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          丁酸提高線粒體功能,減輕氧化應激,改善脂肪肝
          發布時間:2020/6/5 17:02:19 來源:浩華生物.


          1、畜禽脂肪肝

          Fatty liver of livestock and poultry

          脂肪肝問題在豬、雞、牛、羊、魚等各種動物中均普遍發生,成為影響動物健康和畜禽肉品質的重要因素,遺傳、營養、管理、藥物、毒素等均可導致脂肪肝的發生。脂肪肝的形成與脂肪代謝紊亂有關,肝細胞脂肪合成增加,氧化減少。氧化應激、NO信號通路的中斷和線粒體功能障礙等被認為是加速脂肪變性和啟動脂肪肝和纖維化進程的關鍵機制,并且線粒體損傷和氧化應激之間有著復雜的相互作用。

          Fatty liver disease are widelly found in multiple animals, such as pigs, chickens, cattle, sheep, and fish etc., has become a vital factor to affect animal health and meat quality, and many factors such as genetics, nutrition, management, drugs and toxins etc. are possibly the reasons lead to a fatty liver. The formation of fatty liver is related to a disorder of the fat metabolism that the fatty synthesis of liver cells are increased and the oxidation are decreased. The oxidative stress, disruption of NO signaling pathway and mitochondrial dysfunction are considered to be the key mechanisms to accelerate steatosis and trigger the process of fatty liver and fibrosis’. And at the same, there also are some complicated interactions between mitochondrial damage and oxidative stress.

          2、線粒體功能障礙

          Mitochondrial dysfunction

          線粒體有細胞動力工廠”之稱,除了為細胞提供能量,還參與細胞信號轉導、分化與生長、凋亡等生命過程。作為肝細胞最重要的細胞器之一,線粒體是脂肪酸進行β-氧化和三羧酸循環、腺嘌呤核苷三磷酸(ATP)合成和活性氧(ROS)形成的主要場所。缺血缺氧、藥物、毒素等都可導致線粒體功能障礙,表現為形態結構變化,ATP減少,游離氧產生過度,細胞凋亡、鈣離子紊亂、mtDNA損傷等。

          Mitochondria are known as the "Cell power plant". In addition to supplying energy to cellular, mitochondria are also involved in a range of processes, such  as  signaling, cellular differentiation and growth, and cell death. As one of the most important organelles of hepatocytes, mitochondria are the main site of fatty acid β-oxidation, tricarboxylic acid cycle, adenine nucleoside triphosphate (ATP) synthesis and ROS formation. Ischemia, hypoxia, drugs, and toxins etc. are the possibilties would lead to a mitochondrial dysfunction, which would manifeste as changes of morphological structure, ATP reduction, free oxygen’s excessive production, cell apoptosis, calcium disorder, and mtDNA damage, etc.


          肝線粒體功能障礙可引起脂肪氧化的改變。線粒體脂肪酸β氧化是脂肪代謝的限速步驟,線粒體功能障礙導致肝細胞消耗游離脂肪酸的氧化磷酸化以及β-氧化減少,合成和攝取的甘油三酯增多,從而引起脂肪肝問題。

          Liver mitochondria dysfunction causes some changes on fat oxidation. Mitochondrial fatty acid’s β oxidation is the rate-limiting step of fat metabolism, the mitochondrial dysfunction causes the oxidative phosphorylation of free fatty acids consumed by hepatocytes, the decreasing of β-oxidation, the increasing of the synthesization and ingestion of triglycerides, and that’s how the fatty liver is caused.

           
          肝線粒體功能障礙可引起活性氧(ROS)生成和氧化應激的改變。斷奶、疾病、脂肪肝問題等在細胞水平上都是細胞的氧化應激,線粒體是氧化應激的作用靶點。已有大量研究報道在脂肪肝形成過程中,伴隨著ROS的大量產生,線粒體氧化損傷產物如丙二醛(MDA)累積增加,線粒體內主要抗氧化蛋白GSH、SOD2和GPX 水平顯著降低,抗氧化防御體系受到破壞,出現氧化應激,并進一步降低線粒體氧化呼吸功能。

          The dysfunction of liver mitochondria will cause a production of ROS and change of oxidative stress. At the cellular level, weaning, disease and fatty liver problems are all the oxidative stress of cells and mitochondria is the target of oxidative stress. A large number of studies have reported that in the process of fatty liver formation, with the massive production of ROS, the accumulation of mitochondrial oxidative damage products such as malondialdehyde (MDA) starts to rise up, and the levels of the main antioxidant proteins GSH, SOD2 and GPX in the mitochondria are significantly reduced. The antioxidant defense system is damaged and the oxidative stress occurred, further reducing the mitochondria oxidative respiratory function.   


          3、丁酸改善線粒體功能

          Butyric acid improves mitochondrial function

          丁酸作為一種重要的短鏈脂肪酸(SCFA),具有抗炎、抗癌、抗氧化和免疫調節等作用,既能作為能量基質直接被利用,也能作為信號分子調控基因和蛋白的表達。比如通過抑制組蛋白去乙?;福℉DAC)或激活G蛋白偶聯受體41和43,來調控線粒體基因表達,影響機體代謝活動。

          As an important short chain fatty acid (SCFA), butyric acid has the functions of anti-inflammatory, anti-cancer, anti-oxidation and immune regulation. Butyric acid can not only be directly used as the energy matrix, but also act as a signal molecule to regulate gene and protein expression. For example, by inhibiting histone deacetylase (HDAC) or activating G-protein-coupled receptors 41 and 43, butyric acid regulates mitochondrial gene expression and affects the body metabolic activity.

           
          丁酸可以通過減輕炎癥反應、抑制胰島素抵抗和減弱線粒體氧化應激等機制影響非酒精性脂肪肝的發生和發展。何進田等研究發現三丁酸甘油酯營養干預子宮內發育遲緩(IUGR)仔豬,可提高肝臟抗氧化能力,保護線粒體免受損傷;顯著提高IUGR仔豬肝臟琥珀酸脫氫酶(SDH)、蘋果酸脫氫酶(MDH)及錳超氧化物歧化酶(Mn-SOD)的活性,從而提高肝臟線粒體功能。

          Butyric acid can affect the occurrence and development of nonalcoholic fatty liver by reducing inflammatory response, inhibiting insulin resistance and weakening mitochondrial oxidative stress. He Jintian et al. found out that tributyrin nutrition intervention in intrauterine growth retardation (IUGR) piglets will improve the liver antioxidant capacity, protect mitochondria from damage, and significantly improve the liver SDH, MDH and Mn-SOD activities of IUGR piglets, so as to improve the working performance of liver mitochondrial function.

                                           
          PS:SDH是三羧酸循環中唯一嵌入線粒體內膜的酶
                  MDH是一種重要的氧化還原酶
                  Mn-SOD主要存在于線粒體基質中,作為抗氧化劑
          PS: SDH is the only enzyme embedded in the inner mitochondrial membrane in the tricarboxylic acid cycle
          MDH is an important oxidoreductase
          Mn-SOD is mainly existed in the mitochondrial matrix as an antioxidant


          丁酸可能通過增強肝線粒體功能緩解食源性小鼠肥胖,以及大鼠的非酒精性脂肪肝。Hatzis等研究表明,補充丁酸鈉可以增強腸內褪黑素的合成,進而減弱內毒素誘導的活性氧的生成和肝臟氧化應激,從而對高脂飲食所誘導的肝臟疾病的保護作用。Mollica等也發現,丁酸鹽能夠通過激活AMPK/ACC通路,減少ROS生成,減弱氧化應激,調節線粒體的生物效率和功能狀態,從而降低肝臟脂肪。
          The obesity in mice and nonalcoholic fatty liver in rats would be possibly alleviated by butyric acid through enhancing the function performance of liver mitochondria. Studies of Hatzis et al. showed that a supplement of sodium butyrate could enhance the synthesis of melatonin in the intestine, and by which have reduced the endotoxin-induced active oxygen production and liver oxidative stress, thereby to protect liver diseases induced by high-fat diet. Mollica et al. also found out that the butyrate could reduce the production of ROS, weaken the oxidative stress, and regulate mitochondrial biological efficiency and functional state, by activating AMPK/ACC pathway, thereby reducing liver fat.


           
          線粒體基因表達出現問題對能量代謝有著長期影響,丁酸可顯著上調線粒體β氧化相關基因Acc1和Cpt1α的mRNA表達, 和解耦聯相關的關鍵基因Ucp2的表達,以及線粒體自身編碼的8個基因的mRNA水平的表達。

          An expression trouble in the mitochondrial gene has a long-term effect on energy metabolism. The butyric acid can significantly up regulate the mRNA expression of mitochondrial β-oxidation related genes Acc1 and Cpt1α, and the expression of decoupling-related key genes Ucp2, as well as the mRNA level of eight genes encoded by mitochondria themselves.


          qRT-PCR analysis fomRNA expression levels of the generelated with mitochondrial function in liver 

          (A)The mRNA levels of mitochondrial function associated 
          genes ACC1, CPT 1α and UCP2 


                                                 
          Con, normal diet;HF, high-fat diet;
          HFB, high-fat diet with sodium butyrate by gavage
          PS:PGC 1α是與機體能量代謝較為密切的轉錄輔助激活因子,在線粒體合成等過程中發揮重要作用。
          ACC1 和CPT-1α 是機體調控長鏈脂肪酸進入線粒體進行β氧化的重要酶。
          UCP2 在線粒體中與呼吸鏈電子傳遞和能量物質ATP的產生有重要的作用。
          PS: PGC 1α plays an important role in the process of mitochondrial synthesis.
              ACC1 and CPT1α are important enzymes for regulating the β oxidation of long chain fatty acids into mitochondria.
              UCP2 plays an important role in the electron transfer of respiratory chain and the production of ATP.


          (B)The mRNA expression levels of 13 mtDNA-encoded genes

          4、小結

          Summary

          畜禽脂肪肝的問題是能量攝入過多或者代謝異常,導致脂肪氧化不徹底以及氧化應激產生,根本原因是線粒體的功能不好,不能有效氧化脂肪釋放出ATP,降低線粒體應激。用丁酸類衍生物干預后,線粒體功能改善,營養物質徹底氧化,ATP 的供應量充足,有助于減少脂肪在肝臟中的沉積,脂肪肝問題就解決了,動物也能好好地活下來。

          The problems of fatty liver occured in livestock and poultry are caused on the account of an excessive energy intaken or an abnormal metabolism, and results in the incomplete fat oxidation and oxidative stress. The fundamental reason of this phenomenon is the poor function performance of mitochondria, which can not effectively oxidize fat to release ATP, and reduce mitochondrial stress. After an intervention of butyric acid derivatives, the mitochondrial function now has been improved, the energy substances is completely oxidized, the supply of ATP is sufficient, the problem of fatty liver is solved, and the animals is possible to survive well.

           
          從代謝動力學方面看,丁酸根在體內代謝速度特別快,在血液中6min達到峰值,很難維持有效的作用劑量和作用時間。而使用三丁酸甘油酯,血液中的丁酸根在15min達到效應濃度,然后持續升高,30min 時三丁酸甘油酯的含量達到峰值,丁酸根則在45min 達到峰值,并將效應濃度持續維持至使用后3 小時內,從而使足夠量的三丁酸甘油酯和丁酸根能進入骨髓造血細胞里促進血紅蛋白合成,提高氧氣輸入量,促進線粒體融合和再生,增強線粒體動力,輸出更多的ATP,達到保命、促進腸道發育,降低脂肪肝等功效。

          From the aspect of metabolism kinetics, butyrate root metabolizes very fast in vivo, with a 6-minute time to reach the peak value in blood, it is difficult to maintain an effective dosage and action time. But when tributyrin was used, the concentration of butyrate root in blood reached the effect concentration within 15 minutes, and then increased continuously. At the time of 30 minutes, the content of tributyrin reached the peak, while butyrate root at the time of 45 minutes, and maintained the effect concentration until 3 hours after being used. So that enough doses of tributyrin and butyrate is possible to enter into bone marrow hematopoietic cells to promote hemoglobin synthesis, increase oxygen input, promote mitochondrial fusion and regeneration, enhance mitochondrial power, output more ATP, achieve life-saving, promote intestinal development, reduce fatty liver and many other effects.

          參考文獻:

          [1] 黨文呈, 鄧烽丞, 李兆龍, . 丁酸在非酒精性脂肪性肝病發生發展中的作用[J]. 臨床肝膽病雜志, 2020, 36(4):915-918

          [2] 洪健, 賈逸敏, 趙茹茜. 丁酸通過增強肝線粒體功能緩解高脂誘導的小鼠肥胖[J]. 中國生物化學與分子生物學報, 2017, 33( 12) : 1266 - 1273

          [3] 何進田, 董麗, 白凱, .三丁酸甘油酯對宮內發育遲緩哺乳仔豬肝臟抗氧化和線粒體功能的影響亮.[J]. 食品科學, 2016, 37(3): 191-196

          [4] Hatzis G, Ziakas P, Kavantzas N, et al, Melatonin attenuates high fat diet-induced fatty liver disease in rats[J]. World J Hepatol, 2013,5(4):160-169

          [5] Jin C J, Engstler A J, Sellmann C, et al. Sodium butyrate protects mice from the development of the early signs of non-alcoholic fatty liver disease: Role of melatonin and lipid peroxidation[J]. Br J Nutr, 2016:1-12

          [6] Mollica M P, Mattace Raso G, Cavaliere G, et al. Butyrate regulates liver mitochondrial function, efficiency, and dynamics in insulin-resistant obse mice[J]. Diabetes, 2017,66(5):1405-1418

          [7] Wang Chunchun, Cao Shuting, Shen Zhuojun, et al. Effect of dietary tributyrin on intestinal mucosa development, mitochondrial function and AMPK-mTOR pathway in weaned pigs.[J]. Journal of Amimal Science and Biotechnology, 2019(1):1-10.







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