Growth Hormone Response in the Thinned Obese

Ball, Michael F.; El-Khodary, Ashraf Z.; Canary, John J.

doi:10.1210/jcem-34-3-498

Cited by 64 publications

(18 citation statements)

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“…Indeed, in the ob/ob mouse, plasma PRL and growth hormone levels are already reduced before the onset of obesity [27], Moreover, Ball et al [28] found that in obese patients the growth hormone response to ITT after weight loss was restored only in some patients, whereas the response of others continued to be impaired. In addition, Jung et al [29] reported that, in obese wom en, there was a basic abnormality of thermogenesis which persisted even after they had lost weight.…”

Section: Discussionmentioning

confidence: 99%

Effects of Fenfluramine and Ritanserin on Prolactin Response to Insulin-Induced Hypoglycemia in Obese Patients: Evidence for Failure of the Serotoninergic System

Bernini

Argenio²,

Vivaldi³

et al. 1989

Horm Res

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In order to study the hypothesized impairment of the serotoninergic system in human obesity, an insulin tolerance test (ITT) was carried out on 12 obese normoprolactinemic women and on 6 normal-weight women before (A) and after (B) the administration of a serotoninergic drug, fenfluramine (60 mg twice a day per os for 7 days). After a washout period, a new ITT (C) followed the administration of fenfluramine at the same dose, associated with a specific S2 blocker receptor agent, ritanserin (30 mg/day for the first 2 days and 20 mg/day for a further 5 days). In obese subjects, the prolactin (PRL) response to ITT A was reduced as compared to the controls: in 6 patients (‘nonresponders’) the PRL levels did not change, while in the other 6 (‘responders’) they increased (p < 0.003) but less than in the controls (p < 0.02). In normal-weight subjects, the administration of fenfluramine alone or with ritanserin did not modify the PRL response to ITT. In the responders, the serotoninergic drug normalized the PRL response to ITT while significantly improving it in the nonresponders; these effects were not antagonized by ritanserin. In conclusion, our data suggest that the serotoninergic system of obese patients is impaired and that the different secretory pattern observed in the two groups before and after fenfluramine may reflect differing degrees of this impairment.

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Section: Discussionmentioning

confidence: 99%

Effects of Fenfluramine and Ritanserin on Prolactin Response to Insulin-Induced Hypoglycemia in Obese Patients: Evidence for Failure of the Serotoninergic System

Bernini

Argenio²,

Vivaldi³

et al. 1989

Horm Res

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“…Normal subjects who have been made obese by forced feeding release subnormal amounts of endogenous GH in response to hypoglycemia (49). The blunted endogenous GH response to hypoglycemia that is characteristic of obesity is often improved by weight reduction (50)(51)(52)(53)(54). Thus, expansion of the adipose organ tends to suppress endogenous GH release, but the mechanism for this endocrine effect of obesity remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Impaired growth hormone secretion in the adult population: relation to age and adiposity.

Rudman¹,

Kutner²,

Rogers³

et al. 1981

J. Clin. Invest.

645

290

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A B S T R A C T Growth hormone (GH) release was studied in adults of normal stature, ages 21-86 yr. The subjects were 85-115% of ideal body weight, between the 5th and 95th percentiles in height, and free ofactive or progressive disease. 9 to 12 individuals in each decade from third to ninth were evaluated. The following criteria of GH status were measured: serum GH concentration, analyzed by radioimmunoassay at halfhour intervals for 4 h after onset of sleep, and at 1-h intervals from 8 a.m. to 4 p.m. in 52 subjects; daily retention of N, P, and K in response to 0.168 U human (h)GH/kg body wt314/day in 18 subjects; and plasma somatomedin C (SmC) level before and during exogenous hGH treatment in 18 subjects.All 10 individuals, 20-29 yr old, released substantial amounts of endogenous GH during both day and night (average peak serum GH obtained during day and night was 7.3 and 20.3 ng/ml, respectively); average plasma SmC was 1.43 U/ml (95% tolerance limits, 0.64-2.22 U/ ml). There was no significant effect of exogenous hGH on elemental balances or on plasma SmC. In contrast, 6 of 12 individuals 60-79 yr old showed the following evidences of impaired GH release: peak waking and sleeping seruim GH < 4 nglml; plasma SmC < 0.38 U/ ml; a significant retention in N, P, and K; and a significant rise in plasma SmC, in response to exogenous hGH.Plasma SmC, serum GH during sleep, serum GH during the day, retentions of N, P, and K in response to exogenous hGH, and rise in plasma SmC in response to hGH were all intercorrelated (P < 0.05). Plasma SmC < 0.38 U/ml corresponded to peak nocturnal serum GH < 4 ng/ml. The prevalence of plasma SmC < 0.38 U/ml

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“…In obesity, there is a decrease in basal and stimulated GH secretion [1][2][3]. The recent reports of absent GH secretion after the administration of GHRH [4,5] or pyridostigmine (pvr) [5] to obese subjects indicated that the GH discharge elicited by all the stimuli so far tested is blocked in obesity.…”

Section: Introductionmentioning

confidence: 99%

“…Altered GH release could be related to an abnor mal ty at three sites: (1) a circulating inhibitor of GH release in the systemic blood; (2) a somatotroph cell alteration, and (3) hypothalamic dysfunction, either im 1 Supported by grants FISss 89/0127-3 and 90/0026. pairment in GHRH release or somatostatin hypersecre tion.…”

Section: Introductionmentioning

confidence: 99%

Study of Insulin-Like Growth Factor I in Human Obesity

Cordido¹,

Casanueva²,

Vidal

et al. 1991

Horm Res

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In obesity there is a decrease in basal and stimulated GH secretion. IGF-I, which has negative feedback effects on GH secretion, could be the initial mediator of such alterations. We studied IGF-I levels in obese subjects and their relationship to the obesity level and GH secretion. We determined plasma IGF-I basal and stimulated GH in 30 normal and 30 obese women and related these variables to obesity indices (body mass index, BMI, and % overweight). Baseline plasma GH values were 1.2 ± 0.3 and 2.3 ± 0.6 µg/l in obese subjects and controls, respectively (NS). Mean peak GH secretion after stimuli were 11.2 ± 1.4 and 34.4 ± 5.6 µg/l in obese subjects and controls, respectively (p < 0.001). Plasma IGF-I were 1.0 ± 0.1 U/ml and 0.7 ± 0.1 U/l in obese subjects and controls, respectively (NS). There was a significant negative correlation between plasma IGF-I and age (r = -0.55, p < 0.001) and a significant negative correlation between mean peak GH secretion and weight (r = -0.60, p < 0.001), BMI (r = -0.64, p < 0.001) and percentage of ideal body weight (r = -0.67, p < 0.001). We did not find any correlation between IGF-I and indices of overweight. These data suggest that the reduced GH secretion found in obesity is not related to a negative feedback inhibition by elevated levels of IGF-I and that adiposity is not associated with a decline in IGF-I levels. We confirm the existence of a negative correlation between GH secretion and obesity indices.

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Growth Hormone Response in the Thinned Obese

Cited by 64 publications

References 0 publications

Effects of Fenfluramine and Ritanserin on Prolactin Response to Insulin-Induced Hypoglycemia in Obese Patients: Evidence for Failure of the Serotoninergic System

Effects of Fenfluramine and Ritanserin on Prolactin Response to Insulin-Induced Hypoglycemia in Obese Patients: Evidence for Failure of the Serotoninergic System

Impaired growth hormone secretion in the adult population: relation to age and adiposity.

Study of Insulin-Like Growth Factor I in Human Obesity

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