Growth hormone release in unstable diabetes: Tests with saline, arginine, glucagon, and epinephrine

Cremer, G; Molnar, George D.; Taylor, William F.; Rosevear, John W.; Ackerman, Eugene

doi:10.1007/bf02590712

Cited by 14 publications

(6 citation statements)

References 30 publications

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“…Previous studies have suggested that GH levels are inappropriate (1,2,6,9,21) and that the control of GH secretion is impaired (6)(7)(8)(9) in diabetic patients. The present study was undertaken to explore another parameter that might reflect abnormalities in GH release, namely response to TRH.…”

Section: Discussionmentioning

confidence: 99%

“…An increased GH response to exercise has been reported in poorly controlled insulindependent subjects, although the response was normalized in this same group of patients when control was optimized (4,5). GH release appears abnormal in insulindependent diabetics in that hyperglycemia does not inhibit the response of GH to provocative maneuvers, such as arginine infusion or L-dopa, and an altered glucoreceptor has been postulated to explain this response (6)(7)(8)(9).…”

mentioning

confidence: 86%

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Growth Hormone Response to Thyrotropin-Releasing Hormone in Diabetes*

Dasmahapatra

Urdanivia

Cohen

1981

The Journal of Clinical Endocrinology & Metabolism

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The effect of TRH on GH secretion was assessed in 13 insulin-dependent diabetics. PRL and TSH responses to TRH were also determined. Glycosylated hemoglobin levels and serial fasting glucose concentrations indicated that all but 1 of the patients had a period of poor diabetic control for several months before the study. Peak PRL and TSH levels after TRH injection in these diabetic patients did not differ significantly from values observed in nondiabetic individuals. Six of the patients responded to TRH with a significant rise in GH levels; basal GH concentrations were also elevated in these patients. Five of the 6 responders and none of the nonresponders had proliferative diabetic retinopathy. The results suggest that diabetics with elevated basal GH levels hyperrespond to TRH, and that nonspecific secretion of GH in response to TRH occurs in some patients with proliferative diabetic retinopathy. Chronic hyperglycemia does not appear to be the critical factor in determining this response.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 86%

Growth Hormone Response to Thyrotropin-Releasing Hormone in Diabetes*

Dasmahapatra

Urdanivia

Cohen

1981

The Journal of Clinical Endocrinology & Metabolism

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“…In addition to increased spontaneous growth hormone secretion, patients with diabetes may show an exaggerated response to provocative stimuli (17)(18)(19). Growth hormone levels may also fail to suppress normally with glucose, or even rise paradoxically (20,21), and may rise during insulin administration (22,23).…”

Section: Plasma Growth Hormone (Gh) Levels Before and After Adminismentioning

confidence: 99%

“…Diabetes 41: [17][18][19][20][21]1992 T he raised circulating growth hormone levels characteristic of poorly controlled insulin-dependent diabetes mellitus (IDDM) actively worsen diabetic control and may play a part in the pathogenesis of diabetic retinopathy (1,2). The mechanism or mechanisms underlying the diabetesinduced alterations in growth hormone secretion observed clinically have not been clarified, however.…”

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confidence: 99%

Pituitary Response to Growth Hormone–Releasing Hormone in IDDM: Abnormal Responses to Insulin and Hyperglycemia

et al. 1992

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In poorly controlled insulin-dependent diabetes mellitus (IDDM), hyperglycemia fails to inhibit the pituitary response to growth hormone-releasing factor (GRF). To evaluate whether this derangement is reversed by a simultaneous elevation of circulating insulin, 0.3 micrograms/kg i.v. GRF 1-40 was administered to nine poorly controlled IDDM subjects (HbA1 greater than 11.1%) with and without concomitant infusion of insulin. In the absence of insulin, the poorly controlled IDDM subjects demonstrated a growth hormone response to GRF similar to that of nondiabetic subjects, despite marked hyperglycemia (approximately 16.8 mM). When insulin was infused into these same patients (insulin clamp) to produce combined hyperinsulinemia (528 +/- 90 pM) and hyperglycemia (16.5 +/- 1.98 mM), the GRF-induced growth hormone rise was markedly exaggerated (65 +/- 11 vs. 20 +/- 4 micrograms/L without insulin infusion, P less than 0.001). This enhancement of GRF-stimulated growth hormone release by insulin was strikingly attenuated (22 +/- 7 micrograms/L) in five well-controlled diabetic subjects studied under conditions of similar hyperinsulinemia (486 +/- 84 pM) and hyperglycemia (16.41 +/- 0.95 mM). In contrast, in nondiabetic subjects, acute hyperinsulinemia reduced the growth hormone response to GRF. We conclude that the failure of hyperglycemia to block the pituitary response to GRF in poorly controlled diabetes is not attributable to the lack of a coincident increase in circulating insulin. The paradoxical stimulatory effect of insulin on GRF-induced growth hormone release may contribute to the high spontaneous growth hormone levels characteristically seen in poorly controlled insulin-treated patients, and its attenuation after intensive insulin therapy may contribute to the reversal of growth hormone hypersecretion in well-controlled diabetic patients.

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“…More¬ over, it is well known that in insulin-dependent (Type I) diabetic patients several abnormalities in GH secretion may be observed. Poorly controlled Type I diabetic patients show higher mean 24-h GH levels than normal subjects (3), exaggerated GH responses to provocative tests (4)(5)(6) and para¬ doxical GH secretion after TRH (7). GH secretion is regulated by two hypothalamic peptides: GHRH, which has an excitatory role, and somatostatin, which has an inhibitory role.…”

mentioning

confidence: 99%

Effects of exogenous growth hormone pretreatment on the pituitary growth hormone response to growth hormone-releasing hormone alone or in combination with pyridostigmine in Type I diabetic patients

Giustina

Bossoni²,

Bodini³

et al. 1991

Acta Endocrinologica

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We evaluated the effects of iv pretreatment with exogenous GH on the GH response to GHRH either alone or in combination with pyridostigmine in 14 Type I diabetic patients and 6 normal subjects. All the subjects received an iv bolus injection of biosynthetic human GH, 2 IU; 2 h later they received either a. pyridostigmine, 120 mg orally, or b. placebo, 2 tablets orally, followed 1 h later by iv injection of GHRH(1-29) NH2, 100 \g=m\g. In normal subjects the median GH peak after GH+GHRH was 1.8, range 1.2-6.9 \g=m\g/l .Pyridostigmine enhanced the GH response to GHRH in all subjects. The median GH peak after pyridostigmine+ GH+GHRH was 32.7, range 19.8\x=req-\ 42.1 \g=m\g/l(p<0.001 vs GHRH alone). Seven diabetic subjects had median GH peaks after GH+GHRH >6.9 \ g=m\ g/ l (the maximum GH peak after GH+GHRH in normal subjects) (group A: median GH peak 35.7, range 21.7-55 \g=m\g/l ). The other diabetic subjects had GH peak lower than 6.9 \g=m\g/l(group B: median GH peak 4.4, range 2.1-6.5 \g=m\g/l ).Pyridostigmine significantly increased the GH response to GHRH in group B patients (median GH peak 29.3, range 15.7-93.4 \g=m\g/l,p<0.001 vs GH+GHRH alone), but not in group A patients (median GH peak 39.9, range 21.9-64.9 \g=m\g/l).Group A diabetic patients were younger and had higher HbA1c and blood glucose levels than group B patients. In those diabetic patients with an exaggerated GH response to GH+GHRH, pyridostigmine failed to cause the increase in GH secretion observed in diabetic and control subjects with no responses to GH+GHRH. It can be suggested that elevated 24-h GH levels in some Type I diabetic patients may be due to decreased somatostatinergic tone which in turn causes altered autoregulation of GH secretion. We hypothesize that this finding is a consequence of a reset of the hypothalamic control of GH secretion caused by a chronically elevated blood glucose level in this subpopulation.

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Growth hormone release in unstable diabetes: Tests with saline, arginine, glucagon, and epinephrine

Cited by 14 publications

References 30 publications

Growth Hormone Response to Thyrotropin-Releasing Hormone in Diabetes*

Growth Hormone Response to Thyrotropin-Releasing Hormone in Diabetes*

Pituitary Response to Growth Hormone–Releasing Hormone in IDDM: Abnormal Responses to Insulin and Hyperglycemia

Effects of exogenous growth hormone pretreatment on the pituitary growth hormone response to growth hormone-releasing hormone alone or in combination with pyridostigmine in Type I diabetic patients

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