Protein kinase C activation increases transepithelial transport of biologically active insulin

Protein kinase C activation leads to tight junctional leakiness and, consequently, to increased transepithelial (paracellular) solute flux across epithelial barriers. This leakiness is shown here to result in as much as a 20-fold increase in the transepithelial flux of insulin. Using an epithelial/f...

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Veröffentlicht in:	Cancer research (Chicago, Ill.) Ill.), 1998-04, Vol.58 (8), p.1641-1645
Hauptverfasser:	MULLIN, J. M, GINANNI, N, LAUGHLIN, K. V
Format:	Artikel
Sprache:	eng
Schlagworte:	3T3 Cells Animals Biological and medical sciences Biological Transport Cell physiology Cells, Cultured Coculture Techniques DNA - biosynthesis DNA - drug effects Dose-Response Relationship, Drug Enzyme Activation Epithelium - drug effects Epithelium - physiology Fibroblasts - metabolism Fundamental and applied biological sciences. Psychology General pharmacology Insulin - metabolism Mannitol - metabolism Medical sciences Membrane and intracellular transports Mice Molecular and cellular biology Pharmaceutical technology. Pharmaceutical industry Pharmacology. Drug treatments Protein Kinase C - metabolism Tetradecanoylphorbol Acetate - pharmacology
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