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- 저자 : Amber MacDonald (검색결과 2 건)
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Anna Han,Natalie Bennett,Amber Macdonald,Megan Johnstone,Bettaieb Ahmed,Jay Whelan,Dallas R. Donohoe 한국식품영양과학회 2021 한국식품영양과학회 학술대회발표집 Vol.2021 No.10
Butyrate comes from the bacterial fermentation of dietary fiber in the colon. Butyrate is the primary energy source of the colonocytes and plays an epigenetic role in the colonocytes as a histone deacetylase inhibitor (HDACi). We aimed to understand butyrate oxidation and regulatory mechanisms, influencing butyrate oxidation in cancerous colonocytes. Butyrate oxidation was measured as oxygen consumption rate by Seahorse Analyzer. Normal colonocytes showed a significantly higher butyrate oxidation ability compared to cancerous colonocytes (HCT116). Decreased butyrate oxidation of cancerous colonocytes resulted from pyruvate dehydrogenase (PDH) complex inactivation. PDH kinase inhibitor (dichloroacetate, DCA) significantly increased butyrate oxidation in HCT116 compared to those without DCA. DCA also markedly increased OCNT2 and CPT1A expressions that are necessary to carnitine-dependent butyrate oxidation. Additionally, butyrate decreased its own oxidation in HCT116 by suppressing short chain acyl-CoA dehydrogenase (SCAD) expression as an HDACi. These observations offer insight into butyrate’s selective effect against colorectal cancer cells.
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Metabolomics Approach in the Study of the Well-Defined Polyherbal Preparation Zyflamend
Eric D. Tague,Allen K. Bourdon,Amber MacDonald,Maggie S. Lookadoo,Edward D. Kim,Wesley M. White,Paul D. Terry,Shawn R. Campagna,Brynn H. Voy,Jay Whelan 한국식품영양과학회 2018 Journal of medicinal food Vol.21 No.3
Zyflamend is a highly controlled blend of 10 herbal extracts that synergistically impact multiple cell signaling pathways with anticancer and anti-inflammatory properties. More recently, its effects were shown to also modify cellular energetics, for example, activation of fatty acid oxidation and inhibition of lipogenesis. However, its general metabolic effects in vivo have yet to be explored. The objective of this study was to characterize the tissue specific metabolomes in response to supplementation of Zyflamend in mice, with a comparison of equivalent metabolomics data generated in plasma from humans supplemented with Zyflamend. Because Zyflamend has been shown to activate AMPK, the “energy sensor” of the cell, in vitro, the effects of Zyflamend on adiposity were also tested in the murine model. C57BL/6 mice were fed diets that mimicked the macro- and micronutrient composition of the U.S. diet with and without Zyflamend supplementation at human equivalent doses. Untargeted metabolomics was performed in liver, skeletal muscle, adipose, and plasma from mice consuming Zyflamend and in plasma from humans supplemented with Zyflamend at an equivalent dose. Adiposity in mice was significantly reduced in the Zyflamend-treated animals (compared with controls) without affecting body weight or weight gain. Based on KEGG pathway enrichment, purine and pyrimidine metabolism (potential regulators of AMPK) were particularly responsive to Zyflamend across all tissues, but only in mice. Consistent with the metabolomics data, Zyflamend activated AMPK and inhibited acetyl CoA-carboxylase in adipose tissue, key regulators of lipogenesis. Zyflamend reduces adipose tissue in mice through a mechanism that likely involves the activation of AMPK.
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