ArticleScientific reports2025
The antidiabetic effect of safflower yellow by regulating the GOAT/ghrelin/GHS-R1a/cAMP/TRPM2 pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Precision Exercise in Type 2 Diabetes Mellitus: Targeting Signaling Networks for Lipid Homeostasis.Metabolites · 2026Review
- The Emerging Roles of Protein Lipidation in Fertility and Reproductive Disorders: Mechanisms and Therapeutic Implications.Biomolecules · 2026Review
- Multidisciplinary Management in the Diabetes Reversal Clinic Promotes Diabetes Remission.AACE endocrinology and diabetesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Safflower yellow (SY), derived from Carthamus tinctorius L., is a valuable natural edible pigment that exhibits anti-type 2 diabetes mellitus (T2DM) efficacy; however, its mechanism of action is unclear, which hinders its effective use. In this study, we examined the impact of SY on glucose metabolism and insulin secretion both in vivo and in vitro and elucidated the possible underlying mechanism. First, molecular docking demonstrated a strong binding affinity between SY and ghrelin O-acyltransferase (GOAT) protein, which was validated by a cell heat transfer assay (CETSA) and drug affinity response target stability (DARTS) in MIN6 cells. In MIN6 cells, SY increased insulin secretion and showed time- and dose-dependent inhibition of GOAT expression and acyl ghrelin (AG) secretion without affecting the overall levels of ghrelin. Furthermore, ELISA revealed that SY enhanced high glucose (HG)-induced insulin secretion, and immunofluorescence revealed the co-localization of GOAT and ghrelin in MIN6 cells, which was suppressed by SY treatment. The mechanism analysis by Western blot demonstrated that SY downregulated the protein levels of GOAT and GHS-R1a in MIN6 cells while increasing HG-stimulated cAMP and activation of transient receptor potential melastatin 2 (TRPM2). In in vivo experiments, the intraperitoneal injection of SY significantly improved pathological damage to the pancreas, glucose tolerance, and insulin resistance in a mouse model of high-fat diet (HFD)/streptozotocin (STZ)-induced T2DM in a dose-dependent manner. SY enhanced insulin secretion by inhibiting the GOAT/ghrelin system in vivo. In conclusion, we demonstrated that SY exhibits an observable protective effect on diabetes through the GOAT/ghrelin/GHS-R1a/cAMP/TRPM2 pathway. Our findings provide a basis for further investigation of the hypoglycemic mechanism of SY and its potential for further development and utilization.
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.