Effect of Growth Hormone-Releasing Hormone and Clonidine on Growth Hormone Release in Type 1 Diabetic Patients

Giampietro, Ottavio; Ferdeghini, M; Miccoli, Roberto; Locatelli, Vittorio; Cerri, M; Yanaihara, N; Navalesi, R.; Müller, E. E.

doi:10.1055/s-2007-1011898

Cited by 12 publications

(4 citation statements)

References 16 publications

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“…The pituitary release of GH may be influenced by pharmacological stimuli [24], physical exercise [25], and severe hypoglycemia [13,14], The collection of overnight urine should have reduced the interference of physical exercise on uGH excretion and none of the healthy subjects and diabetic patients was treated by any drug, with the exception of insulin for dia betic patients.…”

Section: Discussionmentioning

confidence: 99%

Urinary Growth Hormone Excretion in Children and Adolescents with Insulin-Dependent Diabetes mellitus

et al. 1996

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Urinary growth hormone (uGH) excretion was evaluated in 96 type-1 insulin-dependent diabetic patients and 37 age-matched healthy subjects. The growth hormone concentration was measured by a solid-phase immunoradiometric assay on 3 consecutive overnight urine collections. uGH excretion was comparable between diabetic patients and healthy subjects: 10.9 (0.1-34.8) vs. 9.1 (2.6-34.5) pg/min. In both groups uGH excretion was lower in prepubertal than in pubescent or pubertal individuals (diabetic patients, H = 29.7, p = 0.001; healthy subjects, H = 10.4, p = 0.006). In diabetic patients uGH excretion was related to β₂-microglobulin excretion (r = 0.308; p = 0.005) and to urinary albumin excretion (r = 0.230; p = 0.02) but it was independent of HbAlc and overnight glycemic values. The coefficient of variation of uGH excretion was higher in diabetic patients with respect to healthy subjects: 50 (3-141) vs. 28 (3-100)% (p = 0.002). Among diabetic patients it was greater in prepubertal than in pubescent or pubertal patients (H = 13.7; p = 0.002); in contrast, it was independent of pubertal stage in healthy individuals (H = 2.4; NS). The coefficient of variation of uGH was not related to HbA1c, the duration of diabetes, the coefficient of variation of urinary albumin excretion and the coefficient of variation of β₂-microglobulin excretion. In conclusion uGH excretion is comparable among diabetic patients and healthy subjects, but its day-to-day fluctuation is greater in the former than in the latter group. Renal function but not metabolic control can influence uGH excretion. The day-to-day fluctuation in uGH excretion is independent of metabolic control and renal function.

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Section: Discussionmentioning

confidence: 99%

Urinary Growth Hormone Excretion in Children and Adolescents with Insulin-Dependent Diabetes mellitus

et al. 1996

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“…Most previous studies have compared responses to TRH in diabetics with those of nondiabetics (Ceda et al, 1982;Blickle et al, 1982;Krassowski et al, 1984;Vanelli et al, 1986), rather than comparing with saline control tests in the diabetics. In one of only two previous studies which employed saline controls, the saline was given before the TRH so that the responses are not strictly comparable, and although mean GH concentrations remained fairly constant after saline, there was wider variability than in non-diabetic controls, and at least two subjects had spontaneous peaks of GH following saline during periods of poor metabolic control (Giampetro et al, 1987a). When Giampetro et al (1987b) directly compared mean GH concentrations in a group of adult males with type I and type I1 diabetes, there was no significant difference after TRH and saline.…”

Section: Discussionmentioning

confidence: 99%

Spontaneous Growth Hormone (Gh) Pulsatility Is the Major Determinant of Gh Release After Thyrotrophin‐releasing Hormone in Adolescent Diabetics

Edge

Human

1989

Clinical Endocrinology

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GH release is abnormally regulated in insulin-dependent diabetes (IDDM), and paradoxical stimulation of GH release after TRH has been reported. However, overnight GH pulsatility is increased in IDDM, and it may be difficult to distinguish TRH-stimulated release from spontaneous secretory episodes. To resolve this question, we carried out two overnight GH profiles followed by either TRH or saline control tests in six adolescents with IDDM; ages 11.4-14.7 years, duration IDDM 2.4-6.7 years. A rise in GH was seen in four of six following TRH, but with no consistent pattern. A rise was also seen in four of six following saline. Peak GH levels were similar after TRH and saline (19.3 +/- 4.4 vs 25.8 +/- 5.5 mU/l; mean +/- SEM). Mean blood glucose was no different during TRH and saline tests (9.5 +/- 1.6 vs 7.5 +/- 0.6 mmol/l). The two subjects who had an early GH peak after TRH were those in whom GH levels had already begun to rise, suggesting the coincident occurrence of a spontaneous GH pulse. The timing of the next GH pulse could be predicted equally well after TRH and saline from the overnight secretory profile using autocorrelation. Paradoxical GH stimulation after TRH is not seen in adolescents with IDDM, but apparent responses may be due to timing coincident with the increased spontaneous pulsatility.

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“…Others have found similar GH responses after i.v. administration of GHRH or clonidine in patients with diabetes and controls, respectively (Giampietro et al, 1987;Kopelman et al, 1988). The differences in GH secretion can be attributed to differences in metabolic control (Press et al, 1984b), test methods, time of the day (Matussek et al, 1984;Devesa et al, 1989), age (Gil-Ad et al, 1984;Shibasaki et al, 1984) and body weight (Pavlov et al, 1986;Kopelman et al, 1988).…”

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confidence: 99%

“…We used GHRH and clonidine intravenously as two different stimulative tests for GH secretion. Both tests have been extensively used for this purpose (Speroni et al, 1983;Gil-Ad et al, 1984;Matussek et al, 1984;Press et al, 1984a;Shibasaki et al, 1984;Masuda et al, 1985;Topper et al, 1985;Pavlov et al, 1986;Giampietro et al, 1987;Pietschmann et al, 1987;Kopelman et al, 1988;Krassowski et al, 1988;Valcavi et al, 1988;Devesa et al, 1989;Ismail et al, 1993).…”

mentioning

confidence: 99%

Growth hormone responses to growth hormone‐releasing hormone and clonidine in patients with type I diabetes and in normal controls: effect of age, body mass index and sex

Jacobs¹,

Nathoe²,

Blankestijn³

et al. 1996

Clinical Endocrinology

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Patients with moderately controlled type I diabetes mellitus have normal baseline and stimulated GH concentrations after the administration of GHRH or clonidine compared with healthy controls, when corrected for age, body mass index and sex. However, these 'normal' GH concentrations must be considered inappropriately high in view of the hyperglycaemia in these patients. The low plasma IGF-I concentrations might be responsible for the GH over-production.

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Effect of Growth Hormone-Releasing Hormone and Clonidine on Growth Hormone Release in Type 1 Diabetic Patients

Cited by 12 publications

References 16 publications

Urinary Growth Hormone Excretion in Children and Adolescents with Insulin-Dependent Diabetes mellitus

Urinary Growth Hormone Excretion in Children and Adolescents with Insulin-Dependent Diabetes mellitus

Spontaneous Growth Hormone (Gh) Pulsatility Is the Major Determinant of Gh Release After Thyrotrophin‐releasing Hormone in Adolescent Diabetics

Growth hormone responses to growth hormone‐releasing hormone and clonidine in patients with type I diabetes and in normal controls: effect of age, body mass index and sex

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