Cortistatin regulates glucose-induced electrical activity and insulin secretion in mouse pancreatic beta-cells

Soriano, Sergi; Castellano-Muñoz, Manuel; Rafacho, Alex; Alonso-Magdalena, Paloma; Marroquí, Laura; Ruiz-Pino, Antonia; Bru-Tarí, Eva; Merino, Beatriz; Irles, Esperanza; Bello-Pérez, Melisa; Iborra, Pau Llàcer; Villar-Pazos, Sabrina; Vettorazzi, Jean Franciesco; Montanya, Eduard; Luque, Raúl M.; Nadal, Ángel; Quesada, Iván

doi:10.1016/j.mce.2018.09.009

Cited by 5 publications

(3 citation statements)

References 45 publications

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“…Studies carried out by Sergi Soriano et al in islets isolated from mice demonstrated that CST reduced glucose-stimulated insulin secretion. 19 This effect was eliminated in the presence of SST receptor antagonists, indicating that CST works mainly through somatostatin receptor subtypes (SSTRs). Moreover, CST was reported to affect the insulin levels through pancreatic β-cell inhibition.…”

Section: Discussionmentioning

confidence: 99%

Serum Cortistatin Level in Type 2 Diabetes Mellitus and Its Relationship with Nonalcoholic Fatty Liver Disease

Sun¹,

Wang²,

Huo³

et al. 2023

IJGM

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Purpose To evaluate serum cortistatin (CST) levels in type 2 diabetes mellitus (T2DM) patients with or without non-alcoholic fatty liver disease (NAFLD) and to examine the relationship between CST and NAFLD. Methods A total of 90 T2DM patients, which included 56 NAFLD patients (referred to as DM+NAFLD group) and 34 patients without NAFLD (DM-only group), and 83 non-diabetes individuals that included 39 NAFLD patients (NAFLD-only group) and 44 without NAFLD that acted as the normal-control group (NC group). The differences in the serum CST levels between the groups were compared, and the correlations between CST and other variables were calculated by applying both correlational analysis and multiple linear regression analysis. Results The mean serum CST levels were significantly lower in the DM+NAFLD and DM groups than in the NC group ( P < 0.05). In addition, the CST levels were lower in the DM group relative to that in the NAFLD group ( P < 0.05). However, no statistical difference was noted in the serum CST between diabetic patients with and without NAFLD ( P > 0.05). Similarly, in the non-diabetic group, the serum CST level was not significantly different between individuals with and without NAFLD ( P > 0.05). Furthermore, the serum CST levels were negatively associated with the levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), fasting plasma glucose (FPG), homeostasis model assessment-insulin resistance (HOMA-IR), and insulin cell function index (HOMA-β). Conversely, the serum CST levels were positively associated with high-density lipoprotein cholesterol (HDL-C). The data obtained through multiple linear regression implied that LDL-C and HOMA-β, but not HOMA-IR, were closely related to serum CST levels. Conclusion T2DM was related to decreased serum CST. However, serum CST was correlated with HOMA-β in T2DM patients, while HOMA-IR was not. There was no correlation between CST and NAFLD.

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Section: Discussionmentioning

confidence: 99%

Serum Cortistatin Level in Type 2 Diabetes Mellitus and Its Relationship with Nonalcoholic Fatty Liver Disease

Sun¹,

Wang²,

Huo³

et al. 2023

IJGM

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“…This action can be reversed by SSTR antagonists. Cortistatin was found to be expressed in mouse and human islets, especially localized in δ-cells at both transcriptomic and protein levels [95][96][97][98]. However, in contrast, recent transcriptomic studies pointed to a minimal cortistatin expression level in purified mouse islets cells [7,8].…”

Section: Cortistatinmentioning

confidence: 96%

“…Other than its ability to activate SSTRs, it has also been determined that cortistatin can bind to GHSR [93,94]. Exposure of β-cells to cortistatin would lead to membrane potential hyperpolarization via activation of GIRK channels, reduction in glucose-induced action potentials and thus inhibition of insulin secretion [95]. This action can be reversed by SSTR antagonists.…”

Section: Cortistatinmentioning

confidence: 99%

δ-Cells: The Neighborhood Watch in the Islet Community

Gao

Yang

Zhang

2021

Biology

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Somatostatin-secreting δ-cells have aroused great attention due to their powerful roles in coordination of islet insulin and glucagon secretion and maintenance of glucose homeostasis. δ-cells exhibit neuron-like morphology with projections which enable pan-islet somatostatin paracrine regulation despite their scarcity in the islets. The expression of a range of hormone and neurotransmitter receptors allows δ-cells to integrate paracrine, endocrine, neural and nutritional inputs, and provide rapid and precise feedback modulations on glucagon and insulin secretion from α- and β-cells, respectively. Interestingly, the paracrine tone of δ-cells can be effectively modified in response to factors released by neighboring cells in this interactive communication, such as insulin, urocortin 3 and γ-aminobutyric acid from β-cells, glucagon, glutamate and glucagon-like peptide-1 from α-cells. In the setting of diabetes, defects in δ-cell function lead to suboptimal insulin and glucagon outputs and lift the glycemic set-point. The interaction of δ-cells and non-δ-cells also becomes defective in diabetes, with reduces paracrine feedback to β-cells to exacerbate hyperglycemia or enhanced inhibition of α-cells, disabling counter-regulation, to cause hypoglycemia. Thus, it is possible to restore/optimize islet function in diabetes targeting somatostatin signaling, which could open novel avenues for the development of effective diabetic treatments.

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