[2] For diagnostic purposes, it is calculated from fasting insulin and glucose concentrations with:
[1] [I](∞): Fasting Insulin plasma concentration (μU/mL) [G](∞): Fasting blood glucose concentration (mg/dL) G1: Parameter for pharmacokinetics (154.93 s/L) DR: EC50 of insulin at its receptor (1,6 nmol/L) GE: Effector gain (50 s/mol) P(∞): Constitutive endogenous glucose production (150 μmol/s) Compared to healthy volunteers, SPINA-GR is significantly reduced in persons with prediabetes and diabetes mellitus, and it correlates with the M value in glucose clamp studies, triceps skinfold, subscapular skinfold and (better than HOMA-IR and QUICKI) with the two-hour value in oral glucose tolerance testing (OGTT), glucose rise in OGTT, waist-to-hip ratio, body fat content (measured via DXA) and the HbA1c fraction.
[3] Together with the secretory capacity of pancreatic beta cells (SPINA-GBeta), SPINA-GR provides the foundation for the definition of a fasting based disposition index of insulin-glucose homeostasis (SPINA-DI).
[3] In combination with SPINA-GBeta and whole-exome sequencing, calculating SPINA-GR helped to identify a new form of monogenetic diabetes (MODY) that is characterised by primary insulin resistance and results from a missense variant of the type 2 ryanodine receptor (RyR2) gene (p.N2291D).
[4] In lean subjects it is significantly higher than in a population with obese persons.
[3] In a longitudinal evaluation of the NHANES study, a large sample of the general US population, over 10 years, reduced SPINA-DI, calculated as the product of SPINA-GBeta times SPINA-GR, significantly predicted all-cause mortality.