TY - JOUR
T1 - Impairment of induction of Δ-aminolevulinic acid synthase by gluconeogenic amino acids and carbohydrates in vitro
AU - Schoenfeld, N.
AU - Greenblat, Y.
AU - Epstein, O.
AU - Beigel, Y.
AU - Atsmon, A.
PY - 1985/2
Y1 - 1985/2
N2 - This study was undertaken in a system of chick embryo liver cells incubated in Earle's Basal Salt Solution with hormones. Impairment of induction of Δ-aminolevulinic acid synthase (ALAS) by allyl-isopropylacetamide (AIA) was observed in the presence of glucose. Fructose and various gluconeogenic substances including gluconeogenic amino acids had a similar effect. Leucine, which is purely ketogenic, did not influence induction of ALAS. SH-containing amino acids increased induction of ALAS by AIA. The glucose analogues 3-0-methylglucose and 2-deoxyglucose did not impair induction of ALAS by AIA. The inhibitory effect of glycerol, fructose, and glycine was not affected by 3-0-methylglucose but was reversed by 2-deoxyglucose. The results indicate that the salutory effects of proteins on acute attacks of hepatic porphyria are probably caused by their gluconeogenic properties and that glucose-6-phosphate, or a metabolite of glucose-6-phosphate that is not in the glycolytic pathway, is the active agent that leads to the glucose-like effect.
AB - This study was undertaken in a system of chick embryo liver cells incubated in Earle's Basal Salt Solution with hormones. Impairment of induction of Δ-aminolevulinic acid synthase (ALAS) by allyl-isopropylacetamide (AIA) was observed in the presence of glucose. Fructose and various gluconeogenic substances including gluconeogenic amino acids had a similar effect. Leucine, which is purely ketogenic, did not influence induction of ALAS. SH-containing amino acids increased induction of ALAS by AIA. The glucose analogues 3-0-methylglucose and 2-deoxyglucose did not impair induction of ALAS by AIA. The inhibitory effect of glycerol, fructose, and glycine was not affected by 3-0-methylglucose but was reversed by 2-deoxyglucose. The results indicate that the salutory effects of proteins on acute attacks of hepatic porphyria are probably caused by their gluconeogenic properties and that glucose-6-phosphate, or a metabolite of glucose-6-phosphate that is not in the glycolytic pathway, is the active agent that leads to the glucose-like effect.
UR - http://www.scopus.com/inward/record.url?scp=0021916196&partnerID=8YFLogxK
U2 - 10.1016/0026-0495(85)90117-9
DO - 10.1016/0026-0495(85)90117-9
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AN - SCOPUS:0021916196
SN - 0026-0495
VL - 34
SP - 106
EP - 111
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 2
ER -