From the Research
Insulin has a significant impact on white blood cell (WBC) mobilization, primarily inhibiting this process during the fed state, as evidenced by a study published in 2018 1. When insulin levels rise after eating, it suppresses the mobilization of neutrophils and other white blood cells from bone marrow reserves into circulation. This relationship is clinically relevant in diabetes management, where insulin dysregulation can contribute to altered immune responses. Some key points to consider include:
- During hyperinsulinemic states, there is reduced WBC mobilization, which may partially explain the increased infection risk in poorly controlled diabetes.
- Conversely, during fasting or insulin-deficient states, enhanced WBC mobilization occurs as this inhibitory effect is removed.
- This insulin-mediated regulation works through direct effects on bone marrow granulocyte precursors and indirect effects on adhesion molecules that control WBC trafficking.
- The mechanism involves insulin's activation of PI3K/Akt signaling pathways in hematopoietic cells, affecting their proliferation, differentiation, and release.
- A high white blood cell count is associated with a worsening of insulin sensitivity and predicts the development of type 2 diabetes, as shown in a study published in 2002 2.
- Understanding this relationship helps explain why diabetic patients with poor glycemic control often show altered leukocyte counts and immune function, highlighting the importance of maintaining proper insulin levels for normal immune system operation.
- Glycemic reduction alters white blood cell counts and inflammatory gene expression in diabetes, as demonstrated in the 2018 study 1, which found that significant glycemic reduction in subjects with poorly controlled diabetes led to reduced circulating WBC counts and inflammatory gene expression.