The Response of Serum and Pancreas Tryptophan to Starving and Re-feeding in the Rat

Fernstrom & Wurtman (1971) showed that re-feeding starved rats with a protein-free meal led to a rise in brain tryptophan and 5-hydroxytryptamine concentrations, and an increase in the total serum tryptophan. The rate-limiting factor in brain S-hydroxytryptamine synthesis is considered to be the availability of tryptophan in the brain; this in turn is regulated, not by the total serum tryptophan, but by that small fraction which is diffusible, the majority being bound to serum albumin. Knott & Curzon (1972) showed that starvation caused a rise in the diffusible fraction without affecting the total serum tryptophan concentration. Madras et al. (1973) have shown that at 1 and 2h after administration of glucose to starved animals there is a significant rise in total serum tryptophan, accompanied by a fall in the diffusible fraction. In the present study, the short-term (10-20min) responses of rats to glucose administration were studied, after food deprivation for one normal feeding period (24h). Courtauld Institute male Wistar rats (150-2OOg) were killed by decapitation, and the blood was collected and allowed to clot. Serum total tryptophan was measured by the method of Denckla & Dewey (1967), non-esterified fatty acids as described by MikaC-DeviE et al. (1973), and the ratio of diffusible to bound tryptophan by equilibrium dialysis at 4"C, by using tracer amounts of high-specific-radioactivity ['4C]tryptophan. The small-scale equilibrium dialysis method used here gave results in good agreement with those reported by Knott & Curzon (1972): diffusible tryptophan