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Verfasst von:Stremmel, Wolfgang [VerfasserIn]   i
 Staffer, Simone [VerfasserIn]   i
 Wannhoff, Andreas [VerfasserIn]   i
 Pathil-Warth, Anita [VerfasserIn]   i
Titel:The overall fatty acid absorption controlled by basolateral chylomicron excretion under regulation of p-JNK1
Verf.angabe:Wolfgang Stremmel, Simone Staffer, Andreas Wannhoff, Anita Pathil
E-Jahr:2017
Jahr:06 June 2017
Umfang:12 S.
Fussnoten:Gesehen am 25.08.2020
Titel Quelle:Enthalten in: Biochimica et biophysica acta / Molecular and cell biology of lipids
Ort Quelle:Amsterdam : Elsevier, 1998
Jahr Quelle:2017
Band/Heft Quelle:1862(2017), 9, Seite 917-928
ISSN Quelle:1879-2618
Abstract:Suppression of fatty acid absorption is one goal to fight obesity. However, the responsible molecular mechanism is poorly understood. Aim of the present study was the search for the key regulator of the overall fatty acid absorption mechanism and its pharmaceutical modulation. As experimental tool we employed the polarized human intestinal tumor derived cell line CaCo2. Here we showed that influx of fatty acids is mediated by an apical heterotetrameric plasma membrane protein complex of which the calcium-independent membrane phospholipase A2 (iPLA2ß) is one constituent. The newly synthesized bile acid-phospholipid conjugate ursodeoxycholate-lysophosphatidylethanolamide (UDCA-LPE) blocked iPLA2ß, which structurally disrupted the fatty acid-uptake complex. Furthermore, the inhibition of iPLA2ß lead to reduction of cytosolic lysophosphatidylcholine (LPC) production which suppressed p-JNK1, as a central regulator of metabolism. In a concerted action low p-JNK1 levels prohibited synthesis of the members of the fatty acid uptake complex as well as of apolipoprotein B and the connected members of the basolateral vesicular chylomicron excretion machinery, thereby inhibiting cellular lipid excretion. The basolateral chylomicron release was shown to determine the overall fatty acid-absorption capacity as rate limiting step, whereas apical uptake replenishes the cellular stores, enabling continuous transcellular movement of fatty acids. In conclusion, the UDCA-LPE mediated inhibition of p-JNK1 represents a powerful tool to control intestinal absorption of fatty acids and, thus may be employed as a drug to treat obesity.
DOI:doi:10.1016/j.bbalip.2017.05.013
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: http://dx.doi.org/10.1016/j.bbalip.2017.05.013
 Volltext: http://www.sciencedirect.com/science/article/pii/S1388198117301051
 DOI: https://doi.org/10.1016/j.bbalip.2017.05.013
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Bile-acid phospholipid conjugate
 CaCo2 cells
 Calcium-independent phospholipase Aß
 Fatty acid transport
 Lysophosphatidylcholine
 Ursodeoxycholate-lysophosphatidylethanolamide
K10plus-PPN:1574987291
Verknüpfungen:→ Zeitschrift

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