by activating the special PPARc [10] . If used alone, although each of the antidiabetic drugs could enhance the insulin sensitivity and hence lower glucose or fatty acid levels in type-2 diabetic patients [9] , some side effects would be caused, such as weight gain, fluid accumulation, and pulmonary edema [11] .