Hepatocytus

Hepatocytus (-i, m.) (e verbis Graecis ἡπατο- 'iecoris' atque κύτος 'cavum') est cellula parenchymatis iecoris (vid. fig. I.). Circiter cellularum dodrans iecoris hepatocyti sunt.^[1] Principalia organismi munera sunt anabolica (synthesis, aedificationis, anabolismi) velut catabolica (degradationis, catabolismi) sic enim substantiae chemicae ex vasorum sanguine et venae portae (hepatis) ab apparatu digestorio et arteriae hepaticae propriae a cetero corpore in iecur intrantes ad hepatocytos adveniunt.

Cave: notitiae huius paginae nec praescriptiones nec consilia medica sunt.

Situs intra iecur (anatomia)

Conferatur pagina principalis iecur.

Fig. II. Trabeculum hepatocytorum. In funiculo ordinatis hepatocytis intra iecur forma cuboidea est. Secundum hepatocytos sanguinis vasorum endothelia fenestrata sunt. Flux sanguinis de triade portali ad venulam centralem est (vid. sagittam nigram, a sinistra ad dextram). portal field trias portalis (Glissonii)^[2], portal venule venula portalis (a vena portae, colore caeruleo), hepatic arteriole arteriola hepatica (ab arteria hepatica propria, colore rubro), sinusoid vena intralobularis (colore caesio), central vein vena centralis, Kupffer cell cellula (sideralis) Kupfferi, space of Disse spatium perisinusoidale (Disse), stellate cell cellula sideralis (Ito), bile ductule ductulus biliaris (colore viridi) cum cellulis minoribus cholangiocytis epithelio (sinistra).

Hepatocyti intra iecur in funiculis ("trabeculum hepatocytorum") ordinati (vid. fig. II.) sunt. Ad metabolismum substantiae chemicae ab apparatu digestorio per venam portae et venulam portalem (colore caeruleo) atque a cetero corpore per arteriam hepaticam propriam et arteriola hepatica communiter (colore rubro) perfluunt venam intralobularem (colore caesio) ubi illae trans spatium perisinusoidalem attingunt hepatocytos, qui substantias chemicas accipiunt. Tum sanguis in venam centralem deinde in corpus defluit. Substantiae non hepatocytis acceptae sed in spatio perisinusoidali remansae non in sanguinem sed in lympham systematis lymphacei transeunt.

Ex adverso ductulus biliaris, qui bilem (colore viridi) in ductum biliarem transfert, cum cholangiocytis epithelio situs est.

Anatomia microscopica

Fig. III. Hepatocytis mitochondria magna sunt. Amplificatio: 400x.

Sub microscopio metitur diametrum hepatocytorum 20 – 30 µm (pilus hominis: 17 - 180 µm).

Polaritas membranis plasmaticis diversis hepatocytorum

Hepatocyti finem inter sanguinem et bilem formant. Pro ea re circum hepatocytum duo typi membranarum plasmaticarum inveniuntur, membrana enim plasmatica basolateralis (sive sinusoidalis) et membrana plasmatica apicalis (sive canalicularis). Haec polaritas in structuram functionesque hepatocyti maximum momentum habet^[3].

Membrana plasmatica basolateralis

Membrana plasmatica basolateralis et venae intralobulari et hepatocytis proximis adversa est. Hepatocyti microvillos in spatio perisinusoidali (Disse, vid. fig. II.) permutationem hoc modo substantiarum permittentes porrigunt.

Membrana plasmatica apicalis

Communiter cum hepatocyto proximo membrana ductulo biliaro apicalis adversa est. Ubi commutatio bilirubinorum fit.

Intra hepatocytum (cytoplasma, cytosceletus, organella)

Capacitas est 3.4 x 10⁻⁹ cm³.^[4] Cellulae cum forma cuboidea multis reticulis endoplasmaticis non granulosis locupletatae. Hepatocytis unus vel duo nuclei et magna mitochondria (vid. Fig. III) sunt. Mitochondriis his multis microscopio spectatum cytoplasma inquisitori eosinophile se dat^[5].

Munera hepatocytorum (biochemia et physiologia)

Ne longum est quidem dicere iecur computatrum metabolismi et hepatocytos suos enim partes illius procestri, nam hepatocyti inter multos organismi reactiones perficiunt:

Glycogenolysis — abscissio glucoso-6-phosphatum et glycogenum (n-1) a glycogeno (n) (in cytoplasmate)
Gluconeogenesis — aedificatio glucosum a substantiis non hydratorum carbonii (in cytoplasmate et mitochondriis)
Glycogenogenesis — additio molecularum glucosi in catenam ita glycogenum formans (in cytoplasmate)
Glycolysis
Metabolismus lipidorum
Conversio ammonii venenati ad uream: cyclus ureae (in mitochondriis)
Proteinorum synthesis et degradatio (in reticulo endoplasmatico granuloso)
Synthesis factorum coagulationis sanguinis (grex prothrombini praeter factores III (factor telarius) et IV (calcium), in reticulo endoplasmatico granuloso)
Synthesis et secretio bilis (in reticulo endoplasmatico non granuloso et apparatu Golgiano)
Secretio α1-antitrypsini (A1AT)^[6]
Substantiarum detoxificatio et modificatio

Zonae metabolicae

Nunc vero flux sanguinis de triade portali ad venulam centralem fit. Etsi reactiones omnibus hepatocytis perficiuntur, pondera omnino reactionum istarum non ubique eadem esse videtur. Iam ab anno 1953 differentiae distributionis enzymorum hepaticorum descriptae sunt^[7]^[8]. Concentratio ipsa oxygenii in sanguine de triade portali ad venulam centralem deminuens expressionem genorum enzymorum iubet ut zonae metabolicae - afferens et efferens - orientur^[9]. Quo fit, ut hepatocytos cum diversis functionum suarum momentis sibi forment: In parte priori enim, circum triadem portalem, hepatocytorum muneribus imprimis glycogenolysis et gluconeogenesis et immunologicis velut bilem formationis, in parte vero posteriori, circum venulam centralem, glycogenogenesis et glycolysis et lipogenesis et glutamini formationis et xenobioticorum metabolismi fusius fungantur^[10].

Iter de microvillis ad cytoplasma (aditus per membranam plasmaticam basolateralem)

In spatio perisinusoidale (Disse) hepatocytus microvillis (cum pluribus enzymis) substantias afferentes absorptionis accipit, sic illae sine vel cum mutatione prima per microfilamenta (actinum) adveniunt in cytoplasma, ubi secundum finem aliae structurae intra cellulam reactiones biochemicas expediant.

Reticulum endoplasmaticum non granulosum

Reticulum endoplasmaticum hepatocyti non granulosum cytochromata (CYP) et UDP-glucuronosyltransferases (UGT) continet^[11].
In inflammatione graviori hepatocytorum reticulum endoplasmaticum corripi atque inflammasoma NLRP3 macrophagocytis stellatis incitari videtur^[12]. Dehinc nonnulli morbi ut diabetes mellitus, obesitas, cancer hepatocellularis prodere queant.

Interactiones alias cellulas (non hepatocytos)

Non paucae functiones solum cum mutuis effectibus aliarum cellularum (cellulae Kupfferi, cellulae siderales, cellulae endotheliales vasorum) iecoris sunt.

Facultas regenerandi

Facultas hepatocytorum iecur regenerandi notabilis est. Per hypertrophiam (capacitatis incrementum) hepatocytorum atque per hyperplasiam (numeri incrementum) fit, ut pars quoque iecoris ad magnitudinem principalem apte perveniatur. Expansio differentiatioque cellularum praecursoriarum non multum valere videtur.^[13]

Numerus circadianus

Conferatur pagina principalis Numerus circadianus.

Ut pluribus corporis textibus etiam hepatocytis horologia interna (horologia peripherica) sunt, quae rhythms circadianos sustinent^[14].

Functionum perturbationes et affectus morbosi (pathobiochemia et pathophysiologia)

Ut indicat quantitas mitochondriorum consumptio enim hepatocytorum oxygenii maior est. Per exemplum, perturbationes functionis phosphorylationis oxidativae perturbationes morbosque efficiant.

Icterus hepatocellularis

Conferatur pagina principalis icterus.

Icterus est signum bilirubini vis in sanguine auctior. Ex typis icteri tribus, qui sunt praehepaticum (icterus haemolyticus) et hepaticum (icterus hepatocellularis) et posthepaticum (icterus cholestaticum), solum autem typus hepaticus causa perturbationum hepatocytorum ipsorum est. Pertubati enim hepatocyti bilem non in ductuli biliares abducunt, igitur multitudo bilirubini maior per venas interlobulares in sanguine apparet. Consumpta, potissimum diutissime multumque, hepatocytis phosphorus, arsenicum, chloroformium velut (de amanita) α-amanitinum, phalloidinum, virotaxinum venena hepatica periculosa sunt seque icterum hepatocellularem praebent.

Carcinoma hepatocellulare

Conferatur pagina principalis carcinoma hepatocellulare.

Carcinoma hepatocellulare in orbe terrarum secunda causarum mortis cancris sociatae^[15]. Plerumque comites aliarum perturbationum chronicarum, ut cirrhosis hepatis, hepatitis B, hepatitis C, steatohepatitis, abusus androgenorum, contagionis aflatoxini aspergilli flavi, haemochromatosis velut vitium α1-antitrypsini (Syndroma Laurell-Eriksson), postremo transformatio in carcinomam accidat. Tractatio istius cancri transplantationem vel ablationem chirurgicam vel chemoembolisationem vel radiotherapiam vel chemotherapiam continet.

Senectus

In senectute hepatocytis non raro sunt inclusiones lipofuscini^[16], quod pigmentum fulvum mutationes et perturbationes membranorum vel mitochondriorum vel lysosomatum indicet.

Nexus interni

Notae

↑ De iecoris organogenesi.
↑ Glissionius F (1681). Anatomia hepatis.
↑ Gissen P, Arias IM (Oct 2015). "Structural and functional hepatocyte polarity and liver disease". J Hepatol 63 (4): 1023-37
↑ Lodish H, Berk A, Zipursky SL, Matsudaira P, Baltimore D, Darnell JE (2000): Molecular Cell Biology (editio quinta). W. H. Freeman et Company. Novum Eboracum, pagg. 10
↑ Universitas civitatis Colorati: De histologia hepatocytorum.
↑ Lockett AD (2017). "Alpha-1 Antitrypsin Transcytosis and Secretion". Methods Mol Biol (1639:173-184)
↑ Chiquoine AD (1953). "The Distribution of Glucose 6-phosphatase in the liver and kidney of the mouse". J Histochem Cytochem 1: 429-35
↑ Schuhmacher HH (1957). "Histochemical Distribution pattern of respiratory enzymes in the liver lobule". Science 125: 501-3
↑ Jungermann K, Kietzmann T (1997). "Role of Oxygen in the zonation of carbohydrate metabolism and gene Expression in liver". Kidney Int 51: 402-12
↑ Jungermann K, Katz N (1989). "Functional specialization of different hepatocyte populations". Physiol Rev 69 (3): 708-64
↑ den Braver-Sewradj S. P., den Braver M. W., Baze A., Decorde J., Fonsi M., Bachellier P., Vermeulen N. P. E., Commandeur J. N. M., Richert L., Vos J. C. (2017). "Direct comparison of UDP-glucuronosyltransferase and cytochrome P450 activities in human liver microsomes, plated and suspended primary human hepatocytes from five liver donors". Eur J Pharm Sci (109:96-110) . Microsomata sunt partes reticuli endoplasmatici non granulosi abruptae artificiosae.
↑ Lebeaupin C., Proics E., de Bieville C. H., Rousseau D., Bonnafous S., Patouraux S., Adam G., Lavallard V. J., Rovere C., Le Thuc O., Saint-Paul M. C., Anty R., Schneck AS., Iannelli A., Gugenheim J., Tran A., Gual P., Bailly-Maitre B. (2015). "ER stress induces NLRP3 inflammasome activation and hepatocyte death". Cell Death Dis 6: e1879
↑ Kholodenko IV, Yarygin KN (2017). "Cellular Mechanisms of Liver Regeneration and Cell-Based Therapies of Liver Diseases". Biomed Res Int (2017:8910821)
↑ Guan D., Xiong Y., et al. (Sep 2020). "The hepatocyte clock and feeding control chronophysiology of multiple liver cell types". Science 369 (6509): 1388-94
↑ Gosalia AJ, Martin P, Jones PD (Iul 2017). "Advances and Future Directions in the Treatment of Hepatocellular Carcinoma". Gastroenterol Hepatol (N Y) 13 (7): 398-410
↑ Gaugler C (1997). Lipofuscin , Stanislaus Journal of Biochemical Reviews

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[1] De iecoris organogenesi.

[2] Glissionius F (1681). Anatomia hepatis.

[3] Gissen P, Arias IM (Oct 2015). "Structural and functional hepatocyte polarity and liver disease". J Hepatol 63 (4): 1023-37

[4] Lodish H, Berk A, Zipursky SL, Matsudaira P, Baltimore D, Darnell JE (2000): Molecular Cell Biology (editio quinta). W. H. Freeman et Company. Novum Eboracum, pagg. 10

[5] Universitas civitatis Colorati: De histologia hepatocytorum.

[6] Lockett AD (2017). "Alpha-1 Antitrypsin Transcytosis and Secretion". Methods Mol Biol (1639:173-184)

[7] Chiquoine AD (1953). "The Distribution of Glucose 6-phosphatase in the liver and kidney of the mouse". J Histochem Cytochem 1: 429-35

[8] Schuhmacher HH (1957). "Histochemical Distribution pattern of respiratory enzymes in the liver lobule". Science 125: 501-3

[9] Jungermann K, Kietzmann T (1997). "Role of Oxygen in the zonation of carbohydrate metabolism and gene Expression in liver". Kidney Int 51: 402-12

[10] Jungermann K, Katz N (1989). "Functional specialization of different hepatocyte populations". Physiol Rev 69 (3): 708-64

[11] Braver-Sewradj S. P., den Braver M. W., Baze A., Decorde J., Fonsi M., Bachellier P., Vermeulen N. P. E., Commandeur J. N. M., Richert L., Vos J. C. (2017). "Direct comparison of UDP-glucuronosyltransferase and cytochrome P450 activities in human liver microsomes, plated and suspended primary human hepatocytes from five liver donors". Eur J Pharm Sci (109:96-110) . Microsomata sunt partes reticuli endoplasmatici non granulosi abruptae artificiosae.

[12] Lebeaupin C., Proics E., de Bieville C. H., Rousseau D., Bonnafous S., Patouraux S., Adam G., Lavallard V. J., Rovere C., Le Thuc O., Saint-Paul M. C., Anty R., Schneck AS., Iannelli A., Gugenheim J., Tran A., Gual P., Bailly-Maitre B. (2015). "ER stress induces NLRP3 inflammasome activation and hepatocyte death". Cell Death Dis 6: e1879

[13] Kholodenko IV, Yarygin KN (2017). "Cellular Mechanisms of Liver Regeneration and Cell-Based Therapies of Liver Diseases". Biomed Res Int (2017:8910821)

[14] Guan D., Xiong Y., et al. (Sep 2020). "The hepatocyte clock and feeding control chronophysiology of multiple liver cell types". Science 369 (6509): 1388-94

[15] Gosalia AJ, Martin P, Jones PD (Iul 2017). "Advances and Future Directions in the Treatment of Hepatocellular Carcinoma". Gastroenterol Hepatol (N Y) 13 (7): 398-410

[gaugler-16] Gaugler C (1997). Lipofuscin , Stanislaus Journal of Biochemical Reviews

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