Captopril reverses high glucose-induced effects on LLC-PK1 cells partly by enhancing facilitative glucose transporter messenger RNA expressions.
One of the mechanisms of angiotensin-converting enzyme inhibitors in treating diabetic nephropathy is the reversal of renal hypertrophy. Hyperglycemia is the common denominator of all diabetic states. Thus, effects of captopril on high glucose (27.5 mM)-induced alterations in LLC-PK1 cells were studied as related to the facilitative glucose transporters. We found that high glucose (27.5 mM) inhibited mitogenesis and induced hypertrophy in these cells after 48 hours of culture concomitantly with decreased glucose transporter I messenger RNA expression. Captopril (1 mM) reversed the above effects concomitantly with enhancement of glucose transporter I and II messenger RNA expressions. We conclude that decreased expression of glucose transporter I may be associated with increased intracellular glucose and the resultant ill effects. Captopril reversed the above high glucose-induced effects partly by enhancing glucose transporter I and II messenger RNA expressions.
Yang
M L
ML
Department of Biochemistry, Kaohsiung Medical College, Taiwan.
Guh
J Y
JY
Yang
Y L
YL
Chang
C C
CC
Chuang
L Y
LY
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D002216:Captopril / Q000494:pharmacology*; D002453:Cell Cycle; D002455:Cell Division / Q000187:drug effects; D015870:Gene Expression; D005947:Glucose / Q000494:pharmacology*; D018374:LLC-PK1 Cells; D009004:Monosaccharide Transport Proteins / Q000235:genetics*; D012333:RNA, Messenger; D013552:Swine
D000806:Angiotensin-Converting Enzyme Inhibitors; D009004:Monosaccharide Transport Proteins; D012333:RNA, Messenger; D002216:Captopril; D005947:Glucose