Substance P preserves pancreatic β-cells in streptozotocin-induced type 1 diabetic mice
- Graduate School of Biotechnology, Kyung Hee University, Yong in, 17104 (Korea, Republic of)
- St. Peter's Hospital and R&D Center, Cell & Bio Inc., Seoul 06286 (Korea, Republic of)
- East-West Medical Research Institute, Kyung Hee University, Seoul 02447 (Korea, Republic of)
Preservation of the pancreatic β-cell population is required for the development of therapies for diabetes, which is caused by a decrease in β-cells. Here, we demonstrate the antidiabetic effects of substance P (SP) in type 1 diabetes (T1D) mice induced with streptozotocin. SP enhanced the compensatory proliferation of β-cells in order to restore β-cells in response to acute injury induced by a single high-dose of streptozotocin. However, SP affected neither the basal proliferation of β-cells nor their apoptosis. In vitro studies by using the INS-1 pancreatic β-cell line showed that SP mediated the increase in the proliferation of β-cells via the activation of Akt. Chronic systemic treatment with SP restored the mass of β-cells and inhibited insulitis in T1D mice induced with multiple low-doses of streptozotocin. Therefore, systemic treatment with SP may be a promising therapeutic strategy for treating diabetes in patients with loss of functional β-cells. - Highlights: • Substance P increased β-cell proliferation in response to acute injury. • Substance P did not protect β-cells from apoptosis. • Substance P preserved β-cell mass and delayed diabetic hyperglycemia.
- OSTI ID:
- 22719095
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 491, Issue 4; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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