Background:

There are conflicting data about the relationship between diabetes mellitus and cancer risk in that growing evidence suggest a possible role of endogenous elevated insulin level which is often found in Non-Insulin-Dependent-Diabetes-Mellitus or an exogenous hyperinsulinemia observed often in Insulin-Dependent-Diabetes-Mellitus. In the last years higher attention focused on the role of immunoregulation both in the insulin production by β-cell of Langerhans-islets and in the insulin sensitivity (resistance) of insulin receptors. Interestingly, cytokines from type-2 innate immune cells, such as M2 macrophages or D2 dendritic cells exhibit a protective effect on both types of diabetes. However, the effect of insulin on the balance between type-1 and type-2 natural immune mechanisms, which is important for the tumor defense, was poorly investigated.

Material and methods:

Streptozotocin (STX)-treated Wister rats was treated per oral with a non-optimal single dose of an evidence based and standardized plant immunomodulator, namely Rice Bran Arabinoxylan Concentrate (RBAC) (also known as Lentin Plus 1000) which has been shown to activate type-1 innate immune cells (such as M1, D1 and NK cells). 24h after a single dose of RBAC (45mg/kg) four parameters of NK cells were determined with flow cytometry using stained CD161-APC and CD314-PE monoclonal antibodies and by hematological examinations. The results were compared with negative controls (without STX or RBAC treatment).

Results:

Since STX caused a significantly reduced lymphocyte production in bone marrow, only the RBAC-induced relative increases in number of NKR-P1+ and LGL cells among the all lymphocyte population parallel with the frequency and intensity of the most important Killing Activator Receptor, namely NKG2D among the total NK cell population were determined. In the STX-untreated group RBAC induced only not significant increases compared with negative control values. However, in STX-treated groups all four NK parameters revealed RBAC-induced significant increases (p<0.05) compared to the negative controls.

Conclusion:

These results suggest the hypothesis that insulin deficit can increase the immunomodulator-induced activation of type-1 innate immune cells indicating that insulin takes part on regulation of the natural immune balance inhibiting the type-1 innate antitumor defense.