Notice: We are currently experiencing a higher volume of orders and emails. Responses and order processing may be delayed by approximately 24–48 hours. Thank you for your understanding.
Growth hormone and autoimmune diabetes: what research shows

Ricardo Villares, Dimitri Kakabadse, Yasmina Juarranz, Rosa P. Gomariz, Carlos Martínez-A, and Mario Mellado

PNAS November 26, 2013 110 (48) E4619-E4627; https://doi.org/10.1073/pnas.1314985110

  1. Edited by Tak W. Mak, The Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute at Princess Margaret Hospital, University Health Network, Toronto, ON, Canada, approved October 18 2013 (received for review August 9, 2013)

Abstract

Evidence supports a relationship between the neuroendocrine and the immune systems. Data from mice that overexpress or are deficient in growth hormone (GH) indicate that GH stimulates T and B-cell proliferation and Ig synthesis, and enhances maturation of myeloid progenitor cells.

The effect of GH on autoimmune pathologies has nonetheless been little studied. Using a murine model of type 1 diabetes, a T-cell–mediated autoimmune disease characterized by immune cell infiltration of pancreatic islets and destruction of insulin-producing β-cells, we observed that sustained GH expression reduced prodromal disease symptoms and eliminated progression to overt diabetes.

The effect involves several GH-mediated mechanisms; GH altered the cytokine environment, triggered anti-inflammatory macrophage (M2) polarization, maintained activity of the suppressor T-cell population, and limited Th17 cell plasticity. In addition, GH reduced apoptosis and/or increased the proliferative rate of β-cells.

These results support a role for GH in immune response regulation and identify a unique target for therapeutic intervention in type 1 diabetes.

Reference / Link

  1. Villares, R., Kakabadse, D., Juarranz, Y., Gomariz, R. P., Martínez-A, C., & Mellado, M. (2013). Growth hormone prevents the development of autoimmune diabetes. Proceedings of the National Academy of Sciences of the United States of America (PNAS), 110(48), E4619–E4627. DOI

Our Reviews

4.9/5  out of 323 reviews
26.03.2026
26.03.2026
26.03.2026
25.03.2026
25.03.2026
25.03.2026
24.03.2026
23.03.2026
23.03.2026
21.03.2026
20.03.2026
19.03.2026
16.03.2026
16.03.2026
16.03.2026
16.03.2026
15.03.2026
15.03.2026
13.03.2026
11.03.2026
group_work Cookie consent