Effects of Arginine Homologues and other Guanidino Compounds on the ATP Level and Glucose Oxidation in Isolated Fat Cells

Abstract

The arginine homologues 2-amino-3-guanidinopropionic acid, 2-amino-4-guanidinobutyric acid and 2-amino-6-guanidinocaproic acid (homoarginine) were synthesized and transformed into their methyl esters. The latter, together with arginine methyl ester, arginine diethylamide and some guanidino compounds without the arginyl structure (agmatine, isopentylguanidine and n-butylbiguanide) were examined with regard to their behavior on isolated rat fat cells, concerning the adrenalin-induced depression of the ATP level and the stimulation of glucose oxidation. The homoarginyl and arginyl deriatives counteracted the effect of adrenaline by re-elevating the ATP level, and thus they exerted an insulin-like activity. The esters were slightly active; the arginine diethylamide and agmatine had a marked effect. The shorter homologues of arginine were totally inactive. Isopentylguanidine and butylbiguanide followed the effect of adrenaline; they additionally lowered the ATP level and acted in oppostion to insulin. For comparative reasons the same compounds were tested with regard to their effects on glucose oxidation. The homoarginyl and arginyl derivatives (agmatine included) forced the glucose oxidation similarly to insulin; the shorter homologues were inactive, and isopentylguanidine and butylibiguanide decreased it.