Plasma samples were obtained throughout pregnancy and pseudopregnancy from Sprague-Dawley (SD) rats and during pregnancy from rats of the Munich Wistar (MW) strain. The concentrations of progesterone, oestradiol, prolactin, plasma renin activity (PRA), aldosterone and corticosterone were measured by radioimmunoassay to establish hormonal profiles in the two strains of rat. Circulating progesterone concentrations in both strains of rat were significantly higher during pregnancy than in virgin controls, except at term in the SD group. The hormonal pattern for pseudopregnancy was similar to that of the first half of pregnancy. Oestradiol concentrations were similar to, or lower than, those in virgin controls throughout pseudopregnancy and for the first 2 weeks of pregnancy in both strains of rat. Increased concentrations of steroid were seen only in the pregnant groups towards term. In SD rats, highest prolactin concentrations were apparent during the first half of pregnancy and pseudopregnancy, and at term in the pregnant group. Pregnant MW rats showed a different profile for this hormone, with low levels throughout pregnancy except at term. In all groups PRA rose to a peak at day 9 and decreased to day 16. Pregnant SD rats also showed a significant increase at term. Aldosterone concentrations were significantly increased at several stages of pregnancy in both strains of rat, particularly during the second half of gestation. Pseudopregnant animals showed a different hormone profile, with no significant changes until day 16 when lower concentrations were recorded. There was little variation in the circulating corticosterone concentration except in pregnant rats at term when levels fell. These findings are discussed in relation to the known renal changes of pregnancy and pseudopregnancy.

SUMMARYA disturbed calcium homeostasis characterizes diabetic pregnancy. This study documents changes in bone mineral composition in diabetic pregnant rats and examines the effect of insulin replacement. Control pregnant (CP), diabetic pregnant (DP) and insulin-treated DP (DP1) rats were assessed for femoral calcium and magnesium content, bone mineral density (BMD) and the ratio of hypertrophic to maturing and proliferative cells in the femoral growth plate. DP rats showed a significantly (P < 0.01) lower body weight, femoral weight and length than CP rats. Femoral calcium and magnesium content was also significantly (P < 0.05) lower in DP rats, as was ash weight. When calcium and magnesium were normalized for ash weight no signflcant differences were apparent. A significantly (P < 0.05) lower total BMD at the distal femur was seen in DP rats. This comprised a significantly (P < 0.01) lower trabecular BMD with no significant change in cortical BMD. A significantly (P < 0.05) higher ratio of hypertrophic to maturing and proliferative cells of the femoral growth plate was evident in DP animals. DPi rats showed normal blood glucose concentrations and femoral growth plate histology. DPi rats also showed normal femoral weight and length but only partially restored femoral ash weight and mineral content. Insulin failed to normalize total or trabecular BMD. Diabetes mellitus clearly has a marked effect on bone growth and mineral content in pregnancy which may be relevant to overall calcium homeostasis. The lower bone growth, bone calcium content and trabecular BMD may be unfortunate consequences of the marked hypercalciuria reported elsewhere in diabetes and may serve to maintain normocalcaemia in the disease.

Metabolic and isotopic dilution techniques were used to investigate fluid balance and fluid volumes in rats made diabetic with streptozotocin before and after infusion. Uninfused diabetic rats had significantly (P less than 0.01) lower total body water than controls (57.7 +/- 2.2 vs 65.7 +/- 1.4% (S.E.M.) fat free mass). This was due exclusively to a significantly (P less than 0.001) reduced intracellular fluid volume (38.2 +/- 1.5 vs 45.4 +/- 1.4% fat free mass). Metabolic studies over the preceding 2 weeks showed that the fluid deficit in the diabetic group had resulted from a failure of the rats to increase their fluid intake to the same extent as their combined fluid losses. A 4-h saline infusion halved the fluid deficit in diabetic animals. The retained fluid was used to restore intracellular fluid volume which became comparable in diabetic and control rats (47.2 +/- 2.0 vs 46.4 +/- 1.0% fat free mass). The retention of infusate by diabetic animals to counteract their intracellular dehydration may partly explain the reduced urine output reported elsewhere in infused anaesthetized diabetic rats.

SUMMARYTracer microinjection studies were used to grossly locate the nephron site of altered calcium transport following D-glucose loading. Superficial proximal and distal nephrons were injected with a solution containing 45Ca and either D-glucose or L-glucose (as control). Tubule calcium transport was assessed from the recovery of radioactivity in the final urine. 45Ca recoveries from early proximal microinjections were comparable in the two groups (2-63 + 0 68 vs. 3-70 + 1l19 %). However, 45Ca recoveries from late proximal microinjections were significantly higher when D-glucose was included in the injectate (7 39 + 1-34 vs. 2-83 + 0-67 %, P < 005). 45Ca recoveries from distal microinjections were also significantly higher in the D-glucose group (87-6 + 2-43 vs. 71-0 + 2-92 %, P < 0-001). These data suggest that the effects of D-glucose on renal calcium handling are mediated at the level of the distal tubule, thick ascending limb of the loop of Henle and/or pars recta. The precise mechanisms involved are not known.