In humans abnormal mitochondrial function has been associated with type II diabetes (T2D; Kelley et al. 2002). We have previously demonstrated poor glucose tolerance in the adult offspring of ewes undernourished (0.5 maintenance) over late gestation (Gardner et al. 2005). Therefore, in the present study, we hypothesize that mitochondrial dysfunction in the kidney accompanies glucose intolerance in these sheep. Blue faced Leicester cross Swaledale sheep were fed a dietary regime as described by Gardner (2005): Control group (C n=7) received 100% metabolizable energy (ME) as defined by the Agricultural and Food Research Council, throughout gestation; early nutrient restricted group (NRE, n=6) 50% ME gestation from days 1-30 with 100% ME thereafter; and late nutrient restricted group (NRL, n=4) 50% ME from days 110-term (~day147) with 100% ME at all other times. Ewes delivered spontaneously and at 3 months, lambs were weaned onto pasture at 10 weeks and remained on grass until 12 months. Renal tissue was then harvested post mortem from the offspring, snap frozen and stored at -80°C. Mitochondrial respiratory chain complexes I to IV and citrate synthase activity were measured spectrophotometrically (Rahman et al. 2001). Respiratory chain enzymes were expressed as a ratio of citrate synthase to compensate for mitochondrial enrichment of the sample. Results were analyzed by ANOVA and expressed as means ± SEM. Higher mitochondrial activities in linked complex II III assay was observed in NRL vs. other groups, C (0.17±0.014) vs. NRL (0.27±0.051) P<0.05 and NRE (0.19±0.018) vs. NRL (0.270±0.051) P<0.05. We conclude that late gestational global under nutrition leads to abnormal renal mitochondrial function that is associated with glucose intolerance. Our data show a direct correlation between poor glucose control that is symptomatic of T2D in humans with abnormalities in mitochondrial complex activities.