ketogenesis

出典: meddic

  • n.
  • ケトン体生成、ケトン体生合成
ケトン体
See also Fatty acids, oxidation of


Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2014/09/20 23:48:26」(JST)

wiki en

[Wiki en表示]

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

英文文献

  • Cdc2-Like Kinase 2 Suppresses Hepatic Fatty Acid Oxidation and Ketogenesis Through Disruption of the PGC-1α and MED1 Complex.
  • Tabata M1, Rodgers JT, Hall JA, Lee Y, Jedrychowski MP, Gygi SP, Puigserver P.Author information 1Department of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.AbstractHepatic ketogenesis plays an important role in catabolism of fatty acids during fasting along with dietary lipid overload, but the mechanisms regulating this process remain poorly understood. Here, we show that Cdc2-like kinase 2 (Clk2) suppresses fatty acid oxidation and ketone body production during diet-induced obesity. In lean mice, hepatic Clk2 protein is very low during fasting and strongly increased during feeding; however, in diet-induced obese mice, Clk2 protein remains elevated through both fed and fasted states. Liver-specific Clk2 knockout mice fed a high-fat diet exhibit increased fasting levels of blood ketone bodies, reduced respiratory exchange ratio, and increased gene expression of fatty acid oxidation and ketogenic pathways. This effect of Clk2 is cell-autonomous, because manipulation of Clk2 in hepatocytes controls genes and rates of fatty acid utilization. Clk2 phosphorylation of peroxisome proliferator-activated receptor γ coactivator (PGC-1α) disrupts its interaction with Mediator subunit 1, which leads to a suppression of PGC-1α activation of peroxisome proliferator-activated receptor α target genes in fatty acid oxidation and ketogenesis. These data demonstrate the importance of Clk2 in the regulation of fatty acid metabolism in vivo and suggest that inhibition of hepatic Clk2 could provide new therapies in the treatment of fatty liver disease.
  • Diabetes.Diabetes.2014 May;63(5):1519-32. doi: 10.2337/db13-1304. Epub 2014 Jan 23.
  • Hepatic ketogenesis plays an important role in catabolism of fatty acids during fasting along with dietary lipid overload, but the mechanisms regulating this process remain poorly understood. Here, we show that Cdc2-like kinase 2 (Clk2) suppresses fatty acid oxidation and ketone body production duri
  • PMID 24458359
  • Fibroblast Growth Factor (Fgf) 21 is a novel target gene of the Aryl Hydrocarbon Receptor (AhR).
  • Cheng X1, Vispute SG2, Liu J3, Cheng C4, Kharitonenkov A4, Klaassen CD5.Author information 1Department of Pharmaceutical Sciences, St. John's University, 8000 Utopia Parkway, Queens, NY 11439, USA. Electronic address: chengx@stjohns.edu.2Department of Pharmaceutical Sciences, St. John's University, 8000 Utopia Parkway, Queens, NY 11439, USA.3Department of Internal Medicine, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA.4Lilly Research Laboratories, Division of Eli Lilly and Co., Indianapolis, IN 46285, USA.5Department of Internal Medicine, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA. Electronic address: curtisklaassenphd@gmail.com.AbstractThe toxic effects of dioxins, such as 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), mainly through activation of the aryl hydrocarbon receptor (AhR) are well documented. Fibroblast growth factor (Fgf) 21 plays critical roles in metabolic adaptation to fasting by increasing lipid oxidation and ketogenesis in the liver. The present study was performed to determine whether activation of the AhR induces Fgf21 expression. In mouse liver, TCDD increased Fgf21 mRNA in both dose- and time-dependent manners. In addition, TCDD markedly increased Fgf21 mRNA expression in cultured mouse and human hepatocytes. Moreover, TCDD increased mRNA (in liver) and protein levels (in both liver and serum) of Fgf21 in wild-type mice, but not in AhR-null mice. Chromatin immunoprecipitation assays showed that TCDD increased AhR protein binding to the Fgf21 promoter (-105/+1 base pair). Fgf21-null mice administered 200μg/kg of TCDD died within 20days, whereas wild-type mice receiving the same treatment were still alive at one month after administration. This indicates that TCDD-induced Fgf21 expression protects against TCDD toxicity. Diethylhexylphthalate (DEHP) pretreatment attenuated TCDD-induced Fgf21 expression in mouse liver and white adipose tissue, which may explain a previous report that DEHP pretreatment decreases TCDD-induced wasting. In conclusion, Fgf21 appears to be a target gene of AhR-signaling pathway in mouse and human liver.
  • Toxicology and applied pharmacology.Toxicol Appl Pharmacol.2014 Apr 22. pii: S0041-008X(14)00153-7. doi: 10.1016/j.taap.2014.04.013. [Epub ahead of print]
  • The toxic effects of dioxins, such as 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), mainly through activation of the aryl hydrocarbon receptor (AhR) are well documented. Fibroblast growth factor (Fgf) 21 plays critical roles in metabolic adaptation to fasting by increasing lipid oxidation and ketog
  • PMID 24769090
  • Mitochondrial respiration as a target for neuroprotection and cognitive enhancement.
  • Gonzalez-Lima F1, Barksdale BR2, Rojas JC3.Author information 1Department of Psychology, University of Texas at Austin, Austin, TX 78712, USA; Department of Pharmacology and Toxicology, University of Texas at Austin, Austin, TX 78712, USA; Institute for Neuroscience, University of Texas at Austin, Austin, TX 78712, USA. Electronic address: gonzalezlima@utexas.edu.2Institute for Neuroscience, University of Texas at Austin, Austin, TX 78712, USA.3Department of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX 75235, USA.AbstractThis paper focuses on brain mitochondrial respiration as a therapeutic target for neuroprotection and cognitive enhancement. We propose that improving brain mitochondrial respiration is an important future direction in research and treatment of Alzheimer's disease (AD) and other conditions associated with cognitive impairment and neurodegeneration. The central thesis is that supporting and improving brain mitochondrial respiration constitutes a promising neurotherapeutic principle, with potential applications in AD as well as in a wide variety of neuropsychological conditions. We propose three different interventional approaches to improve brain mitochondrial respiration based on (a) pharmacology, (b) photobiomodulation and (c) nutrition interventions, and provide detailed examples for each type of intervention. First, low-dose USP methylene blue is described as a pharmacological intervention that can successfully increase mitochondrial respiration and result in memory enhancement and neuroprotection. Second, transcranial low-level light/laser therapy with near-infrared light is used to illustrate a photobiomodulation intervention with similar neurometabolic mechanisms of action as low-dose methylene blue. Finally, a nutrition intervention to improve mitochondrial respiration is proposed by increasing ketone bodies in the diet. The evidence discussed for each intervention supports a fundamental neurotherapeutic strategy based on improving oxidative energy metabolism while at the same time reducing the pro-oxidant tendencies of the nervous system. Targeting brain mitochondrial respiration with these three types of interventions is proposed as part of a holistic neurotherapeutic approach to improve brain energy metabolism and antioxidant defenses. This strategy represents a promising new bioenergetics direction for treatment of AD and other neuropsychological disorders featuring cognitive impairment and neurodegeneration.
  • Biochemical pharmacology.Biochem Pharmacol.2014 Apr 15;88(4):584-593. doi: 10.1016/j.bcp.2013.11.010. Epub 2013 Dec 4.
  • This paper focuses on brain mitochondrial respiration as a therapeutic target for neuroprotection and cognitive enhancement. We propose that improving brain mitochondrial respiration is an important future direction in research and treatment of Alzheimer's disease (AD) and other conditions associate
  • PMID 24316434

和文文献

  • Age-related changes in the diurnal variation of ketogenesis in patients with type 2 diabetes and relevance to hypoglycemic medications
  • , , , , , , , , , , , ,
  • Endocrine Journal 62(3), 235-241, 2015
  • … To assess the significance of ketogenesis in the management of diabetes mellitus, we analyzed the factors associated with the diurnal variation of the plasma ketone body levels. … While excessive ketogenesis leads to critical ketoacidosis, inadequate ketone body production could be associated with a propensity to develop neurohypoglycemia in elderly patients treated with insulin secretagogues. …
  • NAID 130005060853
  • FGF21による代謝制御 (特集 ホルモン作用と臓器相関)
  • 小林 正稔,植木 浩二郎
  • 内分泌・糖尿病・代謝内科 38(1), 53-59, 2014-01
  • NAID 40019957682
  • Age-related changes in the diurnal variation of ketogenesis in patients with type 2 diabetes and relevance to hypoglycemic medications
  • , , , , , , , , , , , ,
  • Endocrine Journal, 2014
  • … To assess the significance of ketogenesis in the management of diabetes mellitus, we analyzed the factors associated with the diurnal variation of the plasma ketone body levels. … While excessive ketogenesis leads to critical ketoacidosis, inadequate ketone body production could be associated with a propensity to develop neurohypoglycemia in elderly patients treated with insulin secretagogues. …
  • NAID 130004704364

関連リンク

ketogenesis / ˌki toʊˈdʒɛn ə sɪs / Show Spelled [kee-toh-jen-uh-sis] Show IPA noun Medicine/Medical. the production of ketone bodies in the body, as in diabetes mellitus or low-carbohydrate weight-loss diets. Origin: 1910–15; keto-+ ...
ketogenesis [kēt′ō jen′ə sis] noun the formation of ketones, such as acetone, in the body as a result of the incomplete oxidation of organic compounds such as fatty acids or carbohydrates Origin: keto- plush -genesis Related ...
ke·to·gen·e·sis noun \ ˌ kē-tō-ˈ je-nə-səs\ Definition of KETOGENESIS: the production of ketone bodies (as in diabetes) — ke·to·gen·ic \-ˈ je-nik\ adjective Origin of KETOGENESIS New Latin First Known Use: 1915 ke·to·gen·e·sis ...

関連画像


押しても画像が表示されない場合はサーバが混雑しています。2週間ほどあけて、再度押下してください。


★リンクテーブル★
先読みケトン体

ケトン体」

  [★]

ketone body, ketone bodies
アセトン体 acetone body
ケトーシス



  • 脂肪酸のβ酸化で生じるアセチルCoATCAサイクル(クエン酸サイクル)に入る。肝ミトコンドリアでは相当な割合のアセチルCoAがケトン体生成経路に入り、ケトン体を生成する。
  • 飢餓状態では、ケトン体が脳血管関門を通り抜け、脳のエネルギー源となる。

ケトン体

ケトン体の生合成

ケトン体の代謝

検査




★コメント★

[メモ入力エリア]
※コメント5000文字まで
ニックネーム:
コメント:




表示
個人用ツール


  meddic.jp

リンク
連絡