MICRODIALYSIS OF GLUCOSE IN SUBCUTANEOUS ADIPOSE-TISSUE UP TO 3 WEEKSIN HEALTHY-VOLUNTEERS

OBJECTIVE - To measure possible changes in dialysate glucose concentra tions over time, to validate the diffusional model for glucose transpo rt from tissue to the probe, and to evaluate the actual glucose concen tration in adipose tissue. RESEARCH DESIGN AND METHODS - Glucose conce ntrations in the subcutaneous adipose tissue of five healthy subjects (age 25 +/- 2.7 years, BMI 23.2 +/- 2.3 kg/m(2) [mean +/- SD]) were me asured by the microdialysis technique and compared with blood glucose. We applied microdialysis probes with hollow fibers of various membran e length (10-35 mm), used eight perfusion flow rates (0.5-20 mu l/min) , and perfused four glucose solutions (0.0, 2.8, 8.3, 11.1 mmol/l). RE SULTS - After implantation, a substantial decrease in glucose recovery to the lowest value of 26 +/- 10% of the final plateau value was note d during the first few hours (n = 4). Recovery increased and stabilize d after 5-9 days at 84.0 +/- 7.4% of capillary blood glucose when a fl ow rate of 0.5 mu l/min was applied. According to the zero net-flux me thod, the glucose concentration in equilibrium, C-equi, with the surro unding tissue can be obtained. This concentration also decreases; howe ver, 1 h after recovery, C-equi increases again over 1 or 2 days to a stable value that is not significantly different from the measured cap illary blood glucose (P < 0.05). Using various perfusion flow rates an d probes (membrane length 10-35 mm), it is shown that diffusion is the rate-limiting process for glucose transport through tissue. CONCLUSIO NS - Insertion of the microdialysis probes causes damage to the adipos e cells and the vascular bed around the probe. Glucose recovery decrea ses because of a lower blood supply. In 5-9 days, glucose recovery inc reases; apparently, this time is needed to repair the microstructure o f tissue around the probe. After stabilization of the recovery, no los s of probe permeability, which is due to biocompatibility problems, wa s seen. The change during the 2 days in equilibrium concentration is p robably caused by an inflammation reaction that consumes glucose aroun d the probe. The individual increase in recovery during the Ist days a fter probe insertion until a stable plateau value is reached (flow rat e >0 mu l/min) is complicated for short-term clinical glucose measurem ents in adipose tissue. After stabilization, the mean equilibrium conc entration of all subjects was equal to the mean capillary blood glucos e concentration. Therefore, we conclude that capillary blood glucose c oncentration probably is the driving force for diffusion through the c apillary wall into the probe and is not some interstitial concentratio n.