ArticleThe Journal of clinical endocrinology and metabolism2026
Insulin Receptor Family Autoantibodies in Patients with Type B Insulin Resistance.
Article in The Journal of clinical endocrinology and metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
1 citing paper in PubMed.
- Type B insulin resistance with glycemic extremes: a case report and literature review.Frontiers in endocrinology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
contextType B insulin resistance (TBIR) is a rare autoimmune disorder characterized by insulin resistance (IR) secondary to insulin receptor autoantibodies (InsR-aAb). A paucity of clinical InsR-aAb assays and incomplete mechanistic understanding complicate diagnosis.
objectiveThis study aimed to (1) validate clinical performance of an immune-luminometric InsR-aAb assay in a relatively large cohort; (2) evaluate its diagnostic accuracy and define thresholds for TBIR diagnosis; and (3) evaluate autoantibody profiles against InsR, type 1 IGF receptor (IGF-1R), and the insulin receptor-related receptor (IRRR) in TBIR and non-autoimmune IR.
methodsWe conducted a cross-sectional analysis of patients with TBIR and non-autoimmune IR. InsR-aAb, IGF-1R-aAb, and IRRR-aAb titers were measured using receptor-specific immune-luminometric assays. Receiver operating characteristic analyses assessed diagnostic performance of the InsR-aAb assay. Multivariate regression models evaluated associations between autoantibody titers and biomarkers of glycemia (glycated hemoglobin [HbA1c], glucose, insulin), growth (IGF-1 z-score [IGF-1z]), and pH regulation (bicarbonate, urine pH).
resultsIn TBIR, higher InsR-aAb titers associated with increased HbA1c, glucose, insulin, and lower IGF-1z (all P < .0001); higher IRRR-aAb titers with lower CO2 (P = .04). An optimal InsR-aAb cutoff for distinguishing TBIR from non-autoimmune IR was determined (area under the curve [AUC] 0.96, sensitivity 91.3%, specificity 93.9%). In non-autoimmune IR, autoantibody titers were not associated with glycemia biomarkers; IGF-1z increased with mild IR (P = .005) and decreased with severe IR (P = .01).
conclusionThis study validates an InsR-aAb assay in the largest TBIR cohort to date and identifies a novel association between IRRR-aAb and bicarbonate excretion. While InsR-aAb were detected in other IR disorders, pathogenic effects were specific to TBIR.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.