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

The responses of plasma growth hormone-releasing hormone (GHRH) and growth hormone (GH) to oral administration of L-dopa were studied in normal subjects and patients with various endocrine and metabolic diseases to clarify the pathophysiological role of the GHRH-GH axis. In normal subjects, the plasma GHRH concentration was increased from the basal value of 9.8 +/- 1.4 pg/ml (mean +/- SE) to 34.8 +/- 3.1 pg/ml at 30 approximately 90 min after oral administration of 500 mg L-dopa, followed by a rise of GH release (plasma GH level from less than 1 ng/ml to 21.7 +/- 4.7 ng/ml) in most cases, indicating that L-dopa stimulates GH secretion via hypothalamic GHRH. On L-dopa administration, no apparent increases in both plasma GHRH and GH concentrations were observed in patients with hypothalamic hypopituitarism, whereas GHRH administration induced almost normal GH response. In patients with acromegaly, the plasma levels of GHRH remained stationary after the L-dopa administration and did not correlate with plasma GH levels. In subjects with simple obesity, the responses of plasma GHRH (peak 13.2 +/- 1.2 pg/ml) and GH (peak 4.3 +/- 1.7 ng/ml) to L-dopa were significantly lower than those in normal subjects (p less than 0.01). In patients with primary hypothyroidism, peak levels of plasma GHRH (12.6 +/- 1.3 pg/ml) and GH (2.4 +/- 0.6 ng/ml) were significantly lower than those in normal subjects (p less than 0.01). In patients with non-insulin dependent diabetes mellitus (NIDDM), the responses of GHRH and GH were divided into 2 groups; in the responder the peak values of GHRH and GH were 19.4 +/- 8.6 pg/ml and 12.2 +/- 1.4 ng/ml and in the low or non responder 14.7 +/- 1.5 pg/ml and 2.0 +/- 0.6 ng/ml, respectively. Between both groups, there was a significant difference in the values of fasting blood sugar and HbA1 and mean suffering period. These findings suggest that GH secretion evoked by the L-dopa administration is induced by GHRH released from the hypothalamus, and impairment of GH secretion associated with simple obesity, primary hypothyroidism, or NIDDM may be in part attributed to insufficiency of GHRH release from the hypothalamus, and indicate that L-dopa test is clinically useful for evaluating the ability of intrinsic GHRH release in such diseased states.
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PMID:[Effect of oral administration of L-dopa on the plasma levels of growth hormone-releasing hormone (GHRH) in normal subjects and patients with various endocrine and metabolic diseases]. 312 83

Increased plasma concentrations of growth hormone (GH) are reported in diabetes and it is suggested that this may be important in the development of complications. We have investigated fasting GH levels and the response to 100 micrograms i.v. growth hormone releasing factor, GRF(1-29)NH2, in age-matched men: six normal weight controls, six obese controls, six insulin-dependent diabetics, six normal weight non-insulin dependent diabetics and six obese non-insulin dependent diabetics. None of the diabetic men had clinical evidence of diabetic complications. Fasting GH values did not differ significantly between the five groups. The peak GH response to GRF was similar in the controls, insulin-dependent diabetics (IDD) and non-insulin dependent (NIDD) normal weight diabetics (mean peak +/- SEM: controls 25.5 +/- 5 mU/l, IDD 26.5 +/- 6 mU/l, NIDD 19.7 +/- 5 mU/l) but was significantly reduced in the two obese groups (obese 6.4 +/- 3 mU/l, obese diabetics 4.5 +/- 1 mU/l, P less than 0.01). This impairment of GH secretion was unrelated to either fasting plasma insulin or glucose concentration. We conclude that our results do not confirm the previous reports of abnormal GH secretion in diabetes but do demonstrate a markedly impaired GH response to GRF to be a feature of obesity.
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PMID:Growth hormone response to growth hormone releasing factor in diabetic men. 313 33

In order to assess the dopaminergic tonus, urinary determinations of HVA and DOPAC and also of noradrenaline (NA), adrenaline (A), and methoxyhydroxyphenylglycol (MHPG) were performed in 86 obese children, 11 growth hormone (GH)-deficient short children and also in 40 control children. Part of the obese patients were subjected to a low carbohydrate, low calorie diet and also to short-term (9-14 days) courses of diethylpropion (DEP) 50 mg/day, meclofenoxate (MEC) 100 mg/day and thyroid extract (THE) 1-2 mg/kg/day. The GH-deficient patients received only THE in substitutive (5-10 mg/kg/day) doses. Significative correlations between DOPAC and age, weight and height were found in controls. In the obese group a significantly increased mean level of HVA was found (1.45 +/- 0.09 mg/24 h vs 1.15 +/- 0.10 in controls). The excretion of DOPAC was slightly greater but far from significance. There was also a significant decrease of HVA but not DOPAC in the DEP-treated obese. The rest of the drugs and the diet alone were not effective in any way. Normal levels in all metabolites except NA and A were found in GH-deficient short children. The therapy with thyroid extract did not alter the excretion levels. These findings indicate that in infantile obesity the dopaminergic tonus is somewhat increased but its pathophysiological significance is doubtful. In GH-deficient short children of standard appearance the dopaminergic tonus seems to be undistinguishable from normal.
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PMID:The assessment of the dopaminergic tonus by urinary determinations of homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC) in normal, obese and GH-deficient short children. 321 82

Obesity is characterized by increased levels of insulin and by subnormal growth hormone (GH) release. Insulin/GH ratio is significantly higher in obese than in lean individuals. Fenfluramine, an anorectic drug, may have some effects on hypothalamic-pituitary function and on insulin secretion, possibly through a serotonergic stimulation. The aim of this work was to study the effects of fenfluramine on the insulin/GH ratio after arginine in obese subjects. Ten volunteer obese females were studied; 10 volunteer women were the normal weight controls. All subjects were given placebo and fenfluramine (60 mg p.o.) in a randomized order and after 120 min underwent arginine infusion (25 g i.v. for 30 min). Blood samples were taken every 30 min until 270 min for GH and insulin radioimmunoassay. In the obese group the GH response to arginine was significantly lower than in controls. Fenfluramine administration restored the subnormal GH response to arginine in obese subjects. Arginine infusion provoked a greater insulin secretion in obese subjects than in lean individuals. Fenfluramine administration diminished the insulin response to arginine. Fenfluramine did not modify the insulin/GH ratio in controls while it significantly lowered the insulin/GH ratio in obese subjects. Because insulin promotes fat and carbohydrate storage while GH stimulates lipolysis, the combination of high insulin and low GH concentrations may worsen the obese condition. A lower insulin/GH ratio can be useful in the treatment of obesity.
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PMID:Effect of fenfluramine on insulin/growth hormone ratio in obese subjects. 328 Nov 73

In order to estimate the neuroendocrine function of the central nervous system eventually leading to growth hormone (GH) secretion in essential hypertension, 17 patients with mild arterial hypertension (7 obese and 10 with normal body weight) were examined. The control group consisted of 16 normotensive volunteers (7 obese and 9 with normal body weight). The GH secretion was determined by radioimmunoassay during nocturnal sleep. In all the subjects, the serum GH was also measured after placebo and after the centrally acting alpha 2-adrenergic agonist-clonidine administered i.v. in a dose of 0.15 mg. The fasting serum insulin concentration was also measured in all the subjects. Clonidine decreased the mean arterial pressure in all the subjects investigated. However, in response to clonidine an increase in GH secretion in all hypertensive and normotensive cases with normal body weight was demonstrated, whereas in all obese hypertensive and normotensive patients no significant GH rise was found. It indicates that inhibition of GH secretion in patients with essential hypertension is related to coexistent obesity rather than with that of arterial hypertension. A strong (r = 0.76) and significant (p less than 0.0005) correlation demonstrated between the maximal GH concentration during the nocturnal sleep and after clonidine suggests that the mechanism of GH inhibition in response to both these stimuli is similar and it probably is related to the inhibition of neurohormonal secretion of the growth hormone releasing factor (GRF). However, the negative correlation between the fasting insulin concentration and GH response to clonidine shown in obese subjects only, points to a more complex mechanism of GH inhibition in obesity.
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PMID:Growth hormone (GH) secretion during nocturnal sleep and after clonidine in patients with essential hypertension. 328 64

Electrolytic lesions of the ventromedial hypothalamus (VMH) result in marked hyperphagia and obesity, but several studies have found the excess food intake and weight gain to be greatly reduced when lesions are produced by electrocauterization with radio-frequency current. Unlike electrolytic lesions, radio-frequency lesions leave few or no deposits of metallic ions that can potentially stimulate adjacent tissue. In the present experiment, weight gain and several endocrine responses previously associated with the VMH syndrome were compared in female rats given either electrolytic, radio-frequency, or sham VMH lesions. Both groups with VMH lesions became obese, but rats with radio-frequency lesions displayed only 63.2% of the weight gain of animals with irritative lesions (120.0 vs. 189.8 g in 20 days). Only rats with electrolytic lesions displayed elevated plasma insulin levels during an initial period of food restriction, but both groups with lesions were hyperinsulinemic when allowed to overeat. Plasma growth hormone levels were decreased by electrolytic lesions but unaffected by radio-frequency lesions. Morning corticosterone levels were elevated in both VMH groups, but only the rats with electrolytic lesions were found to have elevations in plasma adrenocorticotropin. It is concluded that some of the endocrine dysfunctions resulting from electrolytic VMH lesions are due to irritative stimulation rather than to tissue ablation.
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PMID:Radio-frequency vs. electrolytic VMH lesions: differential effects on plasma hormones. 328 3

Diabetes, the most common metabolic disease, is responsible for the deaths of over 300,000 Americans annually. The incidence of the disease increases with age and since the U.S. population is graying, prevalence is also increasing. Obesity and family history are strong predictors of diabetes. The etiology of Type II diabetes is heterogeneous. The hyperglycemia of Type II diabetes can result from a variety of metabolic defects including impaired beta cell secretion, receptor deficiencies, or abnormal hepatic production or uptake of glucose. Other glucoregulatory hormones such as glucagon, growth hormone, cortisol, thyroid hormones, somatostatin, and gastric inhibitory polypeptide may contribute to the aberrations of carbohydrate metabolism. Environmental factors including stress, diet, and exercise may also contribute to the disease. Since most diabetics are obese, weight loss should be the first priority in improving status. A variety of diet and exercise regimens may help achieve this goal or even improve glucose control without weight loss. Due to the heterogeneity of the disease individualized treatment must be used to improve status of patients with the various metabolic defects of Type II diabetes.
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PMID:Dietary sugars and carbohydrate metabolism in type II diabetes. 330 10

Serum thyroid hormones in childhood obesity are not altered but caloric intake affects monoiodination of T4 to T3 and rT3. Plasma cortisol and urinary free cortisol concentrations are normal. Increase in cortisol production and secretion rate is reflected in increased values of urinary 17-hydroxycorticosteroids. Elevated urinary 17-ketosteroids are caused by increased androgen synthesis accounting for the increased height velocity in obese preadolescents and for the accelerated skeletal maturation. In both sexes earlier onset of puberty is noticed without remarkable alterations in gonadal steroids. Whether altered prolactin concentrations reflect neuroendocrine abnormalities remains unclear. Impairment of growth hormone release in face of normal or high somatomedins is not of clinical significance. Basal and stimulated insulin concentrations are high. Insulin resistance exists because glucose tolerance is simultaneously impaired. This is due to reduction in insulin receptor numbers and post-receptor defects in insulin action. Weight loss is effective in normalizing the above mentioned hormonal defects.
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PMID:[Hormonal findings in obese children. A review]. 330 53

The potential was examined for insulin, growth hormone and insulin-like growth factor (IGF-1) alone or in combinations to stimulate glycerophosphate dehydrogenase (GPDH) activity, a sensitive marker of differentiation of adipose precursor cells in primary culture. Insulin, but not growth hormone or IGF-1, stimulated GPDH in the presence of fetal calf serum and cat serum. The content of growth hormone in adult rat heparinised plasma seemed, however, important for such stimulation, but was also dependent on feeding status of the plasma donor, and was abolished by hypophysectomy of the cell donor. GPDH activity was then analysed in heparinised plasma in the over-night fasting state in humans to examine a potential influence of age, obesity and pregnancy. In comparison with non-obese adults, GPDH-stimulatory activity was higher in plasma from infants and small children. A similar trend was seen in plasma from teenagers. This activity was probably partly dependent on growth hormone, because this increase of activity could be inhibited by excess of anti-human growth hormone antiserum. Obesity in adulthood or among teenagers was not associated with any difference in plasma activity to stimulate cellular differentiation, and plasma from women during late pregnancy had a low stimulating capacity. Simultaneous analyses of the potential of plasma to stimulate lipid accumulation in adipose precursor cells was proportional to the triglyceride concentration. Overall, the inhibitory effect of antihuman growth hormone antiserum on the differentiating capacity of human plasma was small or non-existing. It is therefore suggested that in human plasma, factors other than growth hormone might be important for the differentiation of adipocyte precursor cells.
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PMID:Effects of age, obesity and growth-hormone on adipogenic activity in human plasma. 331 49

This overview of nutrient balance suggests the following general conclusions. Nutrient balance is in part regulated by the two limbs of the autonomic nervous system. Hypothalamic and genetic obesity are associated with lower levels of sympathetic activity. Conversely the reduced weight of animals with lateral hypothalamic lesions is associated with increased sympathetic activity. Thus the activity of the sympathetic nervous system appears to be inversely related to energy stores. The levels of hormones such as insulin, adrenal steroids, gonadal steroids and growth hormone play an important role in modulating nutrient intake and storage. The data seem to fit the hypothesis that nutrient stores are regulated systems with afferent feedback systems acting on a central controller which regulates intake, storage and metabolism of nutrients through modulation of the autonomic nervous system and motor control of food seeking.
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PMID:Nutrient balance: new insights into obesity. 332 50


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