To elucidate whether insulin-induced hypoglycemia enhances the release of beta-endorphin in man, plasma extracts obtained from healthy subjects and patients with Graves' disease before and 45 min after insulin injection were subjected to gel chromatography, and the fractions obtained were measured by RIA for beta-endorphin. In four healthy subjects, basal plasma beta-endorphin levels were less than 3 to 3.1 pg/ml, and the levels rose substantially to 47.5 +/- 12.4 pg/ml (mean +/- SE) 45 min after insulin injection. Basal plasma beta-endorphin levels in three hyperthyroid patinets (less than 3 to 3.8 pg/ml) did not seem to be different from those in healthy subjects; however, the rise after insulin injection tended to be higher in cases of hyperthyroidism, with a peak value of 68.5 +/- 9.7 pg/ml. Plasma beta-lipotropin and ACTH levels also rose in parallel with beta-endorphin in response to insulin-induced hypoglycemia in both healthy subjects and hyperthyroid patients. It would thus appear that beta-endorphin, like ACTH or beta-lipotropin, is released in human subjects by hypoglycemic stress.

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A B S T R A C T To elucidate whether or not 3-endorphin exists in plasma of normal subjects, plasma extracts obtained before and after metyrapone administration were subjected to gel exclusion chromatography, and fractions obtained were assayed by a sensitive radioimmunoassay for,B-endorphin. The basal plasma level of ,8-endorphin was 5.8± 1.1 pg/ml (mean-+SE, n = 5), which rose significantly to the level of 48.9 +3.8 pg/ml after a single oral dose (30 mg/kg of body wt) of metyrapone administration (P < 0.001). Plasma ACTH levels also increased from the mean basal level of 73+4 pg/ml to 269+41 pg/ml after metyrapone administration. These results indicate that f-endorphin, distinct from f8-lipotropin, exists in normal human plasma and that it is released from the pituitary concomitantly with ACTH.

Aims/Introduction: Liraglutide, a glucagon-like peptide-1 receptor agonist, is expected to provide a new treatment option for diabetes. However, the suitable timing of liraglutide administration in type 2 diabetic patients has not yet been clarified. Materials and Methods: We reviewed type 2 diabetic patients (n = 155) who visited the Osaka Red Cross Hospital for glycemic control, with administration of liraglutide at a dose of 0.6 mg (average glycated hemoglobin [HbA 1c ] level, 8.7 ± 0.1%). The effect of liraglutide based on the pretreatment status was compared. We also analyzed the background factors of both a successful and failed group of patients who switched to liraglutide from insulin. Results: An improvement in blood glucose levels was confirmed in 122 of 155 patients. During the 4-month observation period, the improvement in HbA 1c levels was significantly greater in the group of drug-naïve/previous oral hypoglycemic agent (9.1 ± 0.2 to 7.2 ± 0.2%) than that in the group switching from insulin (8.6 ± 0.2 to 7.8 ± 0.2%). In addition, C-peptide immunoreactivity levels (fasting > 2.2 ng/mL; delta >1.6 ng/mL; urine > 70 lg/day), younger age and a smaller number of insulin units used per day were considered important when deciding on switching to liraglutide from insulin. Conclusions: Liraglutide was more effective in patients who had not been treated previously or received oral hypoglycemic agents than in patients switching from insulin. With respect to switching to liraglutide from insulin, the most important factors to be considered were C-peptide immunoreactivity levels, age, and the number of insulin units used per day. (J Diabetes Invest,