Peripheral and central consequences of immobilization stress in genetically obese Zucker rats

Peripheral and central effects of acute and chronic immobilization stress were measured in lean and obese Zucker female rats. Thus hypothalamic serotonergic metabolism was analyzed by measuring the concentrations of serotonin (5-hydroxytryptamine, 5-HT), tryptophan (TRP; the precursor of 5-HT), and 5-hydroxyindoleacetic acid (5-HIAA; 5-HT metabolite). In addition, plasma total TRP, free fatty acid (FFA), insulin, and corticosterone concentrations were measured. Analysis of stress-induced changes in food consumption were also included. A single 2-h restraint stress was found to increase TRP availability in the hypothalamus of both rats; this promoted an increase in 5-HIAA in the lean rats and increases in 5-HT and 5-HIAA in the obese (fa/fa) rats. These modifications were associated with marked decreases in plasma total TRP and insulinemia in the lean and obese rats. Whereas stress triggered similar hypercorticosteronemia and hyperglycemia, FFA was increased in the lean rats only. Consecutive hypophagia was noted in all the rats. Twenty-four hours after the last of the four 2-h stress sessions, hypothalamic 5-HIAA was increased in the obese rats and plasma TRP and FFA levels decreased in both rats. Although both groups of rats were normoglycemic, stress-induced hyperinsulinemia was evidenced in the lean rats, thus suggesting that chronic stress promotes insulin resistance. These metabolic variations were associated with normal food consumption and increased body weight gains in the lean and obese Zucker rats.