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a microscopic particle of triglycerides produced in the intestines during digestion; in the bloodstream they release their fatty acids into the blood

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/03/25 10:45:40」(JST)

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Schematic image showing a chylomicron

Chylomicrons (from the Greek chylo, meaning juice or milky fluid, and micron, meaning small particle) are lipoprotein particles that consist of triglycerides (85–92%), phospholipids (6–12%), cholesterol (1–3%), and proteins (1–2%).^[1] They transport dietary lipids from the intestines to other locations in the body. Chylomicrons are one of the five major groups of lipoproteins: chylomicrons (a.k.a. ultra low-density lipoprotein), very low-density lipoprotein, intermediate-density lipoprotein, low-density lipoprotein, high-density lipoprotein, that enable fats and cholesterol to move within the water-based solution of the bloodstream.

Function

Chylomicron structure

ApoA, ApoB, ApoC, ApoE (apolipoproteins); T (triacylglycerol); C (cholesterol); green (phospholipids)

Chylomicrons transport lipids absorbed from the intestine to adipose, cardiac, and skeletal muscle tissue, where their triglyceride components are hydrolyzed by the activity of the lipoprotein lipase, allowing the released free fatty acids to be absorbed by the tissues. When a large portion of the triacylglycerol core have been hydrolyzed, chylomicron remnants are formed and are taken up by the liver, hereby transferring dietary fat also to the liver.

Origin

Chylomicrons are formed in the endoplasmic reticulum in the absorptive cells (enterocytes) of the small intestine. The villi, lined with the microvilli of the brush border, provide a lot of surface area for absorption. Newly formed chylomicrons are secreted through the basolateral membrane into the lacteals, where they join lymph to become chyle. The lymphatic vessels carry the chyle to the venous return of the systemic circulation. From there the chylomicrons supply the tissue with fat absorbed from the diet.^[2] Thus, unlike the saccharides and amino acids that digestion liberates from the carbohydrates and proteins of the diet (respectively), the lipids from the diet bypass the hepatic portal system, meaning the liver does not get "first crack" at them.

Stages

There are three stages in the chylomicron's "lifecycle":

Nascent chylomicron
Mature chylomicron
Chylomicron remnant

Nascent chylomicrons

Triglycerides are emulsified by bile and hydrolyzed by the enzyme lipase, resulting in a mixture of fatty acids and monoglycerides. These then pass from the intestinal lumen into the enterocyte, where they are re-esterified to form triacylglycerol. The triacylglycerol is then combined with phospholipids, cholesterol ester, and apolipoprotein B-48 to form a nascent chylomicron. These are then released by exocytosis from enterocytes into lacteals, lymphatic vessels originating in the villi of the small intestine, and are then secreted into the bloodstream at the thoracic duct's connection with the left subclavian vein.

Nascent chylomicrons are composed primarily of triglycerides (85%) and contain some cholesterol and cholesteryl esters. The main apolipoprotein component is apolipoprotein B-48 (apo B-48).

Mature chylomicron

While circulating in blood, chylomicrons exchange components with high-density lipoproteins (HDL). The HDL donates apolipoprotein C-II (APOC2) and apolipoprotein E (APOE) to the nascent chylomicron and, thus, converts it to a mature chylomicron (often referred to simply as "chylomicron"). APOC2 is the coenzyme for lipoprotein lipase (LPL) activity.

Chylomicron remnant

Once triglyceride stores are distributed, the chylomicron returns APOC2 to the HDL (but keeps APOE), and, thus, becomes a chylomicron remnant, now only 30–50 nm. APOB48 and APOE are important to identify the chylomicron remnant in the liver for endocytosis and breakdown.

References

^ Mahmood Hussain, M (January 2000). "A proposed model for the assembly of chylomicrons". Atherosclerosis. 148 (1): 1–15. doi:10.1016/S0021-9150(99)00397-4.
^ Smith, Sareen S. Gropper, Jack L.; Smith, Jack S (2013). Advanced nutrition and human metabolism (6th ed.). Belmont, CA: Wadsworth/Cengage Learning. ISBN 1133104053.

UpToDate Contents

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English Journal

New Insights In Intestinal Sar1B GTPase Regulation and Role in Cholesterol Homeostasis.

Sané A1, Seidman E2, Spahis S1,3, Lamantia V1, Garofalo C1, Montoudis A1, Marcil V1,2, Levy E1,3.
Journal of cellular biochemistry.J Cell Biochem.2015 Oct;116(10):2270-82. doi: 10.1002/jcb.25177.
Sar1B GTPase is a key component of Coat protein complex II (COPII)-coated vesicles that bud from the endoplasmic reticulum to export newly synthesized proteins. The aims of this study were to determine whether Sar1B responds to lipid regulation and to evaluate its role in cholesterol (CHOL) homeosta
PMID 25826777

The Central Role of PCSK9 in Septic Pathogen Lipid Transport and Clearance.

Walley KR1, Francis GA2, Opal SM3, Stein EA4, Russell JA5, Boyd JH6.
American journal of respiratory and critical care medicine.Am J Respir Crit Care Med.2015 Aug 7. [Epub ahead of print]
Microbial cell walls contain pathogenic lipids including lipopolysaccharide (LPS) in gram-negative bacteria, lipoteichoic acid in gram-positive bacteria, and phospholipomannan in fungi. These pathogen lipids are major ligands for innate immune receptors and figure prominently in triggering the septi
PMID 26252194

Familial hypertriglyceridemia: biochemical, clinical and molecular study in a Moroccan family.

Bouabdellah M1, Iraqi H2, Benlian P3, Berqia I2, Benchekroun L1, Chraïbi A2, Chabraoui L1.
Annales de biologie clinique.Ann Biol Clin (Paris).2015 Aug 1;73(4):474-484.
Familial hypertriglyceridemia is a rare autosomal recessive inborn error of metabolism. Mutation within the LPL gene constitutes the first cause of monogenic etiology. Lipoprotein lipase (LPL) is the key enzyme in triglyceride-rich lipoproteins catabolism. Familial LPL deficiency is expressed by eru
PMID 26104879

Japanese Journal

Ultrastructural Demonstration of the Absorption and Transportation of Minute Chylomicrons by Subepithelial Blood Capillaries in Rat Jejunal Villi

TAKAHARA Ei-ichirou,MANTANI Youhei,UDAYANGA Kankanam Gamage Sanath,QI Wang-Mei,TANIDA Takashi,TAKEUCHI Takashi,YOKOYAMA Toshifumi,HOSHI Nobuhiko,KITAGAWA Hiroshi
Journal of Veterinary Medical Science 75(12), 1563-1569, 2013
… Chylomicrons from villous columnar epithelial cells are generally known to be transported only by central lymph vessels (CLV), whereas antigenic particulates derived from the intestinal lumen can also be transported by subepithelial blood capillaries (sBCs) in rat intestinal villi. … The chylomicrons more abundantly presented in villous venules than in arterioles. …
NAID 130003362268

ELISAによるウサギ血清中のImmuno-reactiveアポリポ蛋白B-48の測定

木下誠,松島照彦,真下大和 [他],KOJIMA Masaaki,KIGURE Megumi,TERAMOTO Tamio
Experimental Animals 59(4), 459-467, 2010
… Apolipoprotein B-48 (apoB-48) is produced by the small intestine, is associated with chylomicrons, and appears to be a suitable marker for clinical studies of postprandial dynamics of lipoproteins. …
NAID 130000298606

食事負荷試験におけるインクレチン分泌とカイロミクロン増加との関係

李相翔,平野勉
日本臨床生理学会雑誌 = Japanese journal of applied physiology 39(6), 291-296, 2009-12-01
NAID 10026438905

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[1] Mahmood Hussain, M (January 2000). "A proposed model for the assembly of chylomicrons". Atherosclerosis. 148 (1): 1–15. doi:10.1016/S0021-9150(99)00397-4.

[2] Smith, Sareen S. Gropper, Jack L.; Smith, Jack S (2013). Advanced nutrition and human metabolism (6th ed.). Belmont, CA: Wadsworth/Cengage Learning. ISBN 1133104053.

v t e Lipids: lipoprotein particle metabolism

Lipoprotein particle classes and subclasses	delivery of TGs: Chylomicron VLDL delivery of C and CE: IDL LDL lb LDL sd LDL Lp(a) HDL

Apolipoproteins	APOA 1 2 4 5 APOB APOC 1 2 3 4 APOD APOE APOH SAA SAA1

Extracellular enzymes	LCAT LIPC LPL

Lipid transfer proteins	CETP MTTP PLTP

Cell surface receptors	HDL: SCARB1 IDL: LRP LRP1 LRP1B LRP2 LRP3 LRP4 LRP5 LRP5L LRP6 LRP8 LRP10 LRP11 LRP12 LDL: LDLR LRPAP1

ATP-binding cassette transporter	ABCA1 ABCG5 ABCG8

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chylomicrons