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Post-transplant diabetes mellitus (PTDM) and impaired glucose tolerance are now considered among the major adverse events following organ transplantation. The present study was aimed at investigating the regulation of glucose metabolism in pediatric recipients of a kidney transplant (KT), receiving tacrolimus or cyclosporine A-based immunosuppression. Twelve subjects, eight males and four females, aged 12.1+/-3.8 yr, and with a mean time from KT of 45.6 months were enrolled in the study. All patients had a basal evaluation of fasting glucose (GF), fasting insulin (IF), C-peptide and glycated hemoglobin (HbA1c) levels. They then underwent oral glucose tolerance test (OGTT), with measurement of blood glucose and insulin concentration. Two children had impaired GF, associated with supernormal HbA1c levels, one patient showed impaired glucose tolerance, none had PTDM. Peripheral insulin resistance, as measured by quantitative insulin sensitivity check index (QUICKI) and homeostasis model assessment estimate of insulin sensitivity (HOMA-IR) index, was enhanced in 3 patients. Subsequently, GF significantly increased with time from transplant (p=0.01), while fasting C-peptide and the area under the curve of insulin correlated with creatinine clearance. In conclusion, our results, although generated in a small sample size, would suggest that long-term follow-up of children receiving a KT should extend to explore the response to oral glucose load and at least the basal measure of insulin response.

Short Communications 247Subcutaneous adipose tissue sampIes (10-20 gm) were obtained from 4 patients undergoing abdominal surgery. Adipose tissues were cut into 20-25 mg fragments and fat cells were isolated essentially according to Rodbell (1964), except that higher concentrations of collagenase (3 mg/mI) were used. Fat cell ghosts were prepared according to Pohl. Birnbaumer and Rod. bell (1970). Adenylate cydase activity was assayed by the method of Salomon, Landos and Rodbell (1974) at pH 8.5 (30 0 C). Sodium clofibrate (lCI-Pharma, Plankstadt, Germany) was dissolved in 0.1 N NaOH, the pH of the solution was adjusted to pH 8.5 and direct1y added to the incubation media. The protein content was determined by the method of Lowry, Rosebrough, Fa" and Randall (1951).Adenylate cyclase activities in the absence of added NaF or nor-adrenaline averaged 1.10 nmol cyclic AMP formed per mg protein/15 min. In the presence of nor-adrenaline (l0-3M) and NaF (20 mM) activities were increased 2-3 fold and 6-8 fold respectively.Increasing concentrations of clofibrate (0.01 to 1 mg/mI) caused a dose-dependent inhibition of basal, sodium fluoride as well as nor-adrenaline stimulated adenylate cyclase activity. 1 mg/mI clofibrate inhibited adenylate cyclase activity by about 35-45% (Table). Hormone and NaF stimulated adenylate cyclase activity was decreased to about the same extent. The inhibitory action of clofibrate was detectable after 2.5 min. Time course was linear up to 25 min. The fact that basal, NaF and nor-adrenaline stimulated enzyme activity is inhibited by about the same extent suggests that the drug action is related to sites essential for catalytic activity. The rapid onset of clofibrate action suggests further that no in-vivo transformation is necessary for inhibition of adenylate cyclase. This finding is in contrast to the results of Greene, Herman and Zakim (1970) who observed inhibition of adenylate cyclase by clofibrate only after pretreatment of the animals. Our results support the conelusion that inhibition of adenylate cyclase activity may contribute to the well-known antilipolytic effect of dofibrate.

To evaluate residual pituitary GH, GH responses to continuous 1 80-min infusion of increasing doses of GHRH t-29 followed by iv bolus injection of GHRH were studied in 28 hypopituitary patients, 21 of whom had pituitary abnormalities on MRI. Pituitary hypoplasi a, stalk agenesis and ectopic posterior pituitary lobe in 7 patients with isolated GH deficiency (IGHD) and 6 with multiple pituitary hormone deficiencies (group I); isolated hypoplasia in 8 IGHD (group II); normal pituitary gland morphology in 7 IGHD (group Ill). Pituitary volume was not significantly differ&nt in the groups I and II.