Binds insulin receptor at a site distinct from insulin, activating downstream pathways (PI3K/Akt, MAPK) .
Reduces hepatic glucose output and enhances glucose uptake in adipocytes/muscle .
Catalyzes rate-limiting step: Nicotinamide + PRPP → NMN + PPi ( ) .
Regulates sirtuins, PARPs, and CD38/157 via NAD+ modulation .
Induces IL-6, TNF-α, and IL-1β secretion in monocytes via NF-κB and MAPK pathways .
Upregulated in atherosclerosis, acute coronary syndrome, and metabolic syndrome .
Expressed in human granulosa cells, oocytes, and placental trophoblasts .
Enhances IGF-1-induced progesterone/estradiol secretion and cell proliferation .
Obesity: Elevated plasma levels correlate with visceral fat mass (r = 0.65, p < 0.001) .
Type 2 Diabetes: Serum visfatin levels are 2.3-fold higher in obese diabetics vs. non-diabetics .
Genetic associations: SNPs rs2302559 (OR = 129.4) and rs1215113036 (OR = 44.6) linked to metabolic syndrome .
Promotes endothelial dysfunction, smooth muscle proliferation, and atherosclerotic plaque formation .
Plasma levels correlate with troponin in STEMI patients, suggesting biomarker potential .
Regulated by progesterone, estradiol, and hCG in placental cells .
Altered expression in gestational diabetes and preeclampsia placentas .
Visfatin SNPs increase metabolic syndrome risk (p < 0.001) .
Evolutionary conservation: 96% homology between human and canine visfatin .
Inhibitors: FK866 and CHS828 reduce NAD+ levels in cancer models .
Recombinant visfatin (8424-VF) induces VEGF secretion (ED₅₀ = 1–5 μg/mL) .
The SNP rs2302559 is strongly associated with metabolic syndrome (OR: 18.22; 95% CI: 10.23–32.47), while rs1215113036 shows population-specific effects . Methodological considerations:
Case-control studies: Compare allele frequencies in 150 metabolic syndrome patients vs. 150 controls using PCR-RFLP or sequencing.
Statistical adjustments: Control for confounders (age, BMI) via multivariate regression .
Contradiction analysis: Cell-type-specific responses (e.g., immune vs. placental cells) and differential receptor interactions explain divergent outcomes .
In vitro assays: Treat JEG-3 cells with progesterone, estradiol, hCG, or insulin for 24–48 hours.
Pathway inhibition: Use blockers for PI3K (LY294002) or MAPK (PD98059) to confirm signaling mechanisms .
Outcome measures: Quantify visfatin mRNA (RT-PCR) and protein (Western blot) levels .
Paired sampling: Analyze visceral and subcutaneous adipose tissue from the same donor to control for inter-individual variability .
Normalization: Use stable reference genes (e.g., 36B4) resistant to hormonal fluctuations .
Blinding: Ensure technicians are blinded to clinical status (e.g., unstable angina vs. healthy) during cytokine assays .
Glucose tolerance tests: Administer recombinant visfatin (0.5–5 mg/kg) to insulin-resistant mice and monitor glucose clearance .
Receptor binding assays: Use radiolabeled insulin/visfatin to confirm non-competitive binding to insulin receptors .
Visfatin is a dimeric type II phosphoribosyltransferase, which means it functions as an enzyme that catalyzes the transfer of phosphoribosyl groups. The recombinant human visfatin protein is typically expressed in Escherichia coli and purified to a high degree of purity (≥90%) for research purposes .
Visfatin has been implicated in several physiological and pathological processes:
The role of visfatin in metabolic diseases such as obesity and diabetes has been a subject of extensive research. However, there are conflicting results regarding its association with these conditions. Some studies suggest that visfatin levels correlate with obesity and insulin resistance, while others do not find such associations .
Recombinant human visfatin is produced for research purposes to study its biological functions and potential therapeutic applications. The recombinant protein is often used in cell culture experiments to investigate its effects on various cell types. For example, it has been shown to induce VEGF secretion by PC-3 human prostate cancer cells .