Substance P preserves pancreatic β-cells in type 1 and type 2 diabetic mice
- Graduate School of Biotechnology, Kyung Hee University, Yongin 17104, South (Korea, Republic of)
- Kyung Hee University Hospital at Gangdong, Seoul 05278, South (Korea, Republic of)
- Department of Biomedical Science and Technology, Graduate School, Kyung Hee University, Seoul 02447, South (Korea, Republic of)
Highlights: • Substance P preserved β-cells in nonobese diabetic mice with type 1 diabetes. • Substance P preserved β-cells in db/db mice with type 2 diabetes. • Substance P inhibited the activation of pancreatic stellate cells. Preservation of pancreatic β-cells is required for the development of therapies for type 1 and type 2 diabetes (T1D and T2D, respectively). Our previous study demonstrated that substance P (SP) preserves β-cell populations in mice with streptozotocin-induced T1D. Here, we demonstrated that chronic systemic treatment with SP restored the mass of β-cells both in nonobese diabetic (NOD) mice with T1D or db/db mice with T2D. SP delayed the onset of T1D in NOD mice via immune modulation. SP inhibited immune infiltration into islets and the salivary glands of NOD mice. In db/db mice, SP treatment rescued glucose intolerance. Moreover, SP inhibited apoptosis, as well as the activation of pancreatic stellate cells in pancreatic islets of db/db mice. SP downregulated the number of α-smooth muscle actin (α-SMA) expressing cells in db/db pancreatic islets. Cleaved-caspase-3 expression was reduced in islets of SP-treated db/db mice compared to that in the control. Therefore, these results suggested that SP may preserve pancreatic β-cells through immune modulation and protection from the stimulated activation of pancreatic stellate cells and apoptosis in T1D and T2D, respectively.
- OSTI ID:
- 23137158
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 499, Issue 4; Other Information: Copyright (c) 2018 Elsevier Inc. 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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