ReviewAnnals of the New York Academy of Sciences2018
Nutrient sensing in pancreatic islets: lessons from congenital hyperinsulinism and monogenic diabetes.
Review in Annals of the New York Academy of Sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Nutritional considerations for athletes with diabetes: optimizing performance and glycemic control.Frontiers in nutrition · 2026Review
- In Vitro Assessment of the Bioaccessibility and Hypoglycemic Properties of Essential Amino Acids Blend: Implication for Diabetes Management.Nutrients · 2025Article
- Multi-omic human pancreatic islet endoplasmic reticulum and cytokine stress response mapping provides type 2 diabetes genetic insights.Cell metabolism · 2024Article
- Article
- Revisiting pancreatic islet isolation in murine models: A practical and effective technical protocol.Physiological reports · 2024Article
- How dietary amino acids and high protein diets influence insulin secretion.Physiological reports · 2023Review
- Integrated human pseudoislet system and microfluidic platform demonstrate differences in GPCR signaling in islet cells.JCI insight · 2020Article
- MODY2 in Asia: analysis of GCK mutations and clinical characteristics.Endocrine connections · 2020Article
- Factors Influencing Mitochondrial Function as a Key Mediator of Glucose-Induced Insulin Release: Highlighting Nicotinamide Nucleotide Transhydrogenase.International journal of molecular and cellular medicine · 2020Review
- The relevance of AMP-activated protein kinase in insulin-secreting β cells: a potential target for improving β cell function?Journal of physiology and biochemistry · 2019Review
- Article
- The Genetic and Molecular Mechanisms of Congenital Hyperinsulinism.Frontiers in endocrinology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Pancreatic beta cells sense changes in nutrients during the cycles of fasting and feeding and release insulin accordingly to maintain glucose homeostasis. Abnormal beta cell nutrient sensing resulting from gene mutations leads to hypoglycemia or diabetes. Glucokinase (GCK) plays a key role in beta cell glucose sensing. As one form of congenital hyperinsulinism (CHI), activating mutations of GCK result in a decreased threshold for glucose-stimulated insulin secretion and hypoglycemia. In contrast, inactivating mutations of GCK result in diabetes, including a mild form (MODY2) and a severe form (permanent neonatal diabetes mellitus (PNDM)). Mutations of beta cell ion channels involved in insulin secretion regulation also alter glucose sensing. Activating or inactivating mutations of ATP-dependent potassium (K
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.