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Biochem Biophys Res Commun. 2018 May 23;499(4):960-966. doi: 10.1016/j.bbrc.2018.04.028. Epub 2018 Apr 9.

Substance P preserves pancreatic β-cells in type 1 and type 2 diabetic mice.

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Graduate School of Biotechnology, Kyung Hee University, Yongin 17104, South Korea.
Kyung Hee University Hospital at Gangdong, Seoul 05278, South Korea.
Department of Biomedical Science and Technology, Graduate School, Kyung Hee University, Seoul 02447, South Korea; East-West Medical Research Institute, Kyung Hee University, Seoul 02447, South Korea; College of Medicine, Kyung Hee University, Seoul 02447, South Korea; Kyung Hee University Medical Center, Seoul 02447, South Korea. Electronic address:


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.


Pancreatic β-cells; Substance P; Type 1 diabetes; Type 2 diabetes

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