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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth hormone (HGH) response to glucose-induced hyperglycemia and insulin-induced hypoglycemia in 13 obese adults without carbohydrate intolerance and with normal thyroid function were compared with 16 normal weight subjects. HGH levels measured 30 min after placing an indwelling needle in an antecubital vein were significantly lower in obese than in the non-obese controls. HGH concentrations were inversely related to the body weight in all subjects. In the obese group a suppression of serum HGH level was lacking during glucose-induced hyperglycemia and furthermore it was recorded that HGH response to insulin was significantly less as compared with controls. These data indicate that abnormal HGH response is a characteristic in obesity with normal carbohydrate tolerance and normal thyroid function. HGH is a potent physiological stimulatory of lipolysis and it is thus tempting to speculate that an impaired HGH secretion leads to a diminished lipolysis and further deposition of excessive fat in obesity.
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PMID:Abnormal growth hormone response in obesity with normal carbohydrate tolerance and normal thyroid function. 73 10

Growth hormone (GH), which has been extracted from the pituitary gland since early times, has become easily available by the advance of genetic engineering in recent year. Its clinical application to treatment in various fields, involving obesity, wounds, fractures, gastric ulcers and so on, is being increasingly discussed. The presence or absence of the effect of GH on leukopoiesis was studied in vivo and in vitro experiments. In the in vivo experiment, GH was administered to rats whose bone marrow production had been suppressed by the injection of mitomycin C, and time-course changes in the peripheral blood leukocyte count in these rats were compared with those in rats given physiological saline solution alone (control group). The in vitro experiment was performed by colony assay of mouse marrow cells. Insulin growth factor-1 (IGF-1) was also studied in the in vitro experiment. The in vivo experiment revealed that GH promoted recovery of leukocytes from the nadir, and in the in vitro experiments GH and IGF-1 were demonstrated to increase the number of colonies in the presence of granulocyte macrophage colony stimulating factor (GM-CSF). GH was considered to exert effects on myeloid progenitor cells and the hemopoietic microenvironment simultaneously, resulting in an increase in leukocytes.
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PMID:[The effect of growth hormone on leukopoiesis: in vivo and in vitro studies]. 188 15

Destruction of the ventromedial hypothalamus produces hyperphagia, hyperinsulinemia and hypertriglyceridemia. These changes appear to be partly the result of increased firing rate of the vagus nerve and reduced firing rate of the sympathetic nerves. These reciprocal changes in the function of the autonomic nervous system appear to provide an adequate explanation for the hyperinsulinemia in this syndrome, and for the reduced heat expenditure. Destruction of the lateral hypothalamus, has effects opposite to those of the ventromedial hypothalamus with a reduction in food intake, a decrease in body fat, and an increase in the activity of the sympathetic nervous system. These reciprocal functions of the hypothalamus are associated with different adrenergic receptors. A medial hypothalamic alpha-adrenergic system mediates the epinephrine stimulation of feeding, and a beta-adrenergic system mediates the lateral hypothalamic inhibition of eating. Peptides from the endorphin family can stimulate food intake, but most other peptides are inhibitory. Growth hormone and thyroid hormone stimulate food intake under appropriate conditions. Insulin and adrenal steroids appear to play the most important role of all the hormones in regulating food intake. Deficiency of adrenal glucocorticoids is associated with decreased food intake and a wasting of body flesh. Increased levels of glucocorticoids, on the other hand, produce a variety of truncal obesity. In animals with ventromedial hypothalamic lesions and obesity, adrenalectomy will reverse the obesity. In genetically obese rats and mice, adrenalectomy will attenuate the progression of the syndrome. These effects appear to be through a reduction of food intake, and an increase in energy expenditure. Injections of insulin will stimulate food intake and may lead to obesity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Autonomic and endocrine factors in the regulation of food intake. 286 66

Growth hormone (GH) responses to GRF (1 microgram/kg BW i.v.) were investigated. Comparison between GRF(1-40) and GRF(1-29)NH2 in 11 young adult volunteers gave identical results. One hundred and thirty-one children and adolescents (45 with idiopathic GHD) were tested with GRF (1-29)NH2. The maximal GH levels (max GH) in response to GRF during the 120 min test period were found suitable to characterize the response. In cases without GHD no correlation to age, sex and pubertal development was observed. A maximal GH level of above 10 ng/ml was found to be normal. In 3 out of 86 children without GHD (one with Turner syndrome; two with simple obesity) max GH fell short of 10 ng/ml, while 11 of 45 cases with GHD exceeded this margin. In GHD, max GH was inversely correlated with age. There was no difference in max GH between groups with or without perinatal pathology as a presumed cause of GHD. GH levels to GRF were positively correlated with maximal GH level during sleep in GHD, but not correlated with responses seen to insulin or arginine. The value of GRF testing for the confirmation of GHD is discussed in the light of other GH stimulatory tests and basal somatomedin C measurements. It is suggested that the combination of testing with GRF and the determination of a basal SmC level offers a safe and convenient way to diagnose GHD in clinically suspected cases, though in some cases further diagnostic tests may be needed.
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PMID:Testing with growth hormone-releasing factor (GRF(1-29)NH2) and somatomedin C measurements for the evaluation of growth hormone deficiency. 288 Jul 20

Growth hormone levels following an intravenous bolus injection of 1 micrograms/kg body weight growth hormone releasing hormone were measured in 21 non-obese and 26 obese patients with Type 2 (non-insulin-dependent) diabetes mellitus and in 13 control subjects. Growth hormone responses in non-obese Type 2 diabetic patients were not statistically different from control subjects. However, obese Type 2 diabetic patients had significantly decreased growth hormone responses to growth hormone releasing hormone when compared with non-obese Type 2 diabetic patients (p less than 0.02). In 9 Type 2 diabetic patients growth hormone releasing hormone tests were performed both during hyperglycaemia and after metabolic improvement by insulin treatment. Growth hormone responses before and after insulin treatment were not statistically different. Our data demonstrate that growth hormone responses to growth hormone releasing hormone in non-obese Type 2 diabetic patients do not differ significantly from control subjects; obesity blunts growth hormone responses to growth hormone releasing hormone in Type 2 diabetes mellitus; and growth hormone responses following growth hormone releasing hormone administration in Type 2 diabetes mellitus are not influenced by the state of metabolic control.
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PMID:Effect of growth hormone releasing hormone on growth hormone secretion in type 2 (non-insulin-dependent) diabetes mellitus. 310 23

Cushing's syndrome in childhood is generally recognized by classical features such as truncal obesity, striae, easy bruising, moon facies, hypertension and growth retardation. Exceptionally, Cushing's syndrome has been reported to present as growth failure alone. We diagnosed transient hypercortisolism in 6 children who had poor growth as their only presenting abnormality. The 6 children all had integrated concentrations of cortisols (IC-F) (14.1 +/- 1.7 micrograms/dl; mean +/- 1 SD) which exceeded the IC-F in healthy children and adults (5.7 +/- 1.5 micrograms/dl; P less than 0.001). The IC-F of these 6 index cases overlapped the range of IC-F in patients with pathologically proven Cushing's syndrome (20.2 +/- 4.7 micrograms/dl). Four of the 6 patients were treated with human growth hormone for 8 months and showed a marked improvement in their growth rates. Four patients have entered puberty and are growing at normal rates. Three of the 6 children had normal repeat IC-Fs, subsequently, at a time they had normal growth rates. In 1-1/2 to 3 years of follow-up, none of the patients developed any other stigmata of Cushing's syndrome. We conclude that transient hypercortisolism, documented by the IC-F, may cause growth failure without other symptoms of Cushing's syndrome. Growth hormone therapy may improve the growth rate of these children at the time of their poor growth.
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PMID:Growth impairment due to transient hypercortisolism. 346 64

We determined the effect of pituitary human growth hormone treatment on the growth rate of 52 children with Turner syndrome. The pretreatment growth rate was 3.2 +/- 0.8 cm/yr. Growth hormone treatment (0.2 IU/kg three times per week) resulted in enhancement of the growth rate to 5.9 +/- 1.4 cm/yr for the first year of therapy. The bone age advanced approximately 1 year during the year of therapy. The growth hormone therapy was discontinued at 12 months, and the mean growth rate decreased to pretreatment levels, 3.1 +/- 1.9 cm/yr; 26 of 41 patients actually had post-treatment growth rates that were less than the pretreatment rate. Glucose tolerance tests at 6-month intervals did not indicate an effect of hGH treatment on glucose intolerance. Several patients had glucose intolerance that preceded hGH treatment, but this remained stable during treatment; glucose intolerance likely was related to obesity in this group of patients. Basal and hGH-stimulated somatomedin C levels (32 patients) correlated with age of the patient but not with growth rate during therapy. We conclude that hGH therapy can accelerate the growth rate of patients with Turner syndrome. The growth rate increased to "normal" levels and was dependent on continued treatment with hGH. If the response continues, long-term treatment of Turner syndrome may result in increased adult height.
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PMID:Growth-stimulating effects of human growth hormone therapy in patients with Turner syndrome. 353 50

Oral glucose tolerance tests were performed in the morning and afternoon of separate days on 31 people derived from a normal population sample. Blood sugar levels were higher in the afternoon test from and including 60 minutes after the glucose load. The degree of diurnal variation was similar in men and women, but greater in the older half of the group. It was negatively correlated with the degree of obesity. The plasma insulin response was less at the 30 minute time point in the afternoon, but significantly exceeded the morning values at 120 and 150 minutes after the glucose load. Growth hormone levels were similar in morning and afternoon tests. Fasting non-esterified fatty acid levels were significantly higher before the afternoon test.The relatively impaired glucose tolerance in the afternoon is associated with a delayed insulin response to the glucose load. This seems unlikely to be the sole explanation, however, and increased non-esterified fatty acid metabolism with a consequent decrease in glucose disposal may also contribute.
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PMID:Diurnal variation in glucose tolerance: associated changes in plasma insulin, growth hormone, and non-esterified fatty acids. 481 59

New facts have emerged about growth hormone (hgh) secretion in man giving rise to new conceptions and to new questions.* In well-nourished, lean human beings growth hormone is released in early deep sleep and the pattern of release observed from night to night is fairly constant.* The release of growth hormone in sleep occurs when plasma glucose is not fluctuating and after insulin has fallen to a very low level. Plasma-free fatty acids may rise about two hours later but insulin does not rise in response to nocturnal hgh release.* The releases of growth hormone in sleep appear to meet the needs for a physiological test for the study of problems of growth. Correlations of this test with the many pharmacologic maneuvers in current use for diagnosis remain to be made.* Growth hormone secretion as judged by plasma concentrations relates to protein intake, such that protein depletion initiates compensatory elevation of plasma concentrations of growth hormone. Further elevations may occur with glucose loading-so-called "paradoxical" responses. In contrast, there is compensatory suppression of growth hormone secretion in obesity. Repletion of protein in the malnourished and reduction of weight in obesity cause return toward normal secretion of hgh.* Levodopa as a possible specific stimulus to growth hormone release has just been reported and the implications of this finding for the child of short stature cannot yet be assessed.
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PMID:Changing concepts on the control of growth hormone secretion in man. 493 2

In two girls (14 and 16 years) and one boy (19 years) with PLW-syndrome and pronounced obesity (240, 210 and 77% overweight) endocrine function tests were carried out. Growth hormone secretion was decreased but normalized after reduction of weight. Thyroxin levels as well as basal and TRH stimulated TSH concentrations were normal. HCG application in the boy induced no rise of the normal basal testosterone levels. Oral glucose tolerance test demonstrated an increased stimulation of insulin in two cases, no other symptoms of diabetes mellitus were found. In the LHRH test an insufficient rise of gonadotropins was found. However, after two weeks of pernasal application of an LHRH analogue (D-Leu6-des-Gly10-EA) the gonadotropin stimulation was distinctly improved and onset of puberty was induced in the male patient. These results are indicative of a hypothalamic disturbance in patients with PLW-syndrome.
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PMID:[Endocrine studies on the Prader-Labhart-Willi syndrome: puberty induction in a 19-year-old boy after long-term treatment with an LHRH analog]. 641 33


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