These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Na+-independent sugar transport by cultured renal (LLC-PK1) epithelial cells.
    Author: Mullin JM, McGinn MT, Snock KV, Kofeldt LM.
    Journal: Am J Physiol; 1989 Jul; 257(1 Pt 2):F11-7. PubMed ID: 2750915.
    Abstract:
    The LLC-PK1 cell line has been well characterized concerning its proximal tubule-like Na+-dependent active sugar transporter in the apical membrane. In this study, we investigated the uptake of the glucose analogue, 2-deoxy-D-glucose (2DOG), a paradigm substrate for the facilitated diffusion, Na+-independent sugar transporter in the renal basolateral membrane. The uptake of 0.1 mM 2-[14C]DOG by confluent LLC-PK1 cell sheets at 25 degrees C is linear at least to 10 min, at which time greater than 90% of intracellular radioactivity is 2DOG phosphate. The uptake of this analogue by LLC-PK1 cells is Na+ independent, and the transporter appears to be localized to the basolateral cell membrane. Phlorizin is a much less effective inhibitor than its aglycon, phloretin. Cytochalasin B is also an effective inhibitor, but it causes morphological changes in the cells at concentrations required to inhibit transport. Specificity studies indicate that this transport system requires a hexose with a free hydroxyl at C-1, and that the hydroxyls at C-3 and C-4 be preferably in the equatorial position. Glucose starvation causes an increased rate of 2DOG uptake. Subconfluent (cycling) cultures of LLC-PK1 cells have a threefold greater rate of 2DOG uptake than that seen in confluent (noncycling) LLC-PK1 cells.
    [Abstract] [Full Text] [Related] [New Search]