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,
VERONICA A. VACCARO,
ROBERT A. BOOTH, JR.,
GERMAN LIZARRALDE,
CHRISTOPHER M. ASPLIN and
WILLIAM S. EVANS
Endocrine Section, Veterans Affairs Medical Center (A.I., G.L.) Salem, Virginia 24153
the Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia Health Sciences Center (J.D.V., E.C.C., V.A.V., R.A.B., C.M.A., W.S.E.) Charlottesville, Virginia 22908
Address all correspondence and requests for reprints to: Ali Iranmanesh, M.D., Endocrine Section (111P), Veterans Affairs Medical Center, Salem, Virginia 24153.
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.
* This work was supported by Veterans Affairs Medical Research funds (to A.I.); USPHS General Clinical Research Center Grant RR-00847, Research Career Development Award HD-00634, and University of Virginia Computer Services Grant (to J.D.V.); and Research Career Development Award HD-00711, American Diabetes Association Feasibility Grant, and University of Virginia Computer Services Grant (to W.S.E.).
Visiting Postdoctoral Fellow from Denmark.
Received November 22, 1989.
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