TY - JOUR
T1 - Attenuated pulsatile release of prolactin in men with insulin-dependent diabetes mellitus
AU - Iranmanesh, Ali
AU - Veldhuis, Johannes D.
AU - Carlsen, Elisabeth C.
AU - Vaccaro, Veronica A.
AU - Booth, Robert A.
AU - Lizarralde, German
AU - Asplin, Christopher M.
AU - Evans, William S.
PY - 1990/7
Y1 - 1990/7
N2 - Pulsatile and circadian patterns of PRL release were studied in 11 insulin-dependent diabetic men by sampling blood every 10 min for 24 h and comparing the results to those obtained in 12 normal nondiabetic men. The diabetic men had a mean (±SE) 24-h serum PRL concentration of 5.5 ± 0.42 μg/L, which was significantly lower than that in the nondiabetic men (9.3 ± 0.86; P = 0.0008). Quantitative Cluster analysis of pulsatile PRL time series revealed a normal pulse frequency, but decreased maximal peak amplitude (6.6 ± 0.5 vs. 11.8 ± 1.1 μg/L; P = 0.0009), peak increment (2.6 ± 0.24 vs. 4.0 ± 0.3 μg/L; P = 0.009), peak area (126 ± 15 vs. 192 ± 19 μg/L·min; P = 0.03), and interpulse valley mean concentration (4.8 ± 0.4 vs. 8.6 ± 1.2 μg/L; P = 0.0007). PRL pulse incremental amplitude correlated significantly (r2 = 0.577; P = 0.007) and negatively with duration of disease. Fourier analysis disclosed a normal circadian rhythm of PRL release in diabetic men, with a mean circadian amplitude of 1.5 μg/L ± 0.31, which peaked at 0201 h ± 89 min (±SE). In summary, we have demonstrated significantly reduced mean 24-h serum PRL concentrations in men with poorly controlled insulin-dependent diabetes mellitus. The concomitant suppression of spontaneous PRL pulse amplitude, peak increment, and interpulse valley mean concentrations in the presence of normal pulse frequency is consistent with a reduced mass of PRL secreted per burst and/or accelerated metabolic clearance of PRL in men with type I diabetes mellitus.
AB - Pulsatile and circadian patterns of PRL release were studied in 11 insulin-dependent diabetic men by sampling blood every 10 min for 24 h and comparing the results to those obtained in 12 normal nondiabetic men. The diabetic men had a mean (±SE) 24-h serum PRL concentration of 5.5 ± 0.42 μg/L, which was significantly lower than that in the nondiabetic men (9.3 ± 0.86; P = 0.0008). Quantitative Cluster analysis of pulsatile PRL time series revealed a normal pulse frequency, but decreased maximal peak amplitude (6.6 ± 0.5 vs. 11.8 ± 1.1 μg/L; P = 0.0009), peak increment (2.6 ± 0.24 vs. 4.0 ± 0.3 μg/L; P = 0.009), peak area (126 ± 15 vs. 192 ± 19 μg/L·min; P = 0.03), and interpulse valley mean concentration (4.8 ± 0.4 vs. 8.6 ± 1.2 μg/L; P = 0.0007). PRL pulse incremental amplitude correlated significantly (r2 = 0.577; P = 0.007) and negatively with duration of disease. Fourier analysis disclosed a normal circadian rhythm of PRL release in diabetic men, with a mean circadian amplitude of 1.5 μg/L ± 0.31, which peaked at 0201 h ± 89 min (±SE). In summary, we have demonstrated significantly reduced mean 24-h serum PRL concentrations in men with poorly controlled insulin-dependent diabetes mellitus. The concomitant suppression of spontaneous PRL pulse amplitude, peak increment, and interpulse valley mean concentrations in the presence of normal pulse frequency is consistent with a reduced mass of PRL secreted per burst and/or accelerated metabolic clearance of PRL in men with type I diabetes mellitus.
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U2 - 10.1210/jcem-71-1-73
DO - 10.1210/jcem-71-1-73
M3 - Article
C2 - 2196281
AN - SCOPUS:0025353922
SN - 0021-972X
VL - 71
SP - 73
EP - 78
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 1
ER -