RESUMO
OBJECTIVE: To observe the effects of the flower of Edgeworthia gardneri (Wall.) Meisn (EWM) on glucose and lipid metabolism in KK/upj-Ay/J (KKAy) mice and investigate the possible mechanism of EWM in the liver of KKAy mice by transcriptome analysis. METHODS: Forty KKAy mice were fed a high-sugar and high-fat diet for 3 weeks to establish the animal model of metabolic syndrome. After 5 weeks of continuous administration of EWM, serum high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglycerides (TG), total cholesterol (TC), and free fatty acids (FFA) were detected by radioimmunoassay. Serum fasting insulin (Fins) and adiponectin levels were measured by enzyme-linked immunosorbent assay. Liver tissue fixed with paraformaldehyde was stained with hematoxylin-eosin and oil red O. Transcriptome analysis was used to evaluate the liver tissue. The expressions of lipoprotein lipase (LPL), peroxisome proliferator-activated receptor-γ (PPARγ), adenosine 5'-monophosphate-activated protein kinase (AMPK), sterol regulatory element binding protein-1c (SREBP-1c), and fatty acid synthase (Fas) mRNA and protein in liver tissue were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis. RESULTS: EWM slightly reduced FBG and Fins in KKAy mice. Furthermore, EWM was able to downregulate serum LDL, TG, TC, and FFA and upregulate the expression of serum HDL and adiponectin. Transcriptome analysis revealed the following differential pathways: the peroxisome proliferator-activated receptor (PPAR) signaling pathway and the AMPK signaling pathway. RT-PCR and western blot analysis detected the associated genes and proteins. In addition, EWM was able to upregulate the expression of AMPK and downregulate the expression of PPARγ, SREBP1c, and Fas mRNA and protein and upregulate the expression of LPL mRNA. CONCLUSIONS: EWM can alleviate lipid metabolism disorders and to some extent improve glucose metabolism disorders in KKAy mice. These effects may be related to regulating PPARγ/LPL and activating the AMPK/SREBP1c/Fas pathway.
