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Increasing evidence suggests that DM\u2013HypoT comorbidity arises from reciprocal disturbances in insulin action, thyroid hormone signaling, immune\u2013inflammatory regulation, and cellular energy sensing. Thyroid hormone deficiency may impair glucose utilization, promote insulin resistance, and aggravate metabolic stress, whereas diabetes\u2010associated hyperinsulinemia, oxidative stress, and chronic inflammation may disrupt hypothalamic\u2013pituitary\u2013thyroid axis activity, thyroid hormone synthesis, and peripheral hormone activation. Subclinical hypothyroidism may represent an early biochemical phenotype within this interaction and often intersects with obesity and metabolic syndrome. Additional biological nodes, including gut dysbiosis, micronutrient imbalance, AGE\u2013RAGE signaling, and tissue\u2010specific mitochondrial dysfunction, may further amplify endocrine\u2013metabolic dysregulation. However, causal hierarchy, tissue specificity, phenotype heterogeneity, and responsive patient subgroups remain incompletely defined. This review synthesizes current epidemiological and mechanistic evidence and proposes an integrated pancreatic islet\u2013immune\u2013gut\u2013thyroid axis framework to support mechanism\u2010informed risk stratification, biomarker development, and translational intervention strategies for DM\u2013HypoT comorbidity.<\/jats:p>","DOI":"10.1096\/fj.202602520r","type":"journal-article","created":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T17:24:35Z","timestamp":1789233875000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Endocrine\u2013Metabolic Crosstalk Between Diabetes Mellitus and Hypothyroidism: From Network Mechanisms to Translational Stratification"],"prefix":"10.1096","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0009-0000-0091-9277","authenticated-orcid":false,"given":"Xiuqing","family":"Yang","sequence":"first","affiliation":[{"name":"Institute of Life Sciences &amp; Biomedical 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