Min-Hsiung Pan1,2,3,4, Guliang Yang1, Shiming Li1, Ming-Yi Li5, Mei-Ling Tsai5, Jia-Ching Wu6, Vladimir Badmaev7, Chi-Tang Ho8, Ching-Shu Lai5. 1. Hubei Key Laboratory of Economic Forest Germplasm Improvement and Resources Comprehensive Utilization, Hubei Collaborative Innovation Center for the Characteristic Resources Exploitation of Dabie Mountains, Huanggang Normal University, Huanggang, Hubei, China. 2. Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan. 3. Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan. 4. Institute of Food Science and Technology, National Taiwan University, Taipei, Taiwan. 5. Department of Seafood Science, National Kaohsiung Marine University, Kaohsiung, Taiwan. 6. Department of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan. 7. American Medical Holdings Incorporated, New York, NY, USA. 8. Department of Food Science, Rutgers University, New Brunswick, NJ, USA.
Abstract
SCOPE: SlimTrym® is a formulated product composed of citrus polymethoxyflavones (PMFs), green tea extract, and lychee extract. We investigated the effect of dietary SlimTrym® on diet-induced obesity and associated non-alcoholic fatty liver disease (NAFLD) in mice. METHODS AND RESULTS: Male C57BL/6 mice were fed a normal diet (ND), high fat diet (HFD) or HFD containing 0.1% or 0.5% SlimTrym® for 16 weeks. Dietary SlimTrym® significantly reduced weight gain and relative perigonadal, retroperitoneal, mesenteric fat weight as well as the size of adipocyte in HFD-fed mice. SlimTrym® supplementation also effectively diminished hepatic steatosis and the serum levels of glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), triacylglycerol (TG), and total cholesterol (TCHO). Down-regulation of peroxisome proliferator-activated receptor (PPAR)γ, sterol regulatory element-binding protein (SREBP)-1, and the activation of AMP-activated protein kinase (AMPK) signaling by SlimTrym® in both adipose tissue and liver may be responsible for the observed anti-obesity effects. CONCLUSION: SlimTrym® supplementation potentially diminished diet-induced obesity and hepatic steatosis via regulating AMPK signaling and molecules involved in lipid metabolism.
SCOPE: SlimTrym® is a formulated product composed of citrus polymethoxyflavones (PMFs), green tea extract, and lychee extract. We investigated the effect of dietary SlimTrym® on diet-induced obesity and associated non-alcoholic fatty liver disease (NAFLD) in mice. METHODS AND RESULTS: Male C57BL/6 mice were fed a normal diet (ND), high fat diet (HFD) or HFD containing 0.1% or 0.5% SlimTrym® for 16 weeks. Dietary SlimTrym® significantly reduced weight gain and relative perigonadal, retroperitoneal, mesenteric fat weight as well as the size of adipocyte in HFD-fed mice. SlimTrym® supplementation also effectively diminished hepatic steatosis and the serum levels of glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), triacylglycerol (TG), and total cholesterol (TCHO). Down-regulation of peroxisome proliferator-activated receptor (PPAR)γ, sterol regulatory element-binding protein (SREBP)-1, and the activation of AMP-activated protein kinase (AMPK) signaling by SlimTrym® in both adipose tissue and liver may be responsible for the observed anti-obesity effects. CONCLUSION: SlimTrym® supplementation potentially diminished diet-induced obesity and hepatic steatosis via regulating AMPK signaling and molecules involved in lipid metabolism.
Authors: Stella Baliou; Maria Adamaki; Petros Ioannou; Aglaia Pappa; Mihalis I Panayiotidis; Demetrios A Spandidos; Ioannis Christodoulou; Anthony M Kyriakopoulos; Vassilis Zoumpourlis Journal: Mol Med Rep Date: 2021-06-29 Impact factor: 2.952