The effect of zinc status on the immune function of diabetic rats.

To evaluate the role of zinc status in immune system dysfunction in diabetic animals, the interleukin-2 production and the lymphocyte mitogenic response to phytohaemagglutinin, concanavalin A and lipopolysaccharide were measured in streptozotocin-induced diabetic rats, diabetic rats treated with insulin and their non-diabetic controls maintained on low zinc, normal zinc and high zinc diets for 3 weeks. Unstimulated lymphocyte proliferation was significantly lower in diabetic rats compared to nondiabetic control rats maintained on normal zinc diet (1505 +/- 318 vs 3447 +/- 497 cpm) (p less than 0.005) or low zinc diet (546 +/- 191 vs 4011 +/- 628 cpm) (p less than 0.005). High zinc diet attenuated the difference between the diabetic rats (2404 +/- 833 cpm) and control rats (3929 +/- 713 cpm). Insulinised diabetic rats were similar to control rats. Phytohaemagglutinin-stimulated lymphocyte proliferation was not significantly altered with dietary zinc changes, but diabetic rats on low zinc diet had significantly lower (p less than 0.025) values compared to control rats on the same diet (41470 +/- 7874 vs 72308 +/- 8895 cpm). Insulinisation did not normalise phytohemaegglutinin-stimulated lymphocyte proliferation (40711 +/- 3666 cpm). Similarly, cells from diabetic rats on low zinc diet, unlike their controls, failed to respond to concanavalin A stimulation. Compared to control rats the diabetic rats on either low or normal zinc diets had lower lipopolysaccharide-stimulated lymphocyte proliferation. High zinc diet or insulinisation normalised mitogenic response of lymphocytes to lipopolysaccharide. Unlike the diabetic rats alterations in dietary zinc intake did not significantly affect the lymphocyte proliferation in control rats.(ABSTRACT TRUNCATED AT 250 WORDS)