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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.

Author information

1
Graduate School of Biotechnology, Kyung Hee University, Yongin 17104, South Korea.
2
Kyung Hee University Hospital at Gangdong, Seoul 05278, South Korea.
3
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: kisookpark@khu.ac.kr.

Abstract

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.

KEYWORDS:

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

PMID:
29626466
DOI:
10.1016/j.bbrc.2018.04.028
[Indexed for MEDLINE]

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