{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,27]],"date-time":"2026-05-27T18:15:01Z","timestamp":1779905701258,"version":"3.53.1"},"reference-count":24,"publisher":"The Endocrine Society","issue":"6","funder":[{"name":"German Federal Ministry of Economics and Technology"},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,5,19]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Context<\/jats:title>\n                    <jats:p>Type 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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This 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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We 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).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In TBIR, higher InsR-aAb titers associated with increased HbA1c, glucose, insulin, and lower IGF-1z (all P &amp;lt; .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).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This 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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1210\/clinem\/dgaf692","type":"journal-article","created":{"date-parts":[[2026,1,6]],"date-time":"2026-01-06T12:26:10Z","timestamp":1767702370000},"page":"e1506-e1514","source":"Crossref","is-referenced-by-count":1,"title":["Insulin Receptor Family Autoantibodies in Patients with Type B Insulin Resistance"],"prefix":"10.1210","volume":"111","author":[{"given":"Jennifer E","family":"Lee","sequence":"first","affiliation":[{"name":"National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, MD 20892 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thilo S","family":"Chillon","sequence":"additional","affiliation":[{"name":"Institute for Experimental Endocrinology, Charit\u00e9-Universit\u00e4tsmedizin Berlin , Berlin D-10115 ,","place":["Germany"]},{"name":"Department of Clinical Biochemistry, Odense University Hospital , Odense 5000 ,","place":["Denmark"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Waldemar B","family":"Minich","sequence":"additional","affiliation":[{"name":"Institute for Experimental Endocrinology, Charit\u00e9-Universit\u00e4tsmedizin Berlin , Berlin D-10115 ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brent S","family":"Abel","sequence":"additional","affiliation":[{"name":"National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, MD 20892 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marissa","family":"Lightbourne","sequence":"additional","affiliation":[{"name":"National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, MD 20892 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