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Go, Younghoon,Jeong, Ji Yun,Jeoung, Nam Ho,Jeon, Jae-Han,Park, Bo-Yoon,Kang, Hyeon-Ji,Ha, Chae-Myeong,Choi, Young-Keun,Lee, Sun Joo,Ham, Hye Jin,Kim, Byung-Gyu,Park, Keun-Gyu,Park, So Young,Lee, Chul- American Diabetes Association 2016 Diabetes Vol.65 No.10
<P>Hepatic steatosis is associated with increased insulin resistance and tricarboxylic acid (TCA) cycle flux, but decreased ketogenesis and pyruvate dehydrogenase complex (PDC) flux. This study examined whether hepatic PDC activation by inhibition of pyruvate dehydrogenase kinase 2 (PDK2) ameliorates these metabolic abnormalities. Wildtype mice fed a high-fat diet exhibited hepatic steatosis, insulin resistance, and increased levels of pyruvate, TCA cycle intermediates, and malonyl-CoA but reduced ketogenesis and PDC activity due to PDK2 induction. Hepatic PDC activation by PDK2 inhibition attenuated hepatic steatosis, improved hepatic insulin sensitivity, reduced hepatic glucose production, increased capacity for beta-oxidation and ketogenesis, and decreased the capacity for lipogenesis. These results were attributed to altered enzymatic capacities and a reduction in TCA anaplerosis that limited the availability of oxaloacetate for the TCA cycle, which promoted ketogenesis. The current study reports that increasing hepatic PDC activity by inhibition of PDK2 ameliorates hepatic steatosis and insulin sensitivity by regulating TCA cycle anaplerosis and ketogenesis. The findings suggest PDK2 is a potential therapeutic target for nonalcoholic fatty liver disease.</P>
Jha, Mithilesh Kumar,Song, Gyun Jee,Lee, Maan Gee,Jeoung, Nam Ho,Go, Younghoon,Harris, Robert A.,Park, Dong Ho,Kook, Hyun,Lee, In-Kyu,Suk, Kyoungho Society for Neuroscience 2015 The Journal of neuroscience Vol.35 No.42
<P>Pyruvate dehydrogenase kinases (PDK1–4) are mitochondrial metabolic regulators that serve as decision makers via modulation of pyruvate dehydrogenase (PDH) activity to convert pyruvate either aerobically to acetyl-CoA or anaerobically to lactate. Metabolic dysregulation and inflammatory processes are two sides of the same coin in several pathophysiological conditions. The lactic acid surge associated with the metabolic shift has been implicated in diverse painful states. In this study, we investigated the role of PDK-PDH-lactic acid axis in the pathogenesis of chronic inflammatory pain. Deficiency of <I>Pdk2</I> and/or <I>Pdk4</I> in mice attenuated complete Freund's adjuvant (CFA)-induced pain hypersensitivities. Likewise, <I>Pdk2/4</I> deficiency attenuated the localized lactic acid surge along with hallmarks of peripheral and central inflammation following intraplantar administration of CFA. <I>In vitro</I> studies supported the role of PDK2/4 as promoters of classical proinflammatory activation of macrophages. Moreover, the pharmacological inhibition of PDKs or lactic acid production diminished CFA-induced inflammation and pain hypersensitivities. Thus, a PDK-PDH-lactic acid axis seems to mediate inflammation-driven chronic pain, establishing a connection between metabolism and inflammatory pain.</P><P><B>SIGNIFICANCE STATEMENT</B> The mitochondrial pyruvate dehydrogenase (PDH) kinases (PDKs) and their substrate PDH orchestrate the conversion of pyruvate either aerobically to acetyl-CoA or anaerobically to lactate. Lactate, the predominant end product of glycolysis, has recently been identified as a signaling molecule for neuron-glia interactions and neuronal plasticity. Pathological metabolic shift and subsequent lactic acid production are thought to play an important role in diverse painful states; however, their contribution to inflammation-driven pain is still to be comprehended. Here, we report that the PDK-PDH-lactic acid axis constitutes a key component of inflammatory pain pathogenesis. Our findings establish an unanticipated link between metabolism and inflammatory pain. This study unlocks a previously ill-explored research avenue for the metabolic control of inflammatory pain pathogenesis.</P>
New Virulence Factors of Enterohemorrhagic Escherichia coli (EHEC) O157:H7 in Dairy Food Processing
Moon, Yong-Il,Oh, Sangnam,Park, Mi Ri,Son, Seok Jun,Go, Gwang-woong,Song, Minho,Oh, Sejong,Kim, Sae Hun,Kim, Younghoon Korean Society of Dairy Science and Biotechnology 2015 한국유가공기술과학회지 Vol.33 No.1
Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is well-characterized as an important food-borne pathogen worldwide and causes human diseases such as diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome (HUS) by producing shiga-like toxin (Stx). It has been reported that a number of dairy foods, including cheese, can act as the source of EHEC O157:H7 infections. In addition to the toxicity of Stx, recently it has been indicated that EHEC O157:H7 possesses virulence factors related to attachment, quorum sensing, and biofilms. Moreover, these novel virulence factors might become critical points to be considered in the future production of food derived from animals. Here, we review the evidences that support these insights on new virulence factors and discuss the potential mechanisms mediating the pathogenesis of EHEC O157:H7 in the dairy food industry.
New Virulence Factors of Enterohemorrhagic Escherichia coli (EHEC) O157:H7 in Dairy Food Processing
( Yong Il Moon ),( Sangnam Oh ),( Mi Ri Park ),( Seok Jun Son ),( Gwang Woong Go ),( Minho Song ),( Sejong Oh ),( Sae Hun Kim ),( Younghoon Kim ) 한국유가공기술과학회 2015 한국유가공기술과학회지 Vol.33 No.1
Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is well-characterized as an important food-borne pathogen worldwide and causes human diseases such as diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome (HUS) by producing shiga-like toxin (Stx). It has been reported that a number of dairy foods, including cheese, can act as the source of EHEC O157:H7 infections. In addition to the toxicity of Stx, recently it has been indicated that EHEC O157:H7 possesses virulence factors related to attachment, quorum sensing, and biofilms. Moreover, these novel virulence factors might become critical points to be considered in the future production of food derived from animals. Here, we review the evidences that support these insights on new virulence factors and discuss the potential mechanisms mediating the pathogenesis of EHEC O157:H7 in the dairy food industry.