Microvascular oxygen transport in obese ZDF rats: an early model of type II diabetes

Abstract

Sprague et al. (Diabetes 2006) reported impaired ATP release from human red blood cells (RBC) with type II diabetes that may contribute to impaired regulation of O2 delivery. Our goal was to quantify O2 transport in skeletal muscle of obese ZDF‐370 rats. Using dual wavelength intravital video microscopy we measured hemodynamics (RBC velocity, RBC supply rate, hematocrit) and RBC oxygen saturation in capillaries of extensor digitorum longus muscle as well as capillary density, glucose, TNF‐ α levels, arterial blood gases, arterial hemoglobin and hematocrit levels. Results reported as mean±SD. Two groups, 7 lean ZDF‐380 rats (179±13 g) and 8 obese ZDF‐370 rats (240±10 g), were studied at 7 weeks. Both glucose and TNF‐ α levels were elevated in the obese group compared to lean (glucose: 12.3±5.1 vs 6.8±0.6 mmol/L; TNF‐α: 112±43 vs 19±9 pg/mol). There were no significant differences in total capillary density. RBC supply rate was significantly decreased in obese rats (7.2±1.1 vs 9.0±1.8 RBC/s; p < 0.05); other hemodynamic parameters were unchanged (obese vs lean: velocity 130±26 vs 157±29 μm/sRBC, Hct 14.6±3.3 vs 15.3±1.6 %). There was a trend for decreased O2 saturation in the obese group (54±16% vs 64±5%; p = 0.19). The lower RBC supply rate and O2 saturations suggest the start of impaired regulation of O2 transport in this early diabetic model.Supported by NIH grant (HL‐089125) and a CIHR operating grant to Ellis & Goldman.