ReviewDiabetes2022
ATP-Sensitive Potassium Channels in Hyperinsulinism and Type 2 Diabetes: Inconvenient Paradox or New Paradigm?
Review in Diabetes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Relevance of the KATP channel function for the basal insulin hypersecretion of islets from female NZO mice.Journal of the Endocrine Society · 2026Article
- Is high insulin protective or detrimental? Mathematical modeling reveals the base of the iceberg.American journal of physiology. Endocrinology and metabolism · 2026Article
- Neonatal Hyperinsulinemia and Maternal Diabetes Associated With a Hepatocyte Nuclear Factor 4 Alpha (HNF4A) Variant.Cureus · 2026Article
- Targeted analysis of whole exome sequencing in Thai patients with neonatal diabetes.Human genetics · 2026Article
- Identification and rescue of congenital hyperinsulinism-associated ABCC8 mutations that impair KThe Journal of biological chemistry · 2025Article
- VDAC1 is a target for pharmacologically induced insulin hypersecretion in β cells.Cell reports · 2025Article
- Bayliss-Starling Prize Lecture: KThe Journal of physiology · 2025Article
- Article
- Targeting macrophages and ion homeostasis in T2D: new genes and therapeutic pathways identified.Frontiers in immunology · 2025Article
- Atypical KCNQ1/Kv7 channel function in a neonatal diabetes patient: Hypersecretion preceded the failure of pancreatic β-cells.iScience · 2024Article
- Sildenafil amplifies calcium influx and insulin secretion in pancreatic β cells.Physiological reports · 2024Article
- A loss-of-function mutation in KCNJ11 causing sulfonylurea-sensitive diabetes in early adult life.Diabetologia · 2024Article
- Exploring the Pathophysiology of ATP-Dependent Potassium Channels in Insulin Resistance.International journal of molecular sciences · 2024Review
- CaFrontiers in endocrinology · 2024Review
- Clinical management of diazoxide-unresponsive congenital hyperinsulinism: A single-center experience.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2024Article
- Maternal Western-style diet in nonhuman primates leads to offspring islet adaptations including altered gene expression and insulin hypersecretion.American journal of physiology. Endocrinology and metabolism · 2023Article
- Genome-edited zebrafish model ofIslets · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Secretion of insulin from pancreatic β-cells is complex, but physiological glucose-dependent secretion is dominated by electrical activity, in turn controlled by ATP-sensitive potassium (KATP) channel activity. Accordingly, loss-of-function mutations of the KATP channel Kir6.2 (KCNJ11) or SUR1 (ABCC8) subunit increase electrical excitability and secretion, resulting in congenital hyperinsulinism (CHI), whereas gain-of-function mutations cause underexcitability and undersecretion, resulting in neonatal diabetes mellitus (NDM). Thus, diazoxide, which activates KATP channels, and sulfonylureas, which inhibit KATP channels, have dramatically improved therapies for CHI and NDM, respectively. However, key findings do not fit within this simple paradigm: mice with complete absence of β-cell KATP activity are not hyperinsulinemic; instead, they are paradoxically glucose intolerant and prone to diabetes, as are older human CHI patients. Critically, despite these advances, there has been little insight into any role of KATP channel activity changes in the development of type 2 diabetes (T2D). Intriguingly, the CHI progression from hypersecretion to undersecretion actually mirrors the classical response to insulin resistance in the progression of T2D. In seeking to explain the progression of CHI, multiple lines of evidence lead us to propose that underlying mechanisms are also similar and that development of T2D may involve loss of KATP activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.