| Abstract: | Bitter gourd ( Momordica charantia L.) is a common vegetable in Asia that has been used in traditional medicine for the treatment of Diabetes. PPARs are ligand-dependent transcription factors that belong to the steroid hormone nuclear receptor family and control lipid and glucose homeostasis in the body. We previously reported that the ethyl acetate (EA) extract of bitter gourd activated peroxisome proliferator receptors (PPARs) α and γ. To identify the active compound that activated PPARα, wild bitter gourd EA extract was partitioned between n-hexane and 90% methanol/10% H2O, and the n-hexane soluble fraction was further separated by silica gel column chromatography and finally by preparative HPLC. A transactivation assay employing a clone of CHOK1 cells stably transfected with a (UAS)4-tk-alkaline phosphatase reporter and a chimeric receptor of GAL4-rPPARα LBD was used to track the active component. Based on Mass, NMR, and IR spectroscopy, 9 cis, 11 trans, 13 trans-conjugated linolenic acid (9 c, 11 t, 13 t-CLN) was identified as a PPARα activator in wild bitter gourd. The isolated 9 c, 11 t, 13 t-CLN rich fraction also significantly induced acyl CoA oxidase (ACO) activity in a peroxisome proliferator-responsive murine hepatoma cell line, H4IIEC3, implying that 9 c, 11 t, 13 t-CLN was able to act on a natural PPARα signaling pathway as well. The content of 9 c, 11 t, 13 t-CLN was estimated to be about 7.1 g/kg of our dried wild bitter gourd sample. The concentration of 9 c, 11 t, 13 t-CLN and activation activity in the hydrolyzed EA extract of the seeds was higher than that of the flesh. The potential health benefits of 9 c, 11 t, 13 t-CLN through the PPARα regulated mechanism are worthy to be further characterized in in vivo studies. |
