β-Cell Responses to Nitric Oxide

Broniowska, Katarzyna A.; Oleson, Bryndon J.; Corbett, John A.

doi:10.1016/b978-0-12-800174-5.00012-0

Cited by 48Pancreatic function and diabetesDiabetes and associated disordersNitric Oxide and Endothelin Effects

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β-Cell Responses to Nitric Oxide

Broniowska, Katarzyna A., Oleson, Bryndon J., Corbett, John A.·2014·Vitamins & Hormones

DOI 10.1016/b978-0-12-800174-5.00012-0

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Abstract

Autoimmune diabetes is characterized by the selective destruction of insulin-secreting β-cells that occurs during an inflammatory reaction in and around pancreatic islets of Langerhans. Cytokines such as interleukin-1, released by activated immune cells, have been shown to inhibit insulin secretion from pancreatic β-cells and cause islet destruction. In response to cytokines, β-cells express inducible nitric oxide synthase and produce micromolar levels of the free radical nitric oxide. Nitric oxide inhibits the mitochondrial oxidation of glucose resulting in an impairment of insulin secretion. Nitric oxide is also responsible for cytokine-mediated DNA damage in β-cells. While nitric oxide mediates the inhibitory and toxic effects of cytokines, it also activates protective pathways that allow β-cells to recover from this damage. This review will focus on the dual role of nitric oxide as a mediator of cytokine-induced damage and the activator of repair mechanisms that protect β-cells from cytokine-mediated injury.

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The inhibitory actions of NO on insulin release appear to be due to NOS2-derived NO, which is implicated in the destruction of islet cells in type 1 diabetes.
“The inhibitory actions of NO on insulin release appear to be due to NOS2-derived NO, which is implicated in the destruction of islet cells in type 1 diabetes [309, 310].”
From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [309]

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Background
Proinflammatory Cytokines Perturb Mouse and Human Pancreatic Islet Circadian Rhythmicity and Induce Uncoordinated β-Cell Clock Gene Expression via Nitric Oxide, Lysine Deacetylases, and Immunoproteasomal Activity
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Background
Relationship between nitric oxide- and calcium-dependent signal transduction pathways in growth hormone release from dispersed goldfish pituitary cells
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Proinflammatory Cytokines Mediate Pancreatic β-Cell–Specific Alterations to Golgi Integrity via iNOS-Dependent Mitochondrial Inhibition
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Defining Cytokine Responsive and Non-responsive Human β-cells
Stephens, S. B. (2024) · Function · doi:10.1093/function/zqae039 · Cited by 2
Dysregulated insulin secretion is associated with pancreatic β‐cell hyperplasia and direct acinar‐β‐cell trans‐differentiation in partially eNOS ‐deficient mice
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“…occurring in eNOS +/− mice (Vecoli et al., 2014) as well as in some human polymorphisms (Rittig et al., 2008) may synergistically act with metabolic stress to modify endocrine pancreatic structure and function has not yet been fully elucidated (Broniowska et al., 2014; Sansbury & Hill, 2014).”
Background
Circadian synchronization differentially modifies cytokine-mediated transcriptomic remodeling and cell death in INS-1 cells and mouse islets
Andersen, P. A. K., Reeh, R. H., Sanders, I., Overlund, E. B., Katsioudi, G., Jiménez‐Sánchez, C., Skovhøj, E. Z., Lubberding, A. F., Dibner, C., & Mandrup-Poulsen, T. R. (2025) · iScience · doi:10.1016/j.isci.2025.112431 · Cited by 1
Nitric oxide attenuates PI4P accumulation at the ER membrane to inhibit encephalomyocarditis virus replication selectively in β-cells
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“It is well known that islet exposure to cytokines results in an inhibition of insulin secretion by β -cells (18, 47).”
Influential
Special Issue: Islet Inflammation and Metabolic Homeostasis
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Noge, S., Kumamoto, K., Matsukawa, H., Ando, Y., Suto, H., Kondo, A., Kishino, T., Oshima, M., Suzuki, Y., & Okano, K. (2025) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2025.12813 · Cited by 3
“Although previous reports (28,29) have shown the inhibitory effects of NO on insulin secretion, inhibition of NOS decreased insulin secretion from isolated human pancreas (30) and plasma insulin level in healthy humans (31).”
Proinflammatory cytokines mediate pancreatic β-cell specific alterations to Golgi morphology via iNOS-dependent mitochondrial inhibitionPreprint
Blom, S. E., Behan-Bush, R. M., Ankrum, J. A., Yang, L., & Stephens, S. B. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.01.29.635550 · Cited by 1
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Authors: Broniowska, K. A., Oleson, B. J., & Corbett, J. A.
Affiliations: Medical College of Wisconsin (US)
Corresponding author: Corbett, John A.
ORCID: Broniowska, Katarzyna A.
Venue: Vitamins & Hormones
Publisher: Elsevier
Published: 2014
Volume: 95
Pages: 299-322
ISSN: 0083-6729 (ISSN-L)
DOI: 10.1016/b978-0-12-800174-5.00012-0
OpenAlex: W193185789
Cited by: 48
References: 92
Citations by year: 2026: 1 · 2025: 9 · 2024: 1 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 8 · 2019: 3 · 2018: 2 · 2017: 6 · 2016: 3 · 2015: 4 · 2014: 4
FWCI: 50.28
Type: book chapter
Language: en
Open access: closed
Locations: Vitamins and hormones (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Allergy and Infectious Diseases (R01AI044458)
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK052194)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Keywords: nitric oxide, pancreatic beta cells, autoimmune diabetes, cytokines, interleukin-1, inducible nitric oxide synthase, insulin secretion, islet damage, DNA damage, pancreatic islets
MeSH terms: Insulin Secretion, Animals, Diabetes Mellitus, Type 1, Humans, Insulin, Models, Biological, Necrosis, Nitric Oxide, Cytokines, Apoptosis, Insulin-Secreting Cells, Nitric Oxide Synthase Type II, Endoplasmic Reticulum Stress

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β-Cell Responses to Nitric Oxide

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