Fibrotic Encapsulation is the Dominant Source of Continuous Glucose Monitor Delays.

McClatchey PM, McClain ES, Williams IM, Malabanan CM, James FD, Lord PC, Gregory JM, Cliffel DE, Wasserman DH
Diabetes. 2019

PMID: 31399432 · DOI:10.2337/db19-0229

CGM readings are delayed relative to blood glucose, and this delay is usually attributed to the latency of interstitial glucose levels. However, CGM-independent data suggest rapid equilibration of interstitial glucose. This study seeks to determine the loci of CGM delays. Electrical current was measured directly from CGM electrodes to define sensor kinetics in the absence of smoothing algorithms. CGMs were implanted in mice, and sensor versus blood glucose responses were measured following an intravenous glucose challenge. Dispersion of a fluorescent glucose analogue (2-NBDG) into the CGM micro-environment was observed using intravital microscopy. Tissue deposited on the sensor and non-implanted subcutaneous adipose tissue were then collected for histological analysis. The time to half-maximum CGM response was 35±2 seconds. , CGMs took 24±7 minutes to reach maximum current versus 2±1 minutes to maximum blood glucose (p=0.0017). 2-NBDG took 21±7 minutes to reach maximum fluorescence at the sensor, vs 6±6 minutes in adipose tissue (p=0.0011). Collagen content was closely correlated with 2-NBDG latency (R=0.96, p=0.0004). Diffusion of glucose into the tissue deposited on a CGM is substantially delayed relative to interstitial fluid. A CGM that resists fibrous encapsulation would better approximate real-time deviations in blood glucose.

© 2019 by the American Diabetes Association.

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