FBN1 produces mature matrix fibrillin-1 and the released C-terminal hormone asprosin. These forms must remain distinct when interpreting the literature. Human asprosin corresponds to precursor residues 2732–2871; the 2016 discovery study expressed this human sequence with an N-terminal His tag and tested it in mice and primary mouse hepatocytes. Human plasma immunoblotting and ELISA provide a separate observation of the endogenous circulating product. The study supports hormone activity, extracellular location, glucogenic regulation and a cAMP/PKA response; it does not make the mature matrix chain a circulating hormone or glucose-metabolic enzyme. See Romere et al., 2016, Methods and Figures 1, 2, 4, 5 and 6.
Source identity is preserved in the decision table. Indices 18, 19, 66, 87, 92 and 124 have raw processed-product identity P35555-PRO_0000436882. Index 62 instead names parent P35555 and uses EXP; the 2016 paper's operative extracellular assay is still about asprosin. This distinction is explicit rather than manufactured as a splice-isoform field in the imported annotations. Database-source appetite index 118 is also chain-specific but is not adjudicated in this table.
The 2019 receptor study used mouse Asprosin amplified from mouse liver and an active bacterial GST fusion. Its human OR4M1 experiments do not independently establish human ligand provenance. The exact human-chain IDA context therefore remains unresolved, while the separate human ligand evidence from 2016 is retained. The authors also acknowledge incomplete loss of the glucogenic response after Olfr734 deletion and difficulties obtaining active His-asprosin. See Li et al., 2019, Plasmids and Adenoviruses, Protein Expression and Purification, Discussion and Limitations of Study.
A separate report describes failed replication using other recombinant preparations and hydrodynamic expression. The study includes HEKexpi and bacterial preparations and hydrodynamic expression, so its negative results cannot be reduced to failed His-protein recovery from inclusion bodies. Reproducibility across preparations and laboratories remains unresolved; later GST-positive evidence does not fully explain the negative HEKexpi and hydrodynamic-expression results. The human ligand sequence of every negative construct was not established from the accessed body. Its Case 2 contains original replication observations within an article indexed as a review. See von Herrath et al., 2019, Case 2 and Figure 2 caption. Supplementary construct details were not inspected.
The 2026 study reports matched human HA-Asprosin/PTPRF co-immunoprecipitation and describes mature human asprosin produced in CHO cells. It supports an additional PTPRF mechanism; unchanged Olfr734 expression after Ptprf deletion is not a test excluding the earlier GPCR route. The BLI Methods attach catalog 9377-PF-050 to human Asprosin, but the manufacturer identifies 9377-PF as human LAR/PTPRF. That reagent-label ambiguity remains unresolved, and the reported human affinity is not treated as fully verified. See Liu et al., 2026, Figure 4, Chemicals and Reagents, Co-immunoprecipitation and BLI Methods. Figure 4 pixels were inspected through the ZFIN original-paper figure record; supplemental sequence files were not read.
The glucose-metabolism correction separates regulation from chemical conversion. Asprosin acts as the extracellular signal; hepatocyte machinery performs the reactions. GO:0010907, positive regulation of glucose metabolic process, fits that role without asserting that the original experiment resolves all output into gluconeogenesis. This is a replacement of the existing context, not an added annotation. The GPCR pathway is retained as a supported source-specific route without claiming that it is exclusive.
The 2016 author manuscript was read beyond the normal cache, including operative Methods and figure pixels. The 2019 receptor, replication and 2026 papers were read as original publisher text recovered separately from their abstract-only normal caches; those caches remain unchanged. Original-publisher text captures are private evidence, not missing public source files. The 2016 manuscript contains internal dose/unit inconsistencies, so no dose-sensitive claim is made here. No additional quotations have been introduced.