The LLC-PK1 cell line is unique in its ability to actively transport sugar. Its Na+-dependent sugar transport system makes it an excellent model system for sugar reabsorption by the proximal tubule of mammalian kidney. Like other cell lines, this culture is acclaimed as having inherent advantages relative to the tissue to which it relates, such as: homogeneity of cell type; the ability to return at any future date to the same biological material with which a study was performed by simply thawing cells stored in liquid nitrogen; the ability to grow as much material as is required; the ability to work with both cycling and non-cycling cells; the opportunity to utilize genetic techniques on problems of physiological interest. It is this last advantage which this proposal focuses upon, specifically the isolation of two types of LLC-PD1 mutants: 2) a subline defective in active sugar transport; and 1) a subline capable of gluconeogenesis. The first purpose of this selection scheme will be to acquire a mutant sugar transporter to study structure-function relations of the isolated transport proteins. The second long range goal, in which both types of mutants would be involved, is to study the possible interrelationships of active sugar transport and cellular metabolism, specifically renal gluconeogenesis.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
7R01DK037977-01
Application #
3237053
Study Section
Physiological Chemistry Study Section (PC)
Project Start
1986-03-01
Project End
1989-02-28
Budget Start
1986-03-01
Budget End
1987-02-28
Support Year
1
Fiscal Year
1986
Total Cost
Indirect Cost
Name
Lankenau Hospital
Department
Type
DUNS #
City
Wynnewood
State
PA
Country
United States
Zip Code
19096
Mullin, J M; Kofeldt, L M; Russo, L M et al. (1992) Basolateral 3-O-methylglucose transport by cultured kidney (LLC-PK1) epithelial cells. Am J Physiol 262:F480-7
Mullin, J M; McGinn, M T; Snock, K V et al. (1989) Na+-independent sugar transport by cultured renal (LLC-PK1) epithelial cells. Am J Physiol 257:F11-7
Mullin, J M; Snock, K V; McGinn, M T et al. (1989) Isolation of mutant renal (LLC-PK1) epithelia defective in basolateral, Na(+)-independent glucose transport. Am J Physiol 257:F1039-49
Mullin, J M; McGinn, M T (1988) Epidermal growth factor-induced mitogenesis in kidney epithelial cells (LLC-PK1). Cancer Res 48:4886-91
Mullin, J M; McGinn, M T (1988) Effects of diacylglycerols on LLC-PK1 renal epithelia: similarity to phorbol ester tumor promoters. J Cell Physiol 134:357-66
Mullin, J M; O'Brien, T G (1987) Spontaneous reversal of polarity of the voltage across LLC-PK1 renal epithelial cell sheets. J Cell Physiol 133:515-22
Mullin, J M; McGinn, M T (1987) The phorbol ester, TPA, increases transepithelial epidermal growth factor flux. FEBS Lett 221:359-64