 Routinely in pregnancy, gestational diabetes is diagnosed by the administration of a glucose tolerance test consisting of ingestion of 50g of glucose followed by a serum glucose level one hour later. This is known as a one-hour post-glucola test. A value of 140 mgdL is considered abnormal, and prompts administration of the 3-hour glucose tolerance test. This test consists of a fasting blood sugar, followed by serum glucose levels after a 100g oral glucose challenge at 1-, 2- and 3-hours. A profile with two or more abnormal values is considered diagnostic for gestational diabetes. In 1997 Fisher et al retrospectively compared the incidence of gestational diabetes in those patients who had received tocolytics and antenatal corticosteroids to those who did not, and found a higher incidence of both abnormal one-hour glucose screening tests and gestational diabetes in those patients who received steroids and tocolytics medications used to try to decrease uterine contractions. However, the interval between the receipt of steroids and the administration of the glucose screening test was quite variable in this study. Shelton et al in 2002 evaluated the extent of hyperglycemia in non-diabetic patients who received multiple weekly doses of corticosteroids. They found that the fasting glucose levels increased for several days following the first course of steroids, returned to normal, and then remained persistently elevated in those patients who received three or more courses. Postprandial levels were not significantly altered. A study by Gurbuz et al in 2003 assessed the effects of betamethasone on the one-hour glucola test and found that although there was an initial effect on the screening test, this effect was transient and resolved generally one week after the administration of the second dose of betamethasone. These patients had a one-hour screening test performed prior to the administration of corticosteroids. The dosing regimen of betamethasone, however, was different from that recommended by ACOG. Thus far, no study has reported if: 1 there is significant hyperglycemia in non-diabetic patients who receive corticosteroids and 2 how the magnitude and pattern of the increase in glucose differs in patients with normal and abnormal one-hour glucolas or with diabetes. This study will be conducted as a pilot study, as there is no reports of the extent of hyperglycemia that occurs in non-diabetic patients after administration of corticosteroids to guide a sample size calculation. We will plan to obtain thirty non-diabetic subjects with fifteen diet-controlled diabetic controls for comparison. The hypothesis is that those patients that are not diabetic will not have the same extent of hyperglycemia as those who are diabetic. 