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Áö¹æ»ê : ºÎƼ¸£»ê butyric acid

Áö¹æ»ê Á¾·ù
- ºÎƼ¸£»ê butyric acid
- Linoleic Acid
- oleic Acid

- ÄÉÅæü(ketone body) Àúź¼öÈ­¹°½Ä
- MCT(Áß¼âÁö¹æ)
- ºÎƼ¸£»ê butyric acid

Ä«º¹½Ç»êÀÌÀÚ Áö¹æ»êÀÇ Çϳª. ºÎƼ¸£»ê(Butyric acid), ¹öÅÍ»ê, ³«»ê(լ߫)À̶ó°íµµ Çϴµ¥, ÀÌ°Ô ¹öÅÍ¿¡¼­ ºÐ¸®µÇ¾ú±â ¶§¹®ÀÌ´Ù. ¾î¿øÀº ±×¸®½º¾î·Î ¹öÅ͸¦ ÀǹÌÇÏ´Â ¥â¥ïύ¥ó¥ô¥ñ¥ï. ±Û¸®¼¼·Ñ¿¡ ºÙ¾î¼­ Áö¹æÀ» Çü¼ºÇÑ´Ù. ¸Þź»ê, ¿¡Åº»ê, ÇÁ·ÎÆÇ»êÀº ³Ê¹« °¡º±±â ¶§¹®¿¡ ±Û¸®¼¼·Ñ¿¡ °ÅÀÇ ºÙÁö ¾Ê±â ¶§¹®. Áö¹æ»êÀÇ ¸¶Áö³ë¼±À̶ó°í ÇØ¾ß ÇÒ µí. ´Ù¸¥ Æ÷È­Áö¹æ»êÀÌ ±×·¸µí ¼ø¼öÇÑ ºÎź»êÀº µ¶¼º°ú ºÎ½Ä¼ºÀÌ ÀÖ´Ù. ±×¸®°í ¾öû³­ ¾ÇÃ븦 ÀÚ¶ûÇÑ´Ù. ¾ÖÃÊ¿¡ »ç¶÷ ±¸Åä¿¡¼­ ³ª´Â ³¿»õÀÇ ÁÖ¼ººÐÀÌ ºÎź»êÀÌ´Ù. [1]

ºÎƼ¸£»êÀº õ¿¬ÀÇ Áö¹æÀ» ±¸¼ºÇÏ´Â Áö¹æ»ê Áß¿¡¼­ ź¼Ò¼ö°¡ °¡Àå ÀûÀº À¯±â»êÀ¸·Î n-ºÎƼ¸£»ê°ú À̼ҺÎƼ¸£»ê µÎ°³ÀÇ ±¸Á¶À̼ºÁúü°¡ Á¸ÀçÇÑ´Ù. ÇÕ¼º Çâ·á¿ë ¿¡½ºÅ׸£¸¦ ¸¸µå´Â ¿ø·á, ÇÇÇõÀÇ Å»Ä®½·Á¦·Î »ç¿ëµÈ´Ù. ¼·ÃëÇϸé ÀÎÈÄ¿°, ÀÛ¿­°¨, º¹Åë, ¼îÅ©, ÇãÅ» µîÀ» ÀÏÀ¸Å³ ¼ö ÀÖ´Ù. ´«°ú Á¢ÃËÇϸé ÅëÁõ, ¹ßÀû, ÁßÁõ ½ÉºÎ È­»ó, ½Ã·Â »ó½ÇÀ» ÀÏÀ¸Å³ ¼ö ÀÖÀ¸¸ç ÇǺο¡ ³ëÃ⠽à ÅëÁõ, ¹ßÀû, È­»ó µîÀÌ ³ªÅ¸³¯ ¼ö ÀÖ´Ù. Á¢Ã˽à µ¶¼ºÀ» ³ªÅ¸³»¹Ç·Î Á¢ÃË¿¡ ÁÖÀÇÇÑ´Ù.

ºÎƼ¸£»êÀº »ó¹ÝµÇ´Â 2°¡Áö ±â´ÉÀ» °®°í ÀÖ´Ù. Àΰ£ ´ëÀå¿¡ ÀÖ´Â ¹ßÈ¿ »ê¹°·Î½á Á¤»ó Á÷Àå°áÀå »óÇÇ¿¡¼­ °¡Àå Áß¿äÇÑ ¿¡³ÊÁö¿øÀ¸·Î Á¦°øµÈ´Ù. ÀÌ¿Í ´ëÁ¶ÀûÀ¸·Î ¹è¾çµÈ ¾Ç¼º¼¼Æ÷ÀÇ ºÐÈ­¸¦ ÃËÁøÇÏ´Â ±â´Éµµ °¡Áö°í ÀÖ´Ù. È£±â´ë»ç¿¡¼­ Çø±â´ë»ç·ÎÀÇ ÀüȯÀÌ Á÷Àå°áÀå¿¡¼­ÀÇ Á¾¾ç º¯È¯°ú °ü·ÃÀÌ ÀÖ´Ù. n-ºÎƼ¸£»ê¿°ÀÇ ±¸º°µÇ´Â ±â´ÉÀû ¿ªÇÒÀº ´Ù¸¥ Á¤»óÁ¶Á÷°ú Á¾¾çÁ¶Á÷¿¡¼­ÀÇ ´ë»çÀû È°¼ºÀ» ¹Ý¿µÇÑ´Ù. Á¾¾çÁ¶Á÷¿¡¼­ÀÇ ¿¡³ÊÁö ¿ä±¸°¡ Áõ°¡µÇ°í ÀÌ·Î ÀÎÇØ n-ºÎƼ¸£»êÀÌ °áÇ̵Ǿî Çø±â ´ë»ç·ÎÀÇ ÀüȯÀÌ ÃËÁøµÇ¾ú´Ù. (Jass 1985).
À½½Ä Áß¿¡¼­µµ ƯÈ÷ ¼ÒÀå¿¡¼­ ¼ÒÈ­°¡ ¾ÈµÇ´Â ÀüºÐ¿Í ½ÄÀ̼¶À¯ÀÇ ¾çÀº Àΰ£¿¡¼­ ´ëÀå ±â´ÉÀÇ ÁÖ¿ä °áÁ¤¿äÀÎÀÌ´Ù. À̵é ź¼öÈ­¹°Àº ´ëÀå ±ÕÃÑ¿¡ ÀÇÇÏ¿© ¹ßÈ¿µÇ´Â ÁÖ¿ä ¹°ÁúÀÌ´Ù. ź¼öÈ­¹° ¹ßÈ¿´Â ¸ÍÀåÀÇ pH¸¦ ³·Ãß°í ªÀº »ç½½ Áö¹æ»êÀÇ »ý»êÀ» ¾ß±âÇÑ´Ù. ±×Áß¿¡¼­ ºÎƼ¸£»êÀº Çü¼ºÀÌ»ó º¯È­·ÎºÎÅÍ ´ëÀå »óÇǸ¦ º¸È£ÇÑ´Ù. ´Ü¹éÁú ¼ÒÈ­¿Í ¾Æ¹Ì³ë»ê ¹ßÈ¿µµ ´ëÀå¿¡¼­ ÀϾÁö¸¸ ÃÖÁ¾»ê¹°Àº À¯È¿ÇÑ Åº¼öÈ­¹°ÀÇ ¾ç¿¡ µû¶ó ´Þ¶óÁø´Ù. È°¼º ź¼öÈ­¹°ÀÌ ºÐÇصǴ µ¿¾È ¾Ï¸ð´Ï¾Æ¿Í °°Àº ¾Æ¹Ì³ë»ê ¹ßÈ¿ ÃÖÁ¾»ê¹°Àº ¼¼±ÕÀÌ ´Ü¹éÁú ÇÕ¼ºÀ» Çϱâ À§ÇÑ ¸ñÀûÀ¸·Î »ç¿ëµÈ´Ù. ±×·¯³ª ¹ßÈ¿°¡ Á¦ÇÑµÈ Åº¼Ò¿¡¼­´Â ¾Æ¹Î, ¾Ï¸ð´Ï¾Æ, Æä³î, Àε¹ µîÀÌ ÃàÀûµÈ´Ù. ¹ßÈ¿´Â ¶ÇÇÑ ´ëÀå pHÀÇ º¯È­¸¦ ¾ß±âÇÑ´Ù. pH´Â ´ãÁó»ê, ¾ÆÁú»ê¿°, Ȳ»ê¿°, ±âŸ ´Ù¸¥ ¹°ÁúÀÇ ´ë»ç¸¦ º¯È­½ÃŲ´Ù. ±×·¯¹Ç·Î ¹ßÈ¿´Â »ç¿ëÇÒ ¼ö ÀÖ´Â ¹°Áú¿¡ ÀÇÇÏ¿© ±¤¹üÀ§ÇÏ°Ô Á¶ÀýµÈ´Ù. ƯÈ÷ ½Ä»ç·Î ¼·ÃëÇϴ ź¼öÈ­¹°ÀÇ °æ¿ì´Â ±×·¯ÇÏ´Ù. ´ëÀå »óÇǼ¼Æ÷¿¡¼­ µ¹¿¬º¯À̼º º¯È­¸¦ ÀÏÀ¸Å°°í Á¾¾ç¼ºÀåÀ» ÃËÁøÇÒ ¼ö ÀÖ´Â °¡´É¼ºÀº ¼·ÃëÇÏ´Â ½Ä»ç¿¡ ÀÇÇØ ½±°Ô ¿µÇâÀ» ¹ÞÀ» ¼ö ÀÖ´Ù (Cummings 1987).

 
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Peripheral therapeutic effects[edit]
Butyrate has numerous beneficial effects in humans on energy homeostasis and related diseases (diabetes and obesity), inflammation, and immune function (e.g., it has pronounced antimicrobial and anticarcinogenic effects).[41][46] These effects occur through its utilization by mitochondria to generate ATP during fatty acid metabolism or through one or more of its histone-modifying enzyme targets (i.e., the class I histone deacetylases) and G-protein coupled receptor targets (i.e., FFAR2, FFAR3, and NIACR1).[41]
Immunomodulation and inflammation[edit]
Butyrate's effects on the immune system are mediated through the inhibition of class I histone deacetylases and activation of its G-protein coupled receptor targets: NIACR1 (GPR109A), FFAR2 (GPR43), and FFAR3 (GPR41).[42][47] Among the short-chain fatty acids, butyrate is the most potent promoter of intestinal regulatory T cells in vitro and the only one among the group that is an NIACR1 ligand.[42] It has been shown to be a critical mediator of the colonic inflammatory response. It possesses both preventive and therapeutic potential to counteract inflammation-mediated ulcerative colitis and colorectal cancer.
Butyrate has established antimicrobial properties in humans that are mediated through the antimicrobial peptide LL-37, which it induces via HDAC inhibition on histone H3.[47][48][49] Butyrate increases gene expression of FOXP3 (the transcription regulator for Tregs) and promotes colonic regulatory T cells (Tregs) through the inhibition of class I histone deacetylases;[42][47] through these actions, it increases the expression of interleukin 10, an anti-inflammatory cytokine.[47][42] Butyrate also suppresses colonic inflammation by inhibiting the IFN-¥ã–STAT1 signaling pathways, which is mediated partially through histone deacetylase inhibition. While transient IFN-¥ã signaling is generally associated with normal host immune response, chronic IFN-¥ã signaling is often associated with chronic inflammation. It has been shown that butyrate inhibits activity of HDAC1 that is bound to the Fas gene promoter in T cells, resulting in hyperacetylation of the Fas promoter and up-regulation of Fas receptor on the T-cell surface.[50] It is thus suggested that butyrate enhances apoptosis of T cells in the colonic tissue and thereby eliminates the source of inflammation (IFN-¥ã production).[50]
Similar to other NIACR1 agonists, butyrate also produces marked anti-inflammatory effects in a variety of tissues, including the brain, gastrointestinal tract, skin, and vascular tissue.[51][52][53][54] Butyrate binding at FFAR3 induces neuropeptide Y release and promotes the functional homeostasis of colonic mucosa and the enteric immune system.[55]
Butyric acid is important as an energy (ATP) source for cells lining the mammalian colon (colonocytes). Without butyric acid for energy, colon cells undergo upregulated autophagy (i.e., self-digestion).[56]
Cancer[edit]
Butyrate produces different effects in healthy and cancerous cells; this is known as the "butyrate paradox". In particular, butyrate inhibits colonic tumor cells and promotes healthy colonic epithelial cells.[57] The signaling mechanism is not well understood.[58] A review suggested that the chemopreventive benefits of butyrate depend in part on the amount, time of exposure with respect to the tumorigenic process, and type of fat in the diet.[23] The production of volatile fatty acids such as butyrate from fermentable fibers may contribute to the role of dietary fiber in colon cancer.[23] Short-chain fatty acids, which include butyric acid, are produced by beneficial colonic bacteria (probiotics) that feed on, or ferment prebiotics, which are plant products that contain adequate amounts of dietary fiber. These short-chain fatty acids benefit the colonocytes by increasing energy production and cell proliferation, and may protect against colon cancer.[59]
Conversely, some researchers have sought to eliminate butyrate and consider it a potential cancer driver.[60] Studies in mice indicate it drives transformation of MSH2-deficient colon epithelial cells.[61] It is important to note that these are related to a gene deficiency. Niacin, beta-hydroxybutyrate, and curcumin may be effective adjunct treatments if genetic issues are present.[62][unreliable medical source?]
Diabetes[edit]
A review on the relationship between the microbiome and diabetes asserted that butyrate can induce "profound immunometabolic effects" in animal models and humans with type 2 diabetes;[46] it also noted a relationship between the presence of obesity or diabetes and a state of marked dysbiosis in a host, which is not yet completely understood.[46] While acknowledging that there is strong evidence for the use of butyrate in such disorders, the review called for more research into the pathophysiology (i.e., biomolecular mechanisms) of these diseases, so as to improve therapeutic approaches to these diseases.[46]


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