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Abnormal pulsatile secretion of growth hormone in non‐insulin‐dependent diabetes mellitus
Author(s) -
Franek E.,
Schaefer F.,
Bergis K.,
Feneberg R.,
Ritz E.
Publication year - 1997
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1046/j.1365-2265.1997.2901107.x
Subject(s) - medicine , endocrinology , pulsatile flow , diabetes mellitus , morning , insulin , obesity
OBJECTIVE Studies of GH secretion in patients with non ‐insulin dependent diabetes mellitus (NIDDM) have produced conflicting results. We aimed to differentiate the effects of obesity and metabolic control on pulsatile GH secretion in patients with NIDDM. DESIGN Blood sampling every 15 min from 22.00 hours to 08.00 hours after a fasting period of at least 3 h. Patients: 13 male NIDDM patients, 9 healthy control subjects matched for age and BMI, and 6 lean subjects matched for age. MEASUREMENTS Measurement of GH by a novel ultrasensitive chemiluminescence assay. Analysis of concentration vs time profiles by a multiparameter deconvolution technique. RESULTS GH burst frequency was increased in the NIDDM (0.82 ± 0.28 h −1 ) compared with both control groups (lean: 0.6 ± 0.11; obese: 0.56 ± 0.19). GH burst mass was decreased in patients (1.57 ± 0.98 μg/l.min) and in obese controls (1.46 ± 1.44) compared to lean controls (3.71 ± 3.88). These differences resulted in a significantly higher nocturnal pulsatile GH secretion rate in the lean compared to the obese controls, whereas in the patient group enhanced GH burst frequency compensated for reduced burst mass. The characteristics of GH secretion were not related to nocturnal or early morning blood glucose concentrations. However, GH secretion rate was correlated positively with HbA 1c ( r = 0.57; P = 0.04), and negatively with plasma C peptide concentrations. CONCLUSIONS The specific increase in GH burst frequency previously described in insulin‐dependent diabetes mellitus is also present in NIDDM. However, GH hypersecretion does not occur because GH burst mass is reduced in proportion to the degree of obesity. The effect of diabetes on the hypothalamic control of GH release appears to be determined by the quality of long‐term glycaemic control.