AI Article Synopsis

  • The study explores the effects of Eucommia leaf extract (ELE) on obesity, glycolysis, and lipid metabolism in male rats, showing promising anti-obesity outcomes.
  • Both 5% ELE and ELE aroma treatments resulted in notable changes in metabolic markers, including increased mRNA levels for important metabolic genes in the liver.
  • The findings suggest that ELE enhances lipid metabolism and aerobic glycolysis, potentially aiding in the regulation of metabolic syndrome through the influence of brain-derived neurotrophic factor (BDNF).

Article Abstract

Background: Mutations in the brain-derived neurotrophic factor (BDNF) gene and its receptor, tyrosine receptor kinase B (TrkB), have been reported to cause severe obesity in rodents. Our previous study demonstrated that the oral administration of 5% Eucommia leaf extract (ELE) or ELE aroma treatment (ELE aroma) produced anti-obesity effects.

Objective: In this study, we investigated the effects of ELE on glycolysis and lipid metabolism in male Sprague-Dawley rats, as well as the effects of ELE on BDNF in rat hypothalamus.

Methods And Results: A significant reduction and a reduction tendency in the respiratory quotient were observed in association with 5% ELE and ELE aroma treatment, respectively. Furthermore, RT-qPCR results showed significant increases in Cpt2, Acad, Complex II, and Complex V mRNA levels in the liver with both treatments. In addition, in rat hypothalamus, significant elevations in BDNF, Akt, PLCγ proteins and CREB phosphorylation were observed in the 5% ELE group and the ELE aroma group. Furthermore, the Ras protein was significantly increased in the ELE aroma group. On the other hand, significant dephosphorylation of ERK1/2 was observed by the western blotting in the 5% ELE group and the ELE aroma group.

Conclusion: These findings suggest that the ELE treatment enhances the lipid metabolism and increases the aerobic glycolytic pathway, while ELE-induced BDNF may affect such energy regulation. Therefore, ELE has the possibility to control metabolic syndrome.

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Source
http://dx.doi.org/10.2174/1874467213666200505094631DOI Listing

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