Jt. Tildon et al., DIFFERENTIAL-EFFECTS OF SERUM PROTEIN(S) ON SUBSTRATE OXIDATION BY ISOLATED SYNAPTOSOMES AND CULTURED RAT-BRAIN ASTROCYTES, Developmental neuroscience, 15(3-5), 1993, pp. 226-232
This report extends the finding that serum protein(s) (0.5 mg/ml) caus
ed a 50% decrease in the rate of glucose oxidation by dissociated brai
n cells with only marginal effects on the oxidation of other substrate
s. Since dissociated cells represent a heterogeneous population, studi
es were initiated to determine the effect of serum on the rates of sub
strate oxidation by isolated synaptosomes and cultured rat brain astro
cytes. Experiments revealed that the addition of 5% serum v/v to the r
eaction mixture resulted in a decrease in the rate of (CO2)-C-14 produ
ction from [6-C-14]glucose by isolated synaptosomes by more than 70%.
In contrast, the addition of 5% serum had little or no effect on the (
CO2)-C-14 production from [U-C-14]glutamine by the synaptosomes and on
ly marginal effects (20-25%) on (CO2)-C-14 production from [U-C-14]lac
tate and 3-hydroxy[3-C-14]butyrate. The effect of serum on the rates o
f substrate oxidation were similar for synaptosomal preparations obtai
ned from adult animal brains or 18-day-old rats, except that with the
latter preparation, (CO2)-C-14 production from 3-hydroxy[3-C-14]butyra
te was more attenuated by the presence of serum than with the former s
ynaptosomal preparation (50 vs. 25%). In contrast to the results with
synaptosomes, the presence of 5% serum enhanced the rates of (CO2)-C-1
4 production from [6-C-14]glucose, 3-hydroxy[3-C-14]butyrate and [U-C-
14]lactate by 61, 35 and 69%, respectively, in cultured rat brain astr
ocytes. However, this enhancement did not occur when the cells were gr
own in chemically defined media or when dibutyryl cAMP was added to th
e media. Collectively the results suggest that the presence of serum p
rotein(s) may contribute to the regulation of substrate oxidation by b
rain cells in a yet to be defined manner; either by acting directly wi
th enzymes in the metabolic pathway or via an interim (second messenge
r) factor.