ArticleDiabetes2013
Pathogenesis of A⁻β⁺ ketosis-prone diabetes.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 71 citations in OpenAlex.
- Diminished arginine bioavailability during hyperglycaemia distinguishes individuals with ADiabetologia · 2026Article
- Unmasking Ketosis-Prone Diabetes in a Young Adult.Cureus · 2026Article
- Unraveling A-β+ ketosis-prone diabetes: An evolving diagnosis with an elusive pathogenesis.Journal of diabetes investigation · 2026Review
- Heterogeneity in clinically diagnosed type 1 diabetes: characterising a unique cohort with maintained C-peptide secretion in Ghana.Diabetologia · 2026Article
- Diabetic Ketoacidosis: Considerations and Residual Controversies in Management After the 2024 ADA, EASD, JBDS, AACE, and DST Joint ConsensusEndocrine, metabolic & immune disorders drug targets · 2026Review
- The value of serum creatinine-to-cystatin C ratio in newly diagnosed ketosis-prone diabetes.Endocrine connections · 2026Article
- Higher visceral fat area is inversely associated with ketosis in Chinese patients with type 2 diabetes mellitus: a cross-sectional study.Frontiers in endocrinology · 2026Article
- Amino Acids and CART Distinguish A-β+ Ketosis-Prone Diabetes From Type 1 and Type 2 Diabetes During Hyperglycemic Crises.The Journal of clinical endocrinology and metabolism · 2025Article
- Ketosis-prone Diabetes as a Presentation of New-onset Diabetes in a Patient With Spinal Muscular Atrophy Type III.JCEM case reports · 2025Article
- Article
- Clinical metabolomics in type 2 diabetes mellitus: from pathogenesis to biomarkers.Frontiers in endocrinology · 2025Review
- Random C-Peptide and Islet Antibodies at Onset Predict β Cell Function Trajectory and Insulin Dependence in Pediatric Diabetes.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2024Article
- Atypical Diabetes: What Have We Learned and What Does the Future Hold?Diabetes care · 2024Review
- High Prevalence ofPediatric diabetes · 2024Article
- Plasma amino acid signatures define types of pediatric diabetes.Clinical nutrition ESPEN · 2023Article
- Development and validation of a multivariable risk prediction model for identifying ketosis-prone type 2 diabetes.Journal of diabetes · 2023Article
- The Rare and Atypical Diabetes Network (RADIANT) Study: Design and Early Results.Diabetes care · 2023Article
- Data Mining Framework for Discovering and Clustering Phenotypes of Atypical Diabetes.The Journal of clinical endocrinology and metabolism · 2023Article
- Branched-chain α-keto acids and glutamate/glutamine: Biomarkers of insulin resistance in childhood obesity.Endocrinology, diabetes & metabolism · 2023Article
- A patient with ketosis-prone type 2 diabetes showing nearly normalized glucose tolerance after recovery from severe diabetic ketoacidosis.Diabetology international · 2023Article
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Authors and funding
12 authors at 7 institutions in 1 country.
Funding
Abstract
A⁻β⁺ ketosis-prone diabetes (KPD) is an emerging syndrome of obesity, unprovoked ketoacidosis, reversible β-cell dysfunction, and near-normoglycemic remission. We combined metabolomics with targeted kinetic measurements to investigate its pathophysiology. Fasting plasma fatty acids, acylcarnitines, and amino acids were quantified in 20 KPD patients compared with 19 nondiabetic control subjects. Unique signatures in KPD--higher glutamate but lower glutamine and citrulline concentrations, increased β-hydroxybutyryl-carnitine, decreased isovaleryl-carnitine (a leucine catabolite), and decreased tricarboxylic acid (TCA) cycle intermediates--generated hypotheses that were tested through stable isotope/mass spectrometry protocols in nine new-onset, stable KPD patients compared with seven nondiabetic control subjects. Free fatty acid flux and acetyl CoA flux and oxidation were similar, but KPD had slower acetyl CoA conversion to β-hydroxybutyrate; higher fasting β-hydroxybutyrate concentration; slower β-hydroxybutyrate oxidation; faster leucine oxidative decarboxylation; accelerated glutamine conversion to glutamate without increase in glutamate carbon oxidation; and slower citrulline flux, with diminished glutamine amide-nitrogen transfer to citrulline. The confluence of metabolomic and kinetic data indicate a distinctive pathogenic sequence: impaired ketone oxidation and fatty acid utilization for energy, leading to accelerated leucine catabolism and transamination of α-ketoglutarate to glutamate, with impaired TCA anaplerosis of glutamate carbon. They highlight a novel process of defective energy production and ketosis in A⁻β⁺ KPD.
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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.