Neonates must have functional pancreatic βcells responsive to glucose(G)(Fowden et al. 1982). Newborn foals, especially premature, have poor regulation of glycaemia. This study examined effects of dysmaturity on pancreatic βcell responses & anatomical development in foals during the 1st 10 days postpartum. Over 48h periods at 3 time intervals (days 1-2, 5-6 and 9-10), βcell responses to iv G (0.5g/kg, 40%G, days 1, 5 and 9) or saline (20ml 0.9% NaCl, days 2, 6 and 10) were examined in pony foals delivered either spontaneously (n=7) or induced 2-3 days before fullterm (n=7). Venous jugular blood samples were taken from an indwelling catheter at 5-15 min intervals for 30 before and 60 min after administration. Foals were muzzled throughout this period. Plasma G levels were determined enzymatically. Plasma insulin(I) and total proinsulin(PI) levels were measured by immunoassay validated for equine plasma (Hemmilä et al. 1984). On day 11, all foals were killed. Each pancreas was analysed using stereological methods validated for equids (Beech, 1998). Statistical analyses were ANOVA, paired/unpaired t tests. Data are means±SEM. Induced foals were all classified as dysmature (Rossdale et al. 1984). There were no significant differences in basal levels of G, I and PI between fullterm and dysmature foals on any days. Clearance of iv G was also similar in the 2 groups at all ages studied. However, the maximum increment in plasma I in response to iv G was greater (p<0.02) in dysmature foals on days 1 and 5. On day 1, I levels also remained elevated for longer after iv G in dysmature foals and the area under the I curve was greater (p<0.01). In contrast, PI responses to iv G were similar in the 2 groups. On day 11, pancreatic mass was similar in the 2 groups but total islet volume and percentage of βcells in islets were greater in dysmature foals (Table). Results show that dysmaturity of the foal is associated with enhanced I secretion and resistance. Greater percentage of βcells in islets and total islet volume suggests that the neonatal pancreas is trying to compensate for I resistance by βcell proliferation.