ReviewFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026
Endocrine-Metabolic Crosstalk Between Diabetes Mellitus and Hypothyroidism: From Network Mechanisms to Translational Stratification.
Review in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Diabetes mellitus (DM) and hypothyroidism (HypoT) are common endocrine-metabolic disorders that frequently coexist, forming a biologically complex comorbidity rather than a simple clinical overlap. Increasing evidence suggests that DM-HypoT comorbidity arises from reciprocal disturbances in insulin action, thyroid hormone signaling, immune-inflammatory regulation, and cellular energy sensing. Thyroid hormone deficiency may impair glucose utilization, promote insulin resistance, and aggravate metabolic stress, whereas diabetes-associated hyperinsulinemia, oxidative stress, and chronic inflammation may disrupt hypothalamic-pituitary-thyroid 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-RAGE signaling, and tissue-specific mitochondrial dysfunction, may further amplify endocrine-metabolic 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-immune-gut-thyroid axis framework to support mechanism-informed risk stratification, biomarker development, and translational intervention strategies for DM-HypoT comorbidity.
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.