HORMONAL-REGULATION OF AMINO-ACID-TRANSPORT AND CAMP PRODUCTION IN MONOLAYER-CULTURES OF RAT HEPATOCYTES
HORMONAL-REGULATION OF AMINO-ACID-TRANSPORT AND CAMP PRODUCTION IN MONOLAYER-CULTURES OF RAT HEPATOCYTES
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DOI:
10.1002/jcp.1041030120
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发表时间:
1980-01-01
影响因子:
5.6
通讯作者:
POTTER, VR
中科院分区:
文献类型:
--
作者:
KELLEY, DS;SHULL, JD;POTTER, VR
The effects of insulin [I], glucagon [G] or dexamethasone (DEX) and of G with I or DEX were examined on the uptake of 2-amino [1-14C]isobutyric acid (AIB) and N-Methyl-2-amino [1-14C]isobutyric acid (NMeAIB) in monolayer cultures of rat hepatocytes. I and G stimulated the uptake of both the amino acids and DEX inhibited it, showing that all 3 of these hormones regulate the A system (the Na-dependent system that permits the transport of NMe AIB) for amino acid transport in these cultures. Experiments investigating the transport of aminocyclopentane-1-carboxylic acid, 1- [carboxyl-14C] in the presence of excess AIB or in the absence of Na showed that I had no effect on the activity of the L system (the Na-independent system that prefers leucine). Experiments on the uptake of AIB in the presence of excess NMe AIB showed I had no effect on the transport activity of the ASC system (the Na-dependent system that does not transport NMe AIB). I concentrations ranging from 0.1 nM-100 nM did not antagonize the stimulatory effect of optimum or suboptimum concentrations of G on the uptake of either AIB or NMe AIB. Similarly, G did not antagonize the stimulatory effect of optimum or suboptimum concentrations of I on the uptake of both the amino acids. The combined effect of I and G was additive on the rate as well as the cumulative uptake of both AIB and NMe AIB. DEX alone inhibited the transport of both AIB and NMe AIB by .apprx. 25%, while G caused a 2-3-fold increase; G addition to cultures containing DEX caused a 7-8-fold increase in the uptake of both AIB and NMe AIB when compared to cultures containing DEX alone. The effect of I on the c[cyclic]AMP levels was also investigated. I had no effect on the cAMP levels in cultures treated or untreated with optimum or suboptimum G concentrations.