The index is derived from a mathematical model of insulin-glucose homeostasis.[2] For diagnostic purposes, it is calculated from fasting insulin and glucose concentrations with:
It has the additional advantage that it circumvents the HOMA-blind zone, which renders the calculation of HOMA-Beta impossible if the fasting glucose concentration is 3.5 mmol/L (63 mg/dL) or below.[3] Unlike HOMA-Beta, SPINA-Beta can be sensibly calculated in the whole range of measurements.[1]
In repeated measurements, SPINA-GBeta had higher retest reliability than HOMA-Beta, a measurement for beta cell function from the homeostasis model assessment.[1][4]
In the FAST study, an observational case-control sequencing study including 300 persons from Germany, SPINA-GBeta differed more clearly between subjects with and without diabetes than the corresponding HOMA-Beta index.[4]
Together with the reconstructed insulin receptor gain (SPINA-GR), SPINA-GBeta provides the foundation for the definition of a fasting based disposition index of insulin-glucose homeostasis (SPINA-DI).[4]
In combination with SPINA-GR and whole-exome sequencing, calculating SPINA-GBeta 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).[5]
In several populations, SPINA-GBeta correlated with the area under the glucose curve and 2-hour concentrations of glucose, insulin and proinsulin in oral glucose tolerance testing, concentrations of free fatty acids, ghrelin and adiponectin, and the HbA1c fraction.[4]
^Dietrich, Johannes W.; Böhm, Bernhard (27 August 2015). "Die MiMe-NoCoDI-Plattform: Ein Ansatz für die Modellierung biologischer Regelkreise". GMDS 2015; 60. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik: Biometrie und Epidemiologie e.V. (GMDS). doi:10.3205/15gmds058.
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