Growth Hormone in Thyrotoxicosis: Effect of Insulin-Induced Hypoglycemia1

Burgess, John A.; Smith, Beverly; Merimee, Thomas J.

doi:10.1210/jcem-26-11-1257

Cited by 51 publications

(22 citation statements)

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“…Impoverished plasma HGH responses to insulin-induced hypoglycemia have been reported in patients with hypothyroidism (35,36) and hyperthyroidism (37 results of the present studies suggest that if the blunted plasma HGH responses in patients with hyperthyroidism are encountered, they cannot be explained on the basis of increased peripheral clearance of the hormone. Recent observations, moreover, indicate that plasma HGH responses to hypoglycemia are normal in patients with hyperthyroidism (38).…”

Section: Discussionsupporting

confidence: 42%

Metabolic clearance and production rates of human growth hormone

Taylor¹,

Finster²,

Mintz³

1969

J. Clin. Invest.

115

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A B S T R A C T The metabolic clearance rate (MCR) of human growth hormone (HGH) was determined by the constant infusion to equilibrium technique utilizing HGH-5I. 22 control subjects had a MCR of 229 ±52 ml/min (mean ±sD). No difference was evident between sexes, or between various age groups. Patients with acromegaly demonstrated normal MCR's. Moreover, acute elevations of plasma growth hormone concentrations in normal subjects did not alter the MCR of HGH. The MCR was relatively constant from day to day and within the day when subjects were evaluated in the supine position. In contrast, the assumption of the upright position was associated with a mean 24% decrease in the MCR.These results were contrasted with the MCR of HGH observed in a small number of patients with altered thyroid function or diabetes mellitus. In six patients with hypothyroidism the MCR (131 ±36 ml/min) was significantly decreased (P < 0.001); whereas the MCR in eight patients with hyperthyroidism (240 ±57 ml/min) did not differ from control subjects. The MCR in eight patients with insulin-independent diabetes mellitus (IID) (185 ±41 ml/min) and in eight patients with insulin-dependent diabetes mellitus (IDD) (136 ±31 ml/min) were significantly different from control subjects (P = < 0.05 and P = < 0.001, respectively).These data were interpreted to indicate that the plasma HGH-removing mechanism(s) is not saturated at physiologic plasma HGH of clearance from the plasma, and that the estimation of the MCR of HGH may help clarify the mechanism of abnormal plasma HGH responses to various stimuli.Production rates of HGH (PR) in control subjects (347 ±173 mug/min) were contrasted with hyperthyroid patients (529 ±242 mitg/min, P < 0.05), hypothyroid patients (160 ±69 m/g/min, P < 0.02), lID (245 ±100 m/g/min, NS), and IDD (363 ±153 mug/min, NS). Considerable variability in the determination of the concentrations of immunoprecipitable HGH-l`I and endogenous plasma HGH concentrations was encountered at apparent equilibrium conditions. Since both factors are necessary for the PR calculations, the wide 95% confidence limits of the PR's did not permit a clear interpretation of the significance of these observations. INTRODUCTION Investigators examining the physiologic regulation of plasma human growth hormone (HGH) have been aware that diverse stimuli (1-9) elicit changes in plasma HGH concentrations. Such changes in plasma levels alone, moreover, do not distinguish between the separate contributions of pituitary HGH release and HGH clearance from the plasma, both of which are responsible for a change in plasma concentration.The plasma disappearance of single intravenous injections of radioisotopically labeled HGH has been analyzed to define the distribution and turnover of HGH in humans (10-12). The fractional turnover and production rates of HGH in these studies were derived from calculations which assume first order kinetics and steadystate conditions. Some of the radioisotopic plasma disappearance curves in the literature (10, 11), however, do ...

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Section: Discussionsupporting

confidence: 42%

Metabolic clearance and production rates of human growth hormone

Taylor¹,

Finster²,

Mintz³

1969

J. Clin. Invest.

115

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“…6]. In patients with hyper thyroidism reduced GH responses to pharmacological stimuli [7][8][9] and reduced spontaneous nocturnal GH secretion have been reported [10], In the hyperthyroid rat the GH response to GHRH has also been described to be decreased [11]. Recently, studies in man have shown that the blunted GH response to GHRH in hyperthyroid patients is normalized by long-term antithyroid therapy [9.…”

Section: Introductionmentioning

confidence: 99%

Acute Effects of Clonidine and Growth-Hormone-Releasing Hormone on Growth Hormone Secretion in Patients with Hyperthyroidism

et al. 1991

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Patients with hyperthyroidism have reduced growth hormone (GH) responses to pharmacological stimuli and reduced spontaneous nocturnal GH secretion. The stimulatory effect of clonidine on GH secretion has been suggested to depend on an enhancement of hypothalamic GH-releasing hormone (GHRH) release. The aim of our study was to evaluate the effects of clonidine and GHRH on GH secretion in patients with hyperthyroidism. Eight hyperthyroid females with recent diagnosis of Graves’ disease (age range 20–55 years, body mass index range 19.2–26.2 kg/m²) and 6 healthy female volunteers (age range 22–35 years, body mass index range 19–25 kg/m²) underwent two experimental trials at no less than 7-day intervals: (a) an intravenous infusion of clonidine 150 µg in 10 ml of saline, or (b) a bolus intravenous injection of human GHRH (1–29)NH₂, 100 µg in 1 ml of saline. Hyperthyroid patients showed blunted GH peaks after clonidine (7.1 ± 1.7 µg/l) as compared to normal subjects receiving clonidine (28.5 ± 4.9 µg/l, p < 0.05). GH peaks after GHRH were also significantly lower in hyperthyroid subjects (8.0 ± 1.7 µg/l) as compared to normal subjects receiving GHRH (27.5 ± 4.4 µg/l, p < 0.05). No significant differences in the GH values either after clonidine or GHRH were observed in the two groups of subjects examined. Our data demonstrate that the GH responses to clonidine as well as to GHRH in patients with hyperthyroidism are inhibited in a similar fashion with respect to normal subjects. That clonidine is not able to reverse the blunted GH secretion in hyperthyroidism suggests that hyperthyroxinemia may either cause an increase in somatostatin release by the hypothalamus or block GH secretion acting directly at the pituitary level.

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“…In a series ofreported studies, between 40 and 80% of hypothyroid patients demonstrated a blunted growth hormone response to insulin-induced hypoglycemia, and in the majority ofthese patients the response normalized after thyroid hormone administration and restoration of the euthyroid state (46)(47)(48). In thyrotoxicosis, insulin-induced hypoglycemia tends to result in subnormal growth hormone responses as compared with euthyroid controls, and this is restored to normal levels after restoration of euthyroidism (49,50). Finkelstein et al (50) quantitated the growth hormone plasma halflife and 24-h secretory rates in hyperthyroid patients and euthyroid controls.…”

Section: Introductionmentioning

confidence: 99%

Relationship of receptor affinity to the modulation of thyroid hormone nuclear receptor levels and growth hormone synthesis by L-triiodothyronine and iodothyronine analogues in cultured GH1 cells.

Samuels¹,

Stanley²,

Casanova³

1979

J. Clin. Invest.

122

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A B S T R A C T We have previously demonstrated that L-triiodothyronine (L-T3) induces an increase in growth hormone synthesis and messenger RNA in cultured GH1 cells, a rat pituitary cell line. In addition to regulating the growth hormone response, L-T3 elicits a time-and dose-dependent reduction in the level of its nuclear receptor, which is a direct function of the occupancy of the receptor binding site. In this study we have compared the relative affinity of L-T3, triiodothyroacetic acid, D-triiodothyronine (D-T3), and L-thyroxine (L-T4) for the receptor with the induction ofthe growth hormone synthesis and the ability of these compounds to elicit a reduction in thyroid hormone nuclear receptor levels. Triiodothyroacetic acid and D-T3 were specifically examined because the biologic effect of these compounds in the intact rat is significantly lower than predicted by their affinity for the receptor using isolated rat liver nuclei in vitro. In intact cells each compound demonstrated an excellent relationship between the relative receptor affinity, the induction of growth hormone production, and the concentration-dependent reduction in nuclear receptor levels. With the exception of D-T3, the relative affinity of iodothyronine was identical for the receptor using intact cells in serum-free media, or isolated GH, cell nuclei in vitro. The apparent receptor affinity of D-T3 with intact cells was 5.5-fold lower than with isolated nuclei, which suggests a decrease in cell entry of D-T3 relative

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Growth Hormone in Thyrotoxicosis: Effect of Insulin-Induced Hypoglycemia1

Cited by 51 publications

References 0 publications

Metabolic clearance and production rates of human growth hormone

Metabolic clearance and production rates of human growth hormone

Acute Effects of Clonidine and Growth-Hormone-Releasing Hormone on Growth Hormone Secretion in Patients with Hyperthyroidism

Relationship of receptor affinity to the modulation of thyroid hormone nuclear receptor levels and growth hormone synthesis by L-triiodothyronine and iodothyronine analogues in cultured GH1 cells.

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