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

Health providers examining children of short stature should assess adequacy of growth, determine growth rate, and predict final height with treatment. They can use established standards of growth to compare the child's height with that of other children of the same age to assess growth normalcy. If the child's height is lower than the 3rd/5th percentiles, the health provider must also determine whether the growth velocity is 3 cm/year by following the child for 6 months to 1 year, and whether retardation of skeletal maturity is of more than 2 bone age years to confirm abnormal growth. while the child is being followed for growth velocity, the health provider should prescribe a balanced nutritious diet. If these conditions are met and the child exhibits facial characteristics of growth hormone (GH) deficiency, central obesity, unusually small lower jaw, and prepuberal sex characteristics and behavior after usual age of puberty, the health provider can diagnose GH deficiency. 17% of children of short stature in a certain area of India have GH deficiency. The actual height, chronological age, and bone age are needed to predict the final adult height to monitor the impact of GH therapy. GH levels of less than 7 ng/ml in children not suffering from protein malnutrition suggest total GH deficiency. GH measurements must be done over 24 hours, since GH secretion is pulsatile. Sleep, exercise, and intravenous infusion of 0.5 g/kg body weight of arginine stimulates GH secretion. The most common pharmacologic tests to determine GH secretory status include insulin hypoglycemia and clonidine. Clonidine induces fewer side effects and is more safe than insulin hypoglycemia. Since a child can secrete normal amounts of GH with insulin hypoglycemia, the health provider should conduct 1 physiologic (sleep/exercise) test and 1-2 pharmacologic tests to diagnose GH deficiency.
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PMID:Diagnosis of GH deficiency: auxologic and GH response criteria. 182 77

Hypothalamic noradrenergic mechanisms contribute to altered caloric intake in genetically obese (C57BL/6J, ob/ob) mice. Noradrenergic mechanisms, principally in the paraventricular hypothalamus and of the alpha 2 subtype, have also been implicated in the macronutrient intake regulation of nonpathological models. Accordingly, this study assessed the extent to which clonidine, an alpha 2 agonist, altered macronutrient intake in genetically obese (ob/ob) and lean (C57BL/6J, +/?) mice. Following adaptation to a 6-h feeding regimen, mice were injected intraperitoneally with either clonidine (0.1, 0.5 mg/kg) or 0.15 M NaCl (Experiment 1) or 0.025 mg/kg clonidine or saline (Experiment 2) 30 min prior to simultaneous access to separate sources of carbohydrate, fat, and protein. Clonidine doses of 0.1 mg/kg or greater reduced total energy intake and intake of carbohydrate and fat (p less than 0.005) in all mice (Experiment 1). However, 0.025 mg/kg clonidine selectively increased ingestion of carbohydrate in obese mice by 212% of vehicle-injected values (p less than 0.001) without altering intake in lean mice (Experiment 2). These results implicate an alpha 2 receptor mechanism in genetic obesity.
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PMID:Bidirectional effects of clonidine on carbohydrate intake in genetically obese (ob/ob) mice. 201 43

The role of alpha 2-adrenoceptor stimulation by clonidine on the secretion of beta-endorphin, ACTH, and cortisol in essential hypertension and obesity was studied in 45 subjects: 15 non-obese hypertensives, 10 obese hypertensives, 11 obese normotensives, and 9 healthy subjects. The circadian rhythm of plasma beta-endorphin, ACTH, and cortisol was determined after placebo and after three days on clonidine 0.45 mg daily. Clonidine lowered the blood pressure and blood ACTH and cortisol levels in all the subjects. A significant decrease in beta-endorphin after clonidine occurred in the healthy subjects. In obese normotensives basal beta-endorphin concentrations were significantly higher than in healthy subjects and did not change after clonidine. In about 50% of non-obese and obese hypertensives a significant increase in beta-endorphin secretion after clonidine was noted (responders). In the subgroup of non-obese hypertensive responders no circadian rhythm of beta-endorphin was observed. The results suggest that adrenergic regulation of beta-endorphin secretion is altered in obesity and in certain patients with essential hypertension.
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PMID:Effect of clonidine on beta-endorphin, ACTH and cortisol secretion in essential hypertension and obesity. 284 28

Clonidine, an imidazoline derivative, is an antihypertensive agent which reduces sympathetic tone by acting in the central nervous system to stimulate alpha-2 adrenoceptors. There is evidence that dopamine and norepinephrine modulate the secretion of GH. Stimulation of GH release is a well-known effect of clonidine in man. Obesity is characterized by an impairment of GH release in response to various stimuli. The aim of this work is to study GH release in response to alpha-2 adrenoceptors stimulation by clonidine in obesity. 12 volunteer obese subjects were studied. 10 normal weight subjects, sex and age matched, were controls. The GH responsiveness was tested with a single oral dose of clonidine (0.15 mg). Blood was sampled for GH radioimmunoassay at 0', 30', 60', 90', 120', 150', 180'. Serum GH basal levels were not significant different in obese subjects compared to controls. In obese subjects, no significant changes occurred in blood GH concentration after clonidine. In normal weight controls, instead, a significant increase of GH values was reached at 90' (P less than 0.05) and at 120' (P less than 0.05) after clonidine. The impairment of GH release after clonidine in obese subjects might be in a reduced serotonin release or in a failure of the hypothalamic-pituitary system to stimulate plasma GH caused by a diminished GH releasing factor stimulatory effect or by an excessive endorphin or somatostatin secretion in obesity.
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PMID:Impaired growth hormone response to clonidine in obesity. 324 43

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

Growth hormone (GH) secretion is reduced with age in normal subjects. Aging is furthermore associated with a decline in lean body mass and an increase in relative adiposity, and overt obesity is a negative determinant of GH secretion in all age groups. We tested the hypothesis that differences in body composition and physical fitness rather than age determine stimulated GH secretion in healthy adults. Forty-two clinically nonobese adults [22 women and 20 men, mean age 39.4 yr (range 27-59), mean +/- SE body mass index (BMI) = 23.9 +/- 0.5 kg/m2] underwent 2 GH stimulation tests (arginine and clonidine), determination of maximal oxygen consumption (VO2-max), and a number of anthropometric measurements: body mass index (BMI), waist to hip (W/H)-ratio, intraabdominal fat and thigh muscle to fat (M/F)-ratio (computed tomography scan), total body fat, and lean body mass (DEXA scan). Peak GH levels were lower with clonidine [mean +/- SE (micrograms/L): 9.79 +/- 1.29 (arginine) vs. 3.56 +/- 0.57 (clonidine) (P < 0.001)]. Arginine-stimulated GH peak levels correlated negatively with indices of adiposity and age [intraabdominal fat: r = -0.72, P < 0.001; W/H-ratio: r = -0.58, P < 0.001; age: r = -0.54, P < 0.001], and positively with VO2-max [r = 0.60, P < 0.001]. Clonidine-stimulated GH peak correlated negatively with intraabdominal fat [r = -0.60, P < 0.001] and age [r = -0.46, P = 0.008]. Multiple linear regression revealed multicollinearity among several of the independent variables. In all equations abdominal adiposity and physical fitness, rather than age, contributed significantly to predict changes in arginine stimulated GH secretion. Intraabdominal fat was a more important determinant of the clonidine evoked GH response than age. In clinically nonobese, healthy adults relative adiposity, in particular in the abdominal region, is a major negative determinant of stimulated GH secretion, and physical fitness is an important positive predictor. The cause-effect relationship of these observations remains to be elucidated, but our findings may have clinical implications in the diagnosing of GH-deficiency in adults.
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PMID:Abdominal adiposity and physical fitness are major determinants of the age associated decline in stimulated GH secretion in healthy adults. 896 53

The role that the central sympathetic nervous system plays in the development of obesity hypertension and insulin was evaluated by feeding dogs a high fat diet with or without clonidine treatment. Thirteen adult mongrel dogs were chronically instrumented and randomly assigned to receive either a high fat diet and no clonidine (n=6) or a high fat diet plus clonidine (n=7), 0.3 mg BID. Blood pressure, heart rate, plasma insulin, and electrolytes were measured daily. Insulin resistance was assessed with a multiple-dose euglycemic clamp (1, 2, and 30 mU. kg-1. min-1) before and after 1, 3, and 6 weeks of the high fat diet. Clonidine prevented the hypertension, tachycardia, and insulin resistance associated with feeding dogs the high fat diet but did not affect weight gain. The present study suggests that the central sympathetic nervous system plays a critical role in the development of both insulin resistance and hypertension associated with feeding dogs a high fat diet.
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PMID:Clonidine prevents insulin resistance and hypertension in obese dogs. 993 Nov 63

Basal IGF-I levels and the GH response to at least two among provocative stimuli such as clonidine (CLO, Catapresan, 150 mcg/m2 p.o.), GHRH (1 mcg/kg i.v.)+arginine (ARG, 0.5 g/kg i.v. infusion during 30 min) and GHRH+pyridostigmine (PD, Mestinon cpr 60 mg p.o.) have been evaluated in 43 children with Prader-Willi syndrome (PWS, 17 males and 26 females, age 3-22 yr, 7 normal weight and 36 obese PWS), in 25 normal short children (NC, 17 males and 8 females, 7.7-18.5 yr) and in 24 children with simple obesity (OB, 14 males, 10 females, 7.7-21.5 yr). Both normal weight and obese PWS had mean IGF-I levels lower than those recorded in NC (p<0.001) and OB (p<0.001). The GH responses to GHRH+ARG and GHRH+PD in NC were similar and higher than that to CLO (p<0.001). In PWS the GH response to GHRH+ARG was higher than that to GHRH+PD (p<0.001) which, in turn, was higher than that to CLO (p<0.001); these responses in PWS were lower than those in normal children (p<0.02) and similar to those in OB. In normal weight PWS the GH responses to GHRH+ARG and to GHRH+PD were similar and higher than to CLO (p<0.05); however, each provocative stimulus elicited a GH rise lower than that in NC (p<0.05). In obese PWS as well as in OB the GH response to GHRH+ARG was higher than that to GHRH+PD (p<0.02) which, in turn, was higher than that to CLO (p<0.001); all GH responses in obese PWS and OB were lower than those in NC (p<0.001) but similar to those in normal weight PWS. In conclusion, patients with PWS show clear reduction of IGF-I levels as well as of the somatotroph responsiveness to provocative stimuli independently of body weight excess. These results strengthen the hypothesis that PWS syndrome is frequently connotated by GH insufficiency.
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PMID:GH/IGF-I axis in Prader-Willi syndrome: evaluation of IGF-I levels and of the somatotroph responsiveness to various provocative stimuli. Genetic Obesity Study Group of Italian Society of Pediatric Endocrinology and Diabetology. 1080 Jul 60