Growth Hormone Responses to Sleep, Insulin Hypoglycaemia and Arginine Infusion

1985 ◽  
Vol 22 (1-2) ◽  
pp. 7-11 ◽  
Author(s):  
P.S. Ward ◽  
D.C.L. Savage
Keyword(s):  
Growth Hormone ◽  
Arginine Infusion ◽  
Hormone Responses

GROWTH HORMONE RESPONSES TO FRUCTOSE IN DIABETES MELLITUS

1974 ◽  
Vol 75 (3) ◽  
pp. 497-502
Author(s):  
Mayer B. Davidson ◽  
Roger M. Steele
Keyword(s):  
Diabetes Mellitus ◽  
Growth Hormone ◽  
Fasting Glucose ◽  
Area Under The Curve ◽  
Oral Glucose ◽  
Gh Secretion ◽  
Significant Difference ◽  
Duration Of Disease ◽  
Hormone Responses

ABSTRACT Since fructose is normally metabolized in diabetics and has recently been shown to stimulate GH secretion, it was used to assess GH responses in diabetics. Fourteen diabetics (9 on insulin) and 8 controls matched for weight were studied. Fructose, infused over 10 min, was compared to arginine, infused over 30 min, both at 0.5 g/kg. Samples were collected at 0, 30, 60, 90 and 120 min and GH responses assessed as area under the curve minus the fasting area. There was no significant difference between the GH responses in diabetics and controls to either agent. Responses to arginine and fructose were significantly correlated (r = 0.60, P < 0.01) in all subjects, but not related to therapy, duration of disease or fasting glucose (75–287 mg/100 ml) in the diabetics. Oral glucose blunted the GH response to fructose in 2 controls. It is concluded that 1) fructose can stimulate GH secretion in male diabetics; 2) however, fructose-stimulated GH responses are not increased in diabetes mellitus.

TYPICAL CASES OF ISOLATED GROWTH HORMONE DEFICIENCY WITH AUTOSOMAL RECESSIVE INHERITANCE

1970 ◽  
Vol 63 (4) ◽  
pp. 618-624 ◽  
Author(s):  
Y. Kumahara ◽  
Y. Okada ◽  
K. Miyai ◽  
H. Iwatsubo
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Autosomal Recessive ◽  
Autosomal Recessive Inheritance ◽  
Adult Subject ◽  
Hormone Deficiency ◽  
Recessive Inheritance ◽  
Arginine Infusion ◽  
Isolated Growth Hormone Deficiency ◽  
Male Dwarf

ABSTRACT A 25-year-old male dwarf and his sister, a 31-year-old woman were investigated. Their respective heights were 114 and 97 cm with proportional statures. Their bone ages were that found in the adult subject. Thyroid functions and metyrapone test were normal and the total urinary gonadotrophin was determined in both cases. HGH secretion was not stimulated by insulin-induced hypoglycaemia, arginine infusion or exercise. Their parents and six other siblings were normal in height. The two patients were therefore assumed to be suffering from an isolated growth hormone deficiency with autosomal recessive inheritance.

scholarly journals Growth hormone responses to repeated maximal cycle ergometer exercise at different pedaling rates

2002 ◽  
Vol 92 (2) ◽  
pp. 602-608 ◽  
Author(s):  
K. A. Stokes ◽  
M. E. Nevill ◽  
G. M. Hall ◽  
H. K. A. Lakomy
Keyword(s):  
Growth Hormone ◽  
Area Under The Curve ◽  
Cycle Ergometer ◽  
Mean Power ◽  
Ergometer Exercise ◽  
Hormone Responses ◽  
Sprint Cycling ◽  
Mean Power Output ◽  
Male Subjects ◽  
Serum Gh

The present study examined the growth hormone (GH) response to repeated bouts of maximal sprint cycling and the effect of cycling at different pedaling rates on postexercise serum GH concentrations. Ten male subjects completed two 30-s sprints, separated by 1 h of passive recovery on two occasions, against an applied resistance equal to 7.5% (fast trial) and 10% (slow trial) of their body mass, respectively. Blood samples were obtained at rest, between the two sprints, and for 1 h after the second sprint. Peak and mean pedal revolutions were greater in the fast than the slow trial, but there were no differences in peak or mean power output. Blood lactate and blood pH responses did not differ between trials or sprints. The first sprint in each trial elicited a serum GH response (fast: 40.8 ± 8.2 mU/l, slow: 20.8 ± 6.1 mU/l), and serum GH was still elevated 60 min after the first sprint. The second sprint in each trial did not elicit a serum GH response ( sprint 1 vs. sprint 2, P < 0.05). There was a trend for serum GH concentrations to be greater in the fast trial (mean GH area under the curve after sprint 1vs. after sprint 2: 1,697 ± 367 vs. 933 ± 306 min · mU−1 · l−1; P = 0.05). Repeated sprint cycling results in an attenuation of the GH response.

A Pilot Study of the Mechanism of Action of Desipramine

1981 ◽  
Vol 138 (3) ◽  
pp. 248-251 ◽  
Author(s):  
S. A. Checkley ◽  
A. P. Slade ◽  
E. Shur ◽  
S. Dawling
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Pilot Study ◽  
Mechanism Of Action ◽  
Depressed Patients ◽  
Sedative Effects ◽  
Before And After ◽  
Hormone Responses

SummaryTo test the hypothesis that desipramine alters α adrenoceptor function in depressed patients, the effects of clonidine upon growth hormone sedation and blood pressure have been measured in depressed patients before and after treatment with desipramine. After three weeks of treatment the hypotensive and sedative effects of clonidine were inhibited in all patients even though plasma desipramine concentrations at this time varied from 42 to 560 μg/l. Growth hormone responses to clonidine were enhanced in five of the six patients but this effect was not statistically significant. These findings are consistent with the hypothesis that in these patients desipramine altered α adrenoceptor function: other explanations are discussed.

Impaired prolactin response to arginine infusion and insulin hypoglycaemia in chronic renal failure

1983 ◽  
Vol 102 (4) ◽  
pp. 486-491 ◽  
Author(s):  
O. Schmitz ◽  
J. Møller
Keyword(s):  
Growth Hormone ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Elevated Level ◽  
Matched Control ◽  
Chronic Haemodialysis ◽  
Arginine Infusion ◽  
Pituitary Dysfunction ◽  
Prolactin Response ◽  
Insight Into

Abstract. The elevated level of circulating prolactin present in the majority of uraemic patients on chronic haemodialysis is primarily due to hypothalamic pituitary dysfunction. So far this defect has been illustrated by demonstration of a blunted prolactin response to TRH and failure of l-dopa to suppress prolactin levels. In the present study two powerful prolactin and growth hormone stimuli, namely iv arginine infusion and insulin hypoglycaemia were applied in a group of uraemic patients on chronic haemodialysis and in age matched control subjects. The prolactin increments to arginine infusion (4.4 ± 1.2 ng/ml vs 17.6 ± 4.6 ng/ml, mean ± se) and to insulin hypoglycaemia (7.9 ± 1.7 ng/ml vs 31.5 ± 5.4 ng/ml) were significantly suppressed in the uraemic patients compared to the controls (P < 0.05). In contradistinction the growth hormone rise provoked by the tests were similar in the two groups. Our results provide further insight into the hypothalamic pituitary derangement in uraemic patients and confirm the presumption of an insensitivity of the lactotrophs to stimulation in uraemic patients.

Sign in / Sign up

Export Citation Format

Share Document