1308:
133:
681:. This condition is caused by mutations in genes such as LPL, APOC-II, APOA-V, LMF1, and GPIHBP1, which are involved in the regulation of triglyceride-rich lipoprotein catabolism. Patients with FCS show significantly elevated fasting concentrations of chylomicrons and do not typically develop premature atherosclerosis due to the large size of chylomicrons preventing their traversal through the vascular endothelial barrier. Diagnosis is confirmed by DNA sequencing for pathogenic mutations in these genes.
652:. Patients with CMRD present with chronic diarrhea, failure to thrive, hypocholesterolemia, and low levels of fat-soluble vitamins. The enterocytes of these patients fail to secrete chylomicrons into the lymph, leading to lipid accumulation and characteristic mucosal changes in the small intestine. Unlike ABL and Ho-HBL, CMRD does not cause acanthocytosis, retinitis pigmentosa, or severe neurological symptoms.
1611:
36:
229:
631:. These mutations lead to apoB truncations or amino acid substitutions, resulting in the formation of short, abnormal apoBs that are unable to bind lipids and form chylomicrons. Clinical manifestations vary, ranging from lack of symptoms to features overlapping with those of ABL, including fat malabsorption and vitamin deficiencies.
535:
Hypochylomicronemia refers to abnormally low levels or complete absence of chylomicrons in the blood, particularly after a meal (postprandial). This condition can result from genetic mutations (see below), as well as certain malabsorption syndromes or deficiencies in dietary fat intake.
606:, and fat accumulation in enterocytes and hepatocytes. The condition also results in multiple vitamin deficiencies (E, A, K, and D) due to impaired lipoprotein assembly and transport. If untreated, ABL can cause neurological disturbances such as spinal-cerebellar degeneration,
214:
There is an inverse relationship in the density and size of lipoprotein particles: fats have a lower density than water or smaller protein molecules, and the larger particles have a higher ratio of internal fat molecules with respect to the outer
219:
protein molecules in the shell. ULDLs, if in the region of 1,000 nm or more, are the only lipoprotein particles that can be seen using a light microscope, at maximum magnification. All the other classes are submicroscopic.
279:
to be absorbed by the tissues. When a large portion of the triglyceride core has been hydrolyzed, chylomicron remnants are formed and are taken up by the liver, thereby also transferring dietary fat to the liver.
427:. From here, chylomicrons can supply tissue throughout the body with fat absorbed from the diet. Because they enter the bloodstream in this way, digested lipids (in the form of chylomicrons) bypass the
627:(Ho-HBL; OMIM 107730) is an extremely rare inherited disorder characterized by improper packaging and secretion of apoB-containing lipoproteins due to mutations in both alleles of the
482:
while retaining APOE, transforming into a chylomicron remnant. ApoB48 and APOE are important to identify the chylomicron remnant in the liver for endocytosis and breakdown.
1530:
1510:
1214:
1013:
564:
and become trapped in the subendothelial space. This process enhances the deposition of cholesterol in the arterial wall, which is a critical step in the formation of
1558:
549:
Chylomicron remnants are the lipoprotein particles left after chylomicrons have delivered triglycerides to tissues. Elevated levels of these remnants contribute to
344:
proteins. The transport of nascent chylomicrons within the secretory pathway is facilitated by protein transport vesicles (PCTVs). PCTVs are uniquely equipped with
1307:
132:
602:. This genetic defect leads to nearly undetectable levels of ApoB and very low plasma cholesterol levels. Patients with ABL exhibit fat malabsorption,
1420:
1453:
599:
359:
During transit through the Golgi, nascent chylomicrons undergo enzymatic modification and lipidation processes, resulting in the formation of
967:
842:
349:
321:(smooth ER), where they are re-esterified to form triglycerides. These triglycerides, along with phospholipids and cholesterol, are added to
1485:
1207:
997:
623:
1448:
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119:
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1271:
1200:
57:
1458:
1440:
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100:
1601:
1257:
318:
72:
53:
722:
Gofman, John W.; Jones, Hardin B.; Lindgren, Frank T.; Lyon, Thomas P.; Elliott, Harold A.; Strisower, Beverly (1950).
79:
46:
271:, cardiac, and skeletal muscle tissue, where their triglyceride components are hydrolyzed by the activity of the
495:
Hyperchylomicronemia is characterized by an excessive presence of chylomicrons in the blood, leading to extreme
1292:
479:
455:
298:
774:
Schwenk, Robert W.; Holloway, Graham P.; Luiken, Joost J. F. P.; Bonen, Arend; Glatz, Jan F. C. (2010-04-01).
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554:
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432:
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68:
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proteins, including Sec23/24, which select cargo and facilitate vesicle budding from the ER membrane.
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611:
590:
496:
372:
352:
proteins, which aid in their fusion with the cis-Golgi compartment. This transport is facilitated by
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1007:
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467:
420:
272:
1032:
Julve, Josep; Martín-Campos, Jesús M.; Escolà-Gil, Joan Carles; Blanco-Vaca, Francisco (2016).
775:
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993:
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314:
519:. This condition can be caused by genetic mutations (see below) or secondary factors such as
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93:
1137:
Giammanco, Antonina; Cefalù, Angelo B.; Noto, Davide; Averna, Maurizio R. (2015-03-20).
887:
Giammanco, Antonina; Cefalù, Angelo B.; Noto, Davide; Averna, Maurizio R. (2015-03-20).
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959:
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888:
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550:
512:
440:
240:
776:"Fatty acid transport across the cell membrane: Regulation by fatty acid transporters"
203:. ULDLs are one of the five major groups lipoproteins are divided into based on their
1625:
1033:
947:
561:
416:
345:
302:
1034:"Chylomicrons: Advances in biology, pathology, laboratory testing, and therapeutics"
568:. The retention and modification of these remnants within the arterial wall trigger
1553:
1248:
821:
Kiani, Reza (2018-01-01), Maleki, Majid; Alizadehasl, Azin; Haghjoo, Majid (eds.),
649:
569:
436:
294:
260:
176:
172:
760:
466:(APOE) to the mature chylomicron. APOC2 is a crucial coenzyme for the activity of
614:. Early supplementation of fat-soluble vitamins can prevent these complications.
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1227:
791:
603:
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35:
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863:
1049:
946:
Bodewes, Frank A.J.A.; Wouthuyzen-Bakker, Marjan; Verkade, Henkjan J. (2015),
524:
448:
376:
336:
After synthesis in the smooth ER, nascent chylomicrons are transported to the
310:
306:
196:
1164:
1155:
1098:
914:
905:
799:
560:
Recent studies have demonstrated that chylomicron remnants can penetrate the
317:. Inside these cells, monoglycerides and fatty acids are transported to the
17:
1182:
1116:
1057:
932:
807:
752:
743:
1089:
674:
520:
500:
403:
that contains chylomicrons (and other emulsified fats) is referred to as
228:
478:
Once triglyceride stores are distributed, chylomicrons return APOC2 to
444:
384:
268:
204:
199:
to other locations in the body, within the water-based solution of the
184:
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188:
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1196:
192:
29:
267:
Chylomicrons transport lipids absorbed from the intestine to
470:(LPL), which hydrolyzes triglycerides within chylomicrons.
1139:"The pathophysiology of intestinal lipoprotein production"
988:
Smith, Sareen S. Gropper, Jack L.; Smith, Jack S. (2013).
889:"The pathophysiology of intestinal lipoprotein production"
992:(6th ed.). Belmont, CA: Wadsworth/Cengage Learning.
780:
Prostaglandins, Leukotrienes and
Essential Fatty Acids
1599:
325:
48 to form nascent chylomicrons (also referred to as
598:
disorder caused by mutations in both alleles of the
1567:
1467:
1439:
1410:
1315:
1235:
553:, which is considered an important risk factor for
499:. Clinical manifestations of this disorder include
60:. Unsourced material may be challenged and removed.
1073:"The Chylomicron: Relationship to Atherosclerosis"
948:"Persistent Fat Malabsorption in Cystic Fibrosis"
545:Chylomicron remnants and cardiovascular disease
1208:
458:(HDLs) donate essential components including
371:Mature chylomicrons are released through the
8:
1012:: CS1 maint: multiple names: authors list (
618:Homozygous hypobetalipoproteinemia (Ho-HBL)
27:One of the five major groups of lipoprotein
1215:
1201:
1193:
1077:International Journal of Vascular Medicine
572:, further accelerating the development of
1172:
1154:
1106:
1088:
1071:Tomkin, Gerald H.; Owens, Daphne (2012).
922:
904:
742:
120:Learn how and when to remove this message
724:"Blood Lipids and Human Atherosclerosis"
227:
207:. A protein specific to chylomicrons is
1606:
990:Advanced nutrition and human metabolism
690:
656:Familial chylomicronemia syndrome (FCS)
297:are emulsified by bile and digested by
1005:
1132:
1130:
1128:
1126:
136:Schematic image showing a chylomicron
7:
1027:
1025:
1023:
952:Diet and Exercise in Cystic Fibrosis
648:disorder caused by mutations in the
635:Chylomicron retention disease (CMRD)
58:adding citations to reliable sources
960:10.1016/b978-0-12-800051-9.00041-9
864:"SAR1B gene: MedlinePlus Genetics"
835:10.1016/b978-0-323-51149-0.00018-3
624:Homozygous hypobetalipoproteinemia
25:
662:Familial chylomicronemia syndrome
309:. These lipids are absorbed into
1609:
1306:
673:, abdominal pain, pancreatitis,
301:, resulting in the formation of
293:In the small intestine, dietary
34:
644:(CMRD; OMIM #607689) is a rare
187:(1–2%). They transport dietary
45:needs additional citations for
954:, Elsevier, pp. 373–381,
829:, Elsevier, pp. 303–309,
669:, is characterized by massive
161:ultra low-density lipoproteins
1:
641:Chylomicron retention disease
594:(ABL; OMIM 200100) is a rare
699:"Definition of CHYLOMICRONS"
454:While circulating in blood,
319:smooth endoplasmic reticulum
151:(of plants or animals), and
823:"Chapter 18 - Dyslipidemia"
792:10.1016/j.plefa.2010.02.029
667:Type I hyperlipoproteinemia
1648:
585:Abetalipoproteinemia (ABL)
195:and cholesterol, from the
1304:
1050:10.1016/j.cca.2016.02.004
580:Related genetic disorders
456:high-density lipoproteins
1156:10.3389/fphys.2015.00061
906:10.3389/fphys.2015.00061
275:, allowing the released
1441:Lipid transfer proteins
1143:Frontiers in Physiology
893:Frontiers in Physiology
703:www.merriam-webster.com
608:peripheral neuropathies
566:atherosclerotic plaques
143:(from the Greek χυλός,
1469:Cell surface receptors
744:10.1161/01.cir.2.2.161
570:inflammatory responses
555:cardiovascular disease
264:
237:ApoA, ApoB, ApoC, ApoE
137:
665:(FCS), also known as
521:uncontrolled diabetes
433:first pass metabolism
429:hepatic portal system
415:before it enters the
411:carries chyle to the
409:lymphatic circulation
389:lymphatic capillaries
327:immature chylomicrons
233:Chylomicron structure
231:
169:lipoprotein particles
135:
1571:cassette transporter
1038:Clinica Chimica Acta
827:Practical Cardiology
671:hypertriglyceridemia
612:retinitis pigmentosa
591:Abetalipoproteinemia
525:alcohol use disorder
497:hypertriglyceridemia
491:Hyperchylomicronemia
474:Chylomicron remnants
373:basolateral membrane
289:Nascent chylomicrons
54:improve this article
1298:Remnant cholesterol
1230:particle metabolism
1090:10.1155/2012/784536
646:autosomal recessive
596:autosomal recessive
531:Hypochylomicronemia
460:apolipoprotein C-II
367:Mature chylomicrons
361:mature chylomicrons
679:hepatosplenomegaly
675:eruptive xanthomas
517:acute pancreatitis
509:hepatosplenomegaly
505:lipaemia retinalis
501:eruptive xanthomas
468:lipoprotein lipase
435:, unlike digested
299:pancreatic lipases
273:lipoprotein lipase
265:
138:
1597:
1596:
969:978-0-12-800051-9
844:978-0-323-51149-0
540:Related disorders
381:secretory pathway
315:passive diffusion
159:), also known as
130:
129:
122:
104:
16:(Redirected from
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1239:particle classes
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771:
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728:
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709:
695:
464:apolipoprotein E
447:(in the form of
439:(in the form of
425:subclavian veins
419:of the systemic
331:pre-chylomicrons
323:apolipoprotein B
277:free fatty acids
171:that consist of
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1317:Apolipoproteins
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868:medlineplus.gov
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574:atherosclerosis
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441:monosaccharides
431:and thus avoid
413:lymphatic ducts
397:small intestine
369:
338:Golgi apparatus
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249:triacylglycerol
241:apolipoproteins
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1411:Extracellular
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999:978-1133104056
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786:(4): 149–154.
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737:(2): 161–178.
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551:hyperlipidemia
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513:abdominal pain
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303:monoglycerides
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562:tunica intima
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173:triglycerides
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110:December 2009
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71: –
70:
69:"Chylomicron"
66:
65:Find sources:
59:
55:
49:
48:
43:This article
41:
37:
32:
31:
19:
1632:Lipoproteins
1569:ATP-binding
1262:delivery of
1252:
1247:delivery of
1146:
1142:
1080:
1076:
1066:
1041:
1037:
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52:Please help
47:verification
44:
18:Chylomicrons
1253:Chylomicron
1237:Lipoprotein
1228:lipoprotein
1044:: 134–148.
731:Circulation
604:steatorrhea
449:amino acids
421:circulation
377:enterocytes
311:enterocytes
307:fatty acids
257:cholesterol
217:emulsifying
201:bloodstream
181:cholesterol
975:2024-06-29
873:2022-12-06
850:2022-12-06
708:2024-04-26
685:References
650:SAR1B gene
259:); green (
197:intestines
191:, such as
175:(85–92%),
155:, meaning
147:, meaning
80:newspapers
1165:1664-042X
1099:2090-2824
1008:cite book
915:1664-042X
800:0952-3278
629:APOB gene
486:Pathology
379:(via the
179:(6–12%),
1626:Category
1183:25852563
1117:22007304
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1058:26868089
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753:15427204
600:MTP gene
445:proteins
385:lacteals
224:Function
185:proteins
1616:Biology
1413:enzymes
1174:4367171
1108:3189596
924:4367171
395:of the
391:in the
383:) into
346:v-SNARE
269:adipose
205:density
167:), are
94:scholar
1602:Portal
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284:Stages
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189:lipids
153:micron
145:chylos
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1584:ABCG5
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1536:LRP10
1521:LRP5L
1496:LRP1B
1484:IDL:
1476:HDL:
1354:APOC
1324:APOA
1288:Lp(a)
757:S2CID
727:(PDF)
405:chyle
401:Lymph
393:villi
354:COPII
342:SAR1B
157:small
149:juice
101:JSTOR
87:books
1554:LDLR
1531:LRP8
1526:LRP6
1516:LRP5
1511:LRP4
1506:LRP3
1501:LRP2
1491:LRP1
1459:PLTP
1454:MTTP
1449:CETP
1426:LIPC
1421:LCAT
1400:SAA1
1390:APOH
1385:APOE
1380:APOD
1350:APOB
1266:and
1258:VLDL
1179:PMID
1161:ISSN
1113:PMID
1095:ISSN
1081:2012
1054:PMID
1014:link
994:ISBN
964:ISBN
929:PMID
911:ISSN
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796:ISSN
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480:HDLs
423:via
348:and
313:via
305:and
193:fats
165:ULDL
73:news
1486:LRP
1431:LPL
1395:SAA
1293:HDL
1277:LDL
1272:IDL
1249:TGs
1169:PMC
1151:doi
1103:PMC
1085:doi
1046:doi
1042:455
956:doi
919:PMC
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