ReviewFrontiers in endocrinology2026
Interconnected metabolic and reproductive signaling axis in type 2 diabetes mellitus and polyendocrine metabolic ovarian syndrome.
Review in Frontiers in endocrinology, 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
No grant is acknowledged in the PubMed record.
Abstract
Polyendocrine metabolic ovarian syndrome (PMOS) and type 2 diabetes milletus (T2DM) are interlinked endocrine and metabolic disorders characterized by insulin resistance (IR), hyperinsulinemia and chronic low-grade inflammation. Both these abnormal physiological and metabolic conditions share overlapping cellular and molecular pathways involving insulin signaling, PI3K/Akt dysregulation, oxidative stress (OS) and inflammatory cascades. In PMOS, these disturbances further intersect with reproductive axis dysfunction including hyperandrogenism and follicular arrest. This manuscript reviews the shared metabolic and reproductive signaling pathways in PMOS and T2DM, highlighting insulin signaling defects, AMPK-mTOR imbalance, WNT/β-catenin dysregulation and inflammatory mediators. Understanding these common pathways may facilitate development of unified and more specific therapeutic strategies targeting both metabolic and reproductive dysfunction among these disorders.
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.