Increased lipid fluidity in synaptosomes from brains of hyperosmolal rats.

Taurine, a product of sulfur amino acid metabolism, is important in cerebral osmoregulation. To understand the adaptive changes in transport which accompany different hyperosmolal states, we determined lipid composition and fluorescence anisotropy of synaptosomal liposomes from rats with chronic hypernatremic dehydration (CHD), streptozocin-induced (STZ) diabetes, and insulin treated diabetes. Induction of CHD increased serum osmolality, and enhanced in vitro synaptosomal taurine uptake (P < 0.01, n = 3, vs. control). Fluorescence anisotropy studies showed that the fluidity of lipids from CHD synaptosomes was higher than control (P < 0.05, n = 3). STZ-diabetes resulted in hyperglycemia, increased serum osmolality, and stimulated synaptosomal taurine uptake (P < 0.01, n = 3, vs. control). Insulin treatment of diabetic rats restored serum osmolality and taurine transport to control values. The fluidity of diabetic rat brain synaptosomal lipids was significantly higher than control (P < 0.05, n = 3); fluidity was normalized by insulin administration to diabetic rats. Total fatty acid, cholesterol, and cholesterol/phospholipid molar ratio of CHD, STZ, and insulin treated diabetic rats were similar to control. However, the ratio of saturated to unsaturated fatty acids was decreased in hyperosmolal states. This suggests that adaptive increases in cerebral taurine transport during hyperosmolality may result from a direct effect on membrane composition that alters fluidity and permits enhanced transmembrane flux of osmoprotective molecules.