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

In order to identify factors important in the growth of adipose tissue, four groups of children were studied. Infants of gestational diabetic mothers demonstrated increased fat cell numbers as early as age two months, a finding which accelerated with increasing age, and which was associated with persistent hyperinsulinemia and increasing obesity. Children with growth hormone deficiency increased their adipose cell number following treatment with exogenous hormone. Patients with the Prader-Willi syndrome, who developed obesity after the age of two, did so primarily via increases in fat cell size. Identical twins who were concordant for birthweight continued to have similar weights and total adipocyte numbers, while in those with discordant birthweights the smaller twin displays lower body weight and adipose cell number. The data indicate that growth hormone and insulin, as well as genetic factors, which may be modified by the in-utero environment, are important determinants of human adipose tissue mass.
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PMID:Growth of adipose tissue in infants, children and adolescents: variations in growth disorders. 731 84

Empty sella syndrome (ESS) is a multicausal entity. The incidence of primary empty sella syndrome (PESS) in children with neuroendocrine dysfunction is not known. In the pediatric age group, frequency seems to have been underestimated. A total of 117 cases of neuroendocrine disorders, including complete growth hormone deficiency, primary hypothyroidism with pituitary resistance to thyroid hormone, obesity, central precocious puberty, hypothalamic hypogonadism and central diabetes insipidus, have been studied with computed tomography and/or magnetic resonance imaging of sellar region for etiologic evaluation. Twenty-one patients were found to have PESS. We noted a high incidence of PESS in children with neuroendocrine dysfunction (17.9%). Children with neuroendocrine dysfunction should be investigated with respect to PESS, and children with PESS recognized coincidentally should be studied with the particular consideration of subclinical neuroendocrine dysfunction.
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PMID:Association of empty sella and neuroendocrine disorders in childhood. 764 85

The postoperative course of children undergoing surgery for craniopharyngioma was reviewed. Typically they were below height at presentation. All had an attempt at radical surgical resection of the tumor. Most developed diabetes insipidus in the postoperative period, which was permanent in all but 1 child. 94% required thyroid replacement therapy, and sex steroids were administered in 100% when they reached the age of puberty. 91% required maintenance corticosteroids. 54% required growth hormone replacement, but some children showed continued growth despite apparent growth hormone deficiency. Postoperative obesity develops in one half of patients, and may be improved with administration of growth hormone; a controlled trial is underway.
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PMID:The endocrine outcome after surgical removal of craniopharyngiomas. 784 Oct 75

We report a classical case of Prader-Willi syndrome (PWS) in an adult with typical interstitial deletion of chromosome 15, and emphasize the study of hormonal change. This 21-year-old female had PWS face characteristics, small hands and feet, marked obesity, mental retardation, growth retardation, absence of puberty and amenorrhea. She also had the characteristic history of infantile hypotonia, poor feeding, failure to thrive and then improved appetite, followed by obesity from the age of four years. She had compulsive hyperphagia, to the extent of stealing and lying to take food. Chromosome study with high resolution banding technique revealed a small interstitial deletion at band q12 of chromosome 15, which is characteristically found in a majority of patients with PWS. Hormonal study revealed hypogonadism and growth hormone deficiency of supposed hypothalamic origin. She also had non-insulin-dependent diabetes mellitus with decreased pancreatic insulin reserve.
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PMID:Hormonal change in an adult with Prader-Willi syndrome: report of a case. 791 75

The concept of body composition covers the division of the body into a number of compartments. The most important are the fat mass (FM), the fat-free mass (FFM), the total body protein and the total body bone mineral content. Numerous methods for the measurement of body composition are available. The three classical methods for the measurement of FM and FFM, namely underwater weighing, measurement of total body potassium and measurement of total body water by isotope dilution, are often regarded as reference methods. However, newer methods such as computed tomography, neutron activation analysis and dual energy X-ray absorptiometry are increasingly used because of their reliability and ability for independent measurement of two or more components. Bioelectrical impedance analysis has become popular because of its clinical applicability. Three- or four-compartment models involving combination of two, three or more separate methods are more accurate than single methods, but are usually confined to research purposes because of the laborious measurement procedures. Computed tomography and dual energy X-ray absorptiometry have the unique possibility of regional measurements of body composition. Fat distribution and relative overweight may be estimated by simple anthropometric measures such as skinfold thicknesses. There are many applications for body composition measurements in research and clinical practice. These include treatment of obesity, growth hormone deficiency, diabetes mellitus and climacteric changes, as well as clinical nutrition and estimation of the hydration of dialysis patients and of critically ill intensive or surgical patients.
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PMID:[Non-invasive measurement of body composition]. 806 96

The clinical consequences of growth hormone (GH) deficiency (GHD) in adults have not been defined. Standard methods of measuring GH reserve in children may not be reliable in adults. In addition, obesity in normal adults diminishes GH responsiveness to provocative stimuli; this inhibition of GH release is reversed with pyridostigmine (PD). We investigated the use of GH-releasing hormone (GHRH) as a method to assess pituitary GH secretory reserve (as defined by peak GH response to GHRH) in both non-obese and obese (ie, > 115% ideal body mass index [BMI]) adults with hypothalamic-pituitary tumors. Nine non-obese patients (NOP) and 10 obese patients (OP) were studied with 11 non-obese controls (NOC) and 10 obese controls (OC). All study groups received GHRH (1 microgram/kg intravenous bolus) with blood sampling at -15, 0, 15, 30, 45, 60, 75, and 90 minutes. OC and OP received 120 mg PD orally 1 hour before GHRH injection. Mean serum GH responses in NOC and OC were significantly higher (P < .05) than those in NOP and OP, respectively, 15 minutes after GHRH injection, and remained so throughout the time-course of the test. Mean +/- standard error of the mean (SEM) peak GH level (microgram/L) was lower in NOP than in NOC (5.1 +/- 1.6 v 21.2 +/- 4.4, P < .01) and lower in OP than in OC (4.6 +/- 1.8 v 15.5 +/- 2.2, P < .01). Mean +/- SEM peak GH level was also lower in NOP than in OC (5.1 +/- 1.6 v 15.5 +/- 2.2 micrograms/L, P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum growth hormone response to growth hormone-releasing hormone in non-obese and obese adults with hypopituitarism. 851 May 26

The review examines the evidence that the supply of cholesterol available for incorporation into nascent lipoprotein particles exerts a regulatory influence on apolipoprotein (apo) B secretion by the liver. Support for this hypothesis comes both from in vitro experiments and from recent observations in normal subjects and patients with dyslipidemia associated with familial hypercholesterolemia, obesity, noninsulin dependent diabetes mellitus, growth hormone deficiency and cholesteryl ester storage disease. The findings do not negate a role for triglyceride synthesis in determining apoB secretion in very low density lipoprotein, but the inhibitory effects on the latter process of pharmacological blockade of cholesterol synthesis or esterification suggest that it is conditional upon an adequate supply of cholesteryl ester.
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PMID:Role of cholesterol in regulating apolipoprotein B secretion by the liver. 872 9

Growth hormone deficiency (GHD) is associated with truncal obesity. We aimed at identifying factors that determine the body mass index (BMI) of untreated GHD children and the changes in BMI during 2 years of GH therapy in 348 Dutch GHD children registered in the National GH Registration Database. BMI was expressed as a standard deviation score (SDS). Before GH therapy, the mean (95% CI) BMI-SDS in all GHD children (0.09 (-0.05 to 0.24) SDS) was comparable to normal children. Patients with GHD due to a cranial tumour have a higher BMI (1.03 (0.69-1.36) SDS; p < 0.0001) as well as those with multiple pituitary hormone deficiencies (0.35 (0.14-0.57) SDS; p = 0.005) and patients who are in puberty at start of GH therapy (0.60 (0.13-1.08) SDS; p = 0.036). During GH therapy BMI initially decreased to reach a nadir of -0.28 (-0.35 to -0.21) SDS at 6 months. Thereafter BMI progressively increased to -0.09 (-0.18 to -0.04) SDS after 24 months. A higher initial BMI-SDS resulted in a larger decrease in BMI-SDS. We showed that this can be sufficiently explained by a regression to the mean effect.
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PMID:Body mass index in growth hormone deficient children before and during growth hormone treatment. 943 84

Growth failure is a recognized feature of the Prader-Willi syndrome (PWS). Despite evidence that hypothalamic dysfunction accompanies the syndrome, the etiology of this growth failure remains controversial because most patients with PWS are obese. In order to contribute to resolution of this controversy, we performed a retrospective analysis of 16 obese and non-obese PWS children. GH deficiency was diagnosed in 12 of the 16 subjects and occurred independently of weight status. All of the non-obese subjects were GH deficient. Of the 4 GH-sufficient children, 2 were moderately obese and 2 were morbidly obese. One of these children had clinical evidence of GH deficiency including a low IGF-1 level. Only one of the children had evidence of GH deficiency and a normal IGF-1 level, a pattern that could be attributable to obesity. We conclude that most short children with PWS have growth hormone deficiency and that this deficiency probably results from hypothalamic dysfunction.
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PMID:Growth failure in Prader-Willi syndrome is secondary to growth hormone deficiency. 956 5

The identification and sequencing of the ob gene and its product, leptin, in late 1994 opened new insights in the study of the mechanisms controlling body weight and led to a surge of research activity. During this time, a considerable body of knowledge regarding leptin's actions has been accumulated and the field continues to expand rapidly. Currently there is particular interest in the interaction of leptin with other peripheral and neural mechanisms to regulate body weight, reproduction and immunological response. In this review, we attempt to place the current state of knowledge about leptin in the broader perspective of physiology, including its structural characteristics, receptors, binding proteins, signalling pathways, regulation of adipose tissue expression and production, secretion patterns, clearance mechanisms and functional effects. In addition, leptin's involvement in the pathophysiology of obesity, anorexia nervosa, diabetes mellitus, polycystic ovary syndrome, acquired immunodeficiency syndrome, cancer, nephropathy, thyroid disease, Cushing's syndrome and growth hormone deficiency will be reviewed.
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PMID:Leptin: physiology and pathophysiology. 978 36


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