Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By mating mice heterozygous for the recessive gene, obese (ob/+) (+/+), with mice homozygous for the recessive gene, dwarf (+/+)(dw/dw), and subsequent mating of the offspring, mice homozygous for both the obese and dwarf gene were obtained. It was established that the genes for obese and dwarf mice belong to different linkage groups. The homozygous obese dwarf mice develop obesity and hyperinsulinemia. The degree of hyperglycemia developed by these homozygotes is not significantly different from that of nonobese dwarf mice. Because homozygous dwarf mice are deficient in growth hormone production, it was concluded that obesity and hyperinsulinemia can develop under conditions of extreme growth hormone deficiency.
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PMID:Development of the obese-hyperglycemic syndrome in mice with a growth hormone deficiency. 112 28

Protein C deficiency can lead to cerebrovascular occlusive disease. We describe a patient in whom heterozygous protein C deficiency (type 1) is suspected on the grounds of reduced protein C activity and who suffered from multiple thrombo-embolic events involving the brain and peripheral organs. The patient developed hypothalamic failure with hypernatraemia, hypodipsia, hypersomnolence and hyperkapnia, obesity, hyperprolactinaemia, hypogonadotropic hypogonadism and growth hormone deficiency. We hypothesize that protein C deficiency caused cerebrovascular occlusions which eventually led to hypothalamic insufficiency in this patient. Disorders of the anticoagulant system should be looked for in patients with unexplained hypothalamic disease.
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PMID:Hypothalamic failure as a sequela of heterozygous protein C deficiency? 162 70

Adults with GHD have normal overnight fasting glucose levels and normal overall glucose turnover. In the absence of GH, insulin secretion is reduced and may be associated with impaired glucose tolerance. The lack of GH is associated with normal insulin sensitivity but reduced hypoglycaemic responsiveness, probably due to a reduced supply of gluconeogenic substrates. When GHD is associated with obesity, however, hyperinsulinaemia and insulin resistance ensue and hypoglycaemic responsiveness is restored. In adults with GHD, treatment with recombinant human GH for 6 months increased fasting plasma glucose to within the normal range, with no change in overall glucose turnover and carbohydrate tolerance, in the presence of elevated basal insulin levels.
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PMID:Glucose metabolism in adults with growth hormone deficiency. 178 17

Injections of monosodium glutamate to neonate rats induce chronic growth hormone deficiency by hypothalamic lesions in the regions of the nucleus arcuatus and the eminentia mediana. The glutamate treated rats develop massive obesity. By this type of obesity hyperinsulinemia in the dynamic phase is not evident. The adipose tissue of the GOR (glutamate obese rat) is characterized by hypertrophic adipocytes and diminished number of adipocytes. In the GOR glucose oxidation and glucose lipid conversion are increased, but insulin sensitivity of glucose metabolism is diminished. The enhanced glucose utilization in adipose tissue of the GOR is discussed as being the consequence of the chronic growth hormone deficiency.
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PMID:[Glucose utilization in adipose tissue of rats in chronic somatotropin deficiency]. 267 26

The effects of chronic growth hormone deficiency on the growth hormone-dependent, sexually dimorphic hepatic drug-metabolizing enzymes were studied in adult rats of both sexes. Neonatal administration of monosodium L-glutamate produced the expected syndrome characterized by stunted growth, obesity, prolonged vaginal estrus, and an inhibition in the growth of the pituitaries, adrenals, gonads, sexual accessory organs, and kidneys. Associated with these abnormalities was a 90% reduction in the concentration of serum growth hormone in male and female rats. In contrast, the activities of hepatic aniline hydroxylase, total cytochrome P-450, and the Michaelis constants and maximal velocities for hexobarbital hydroxylase and UDP-glucuronosyltransferase were unaffected by the profound deficiency in growth hormone.
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PMID:Normal levels of hepatic drug-metabolizing enzymes in neonatally induced, growth hormone-deficient adult male and female rats. 287 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

Pre- and postoperative growth was analyzed in 22 children with craniopharyngioma. In 19 children a growth failure preceded the diagnosis by a mean of 4 years. Six children were obese preoperatively. During the first 3 postoperative months relative weight increased greater than 10% in 14/21 children (there was one surgical death). One year after surgery 13/21 were obese. Neither the size of the tumor nor the mode of surgery was decisive in the development of the obesity. Serum insulin and insulin-like growth factor I (IGF-I) were assessed in four children with growth hormone deficiency (GHD) who, after surgery for craniopharyngioma, were growing normally without GH substitution. One of them was normal in weight and had normal insulin and IGF-I levels; the others were obese and had supranormal insulin and subnormal IGF-I levels. One of the four and two other children with unsubstituted GHD reached final height SDS -0.8, -2.0 and -2.4. One child with normal postoperative GH response reached final height SDS -0.7. Final height SDS greater than or equal to -2.5 was gained with GH substitution by 6/11 children. It was greater than 2.0 SD below the height SDS expected from the heights of the parents in 7/11. An adequate monitoring of children's growth would lead to earlier diagnosis and probably better outcome.
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PMID:Children with craniopharyngioma. Early growth failure and rapid postoperative weight gain. 339 13

The deoxyribonucleic acid (DNA) is constant per cell in diploid tissues and in polyploid tissues the DNA content and the cytoplasm increase commensurately. In muscle the DNA unit (protein/DNA) was described on the assumption that each nucleus has jurisdiction over a certain volume of cytoplasm. Such an approach allows a sensible interpretation of metabolic data. Since 66-70% of nuclei are within myofibres muscle represents a reasonably homogeneous tissue. A brief historical review is made concerning the use of DNA as a cell constant. The application of this knowledge to normal human somatic growth and to disease states is considered as well as reduced nutrition and overnutrition. The consequences of reduced nutrition as it related to brain growth are briefly mentioned as is our 7 year study on the fetal primate (Macaca mulatta). Attention is focussed on our work in the early 1960's concerning the role of insulin and growth hormone on the DNA unit. In the last decade this work culminated in the close study of the Little Mouse with isolated growth hormone deficiency--thus exposing the panhypopituitary model (the human pituitary dwarf, Snell Smith mouse or hypophysectomised rat) as non-optimal models. The findings indicate that growth hormone is indeed related to cell replication and insulin to cytoplasmic growth in the postnatal period but the role of other hormones is clearly important, augmenting or opposing these hormones. The concept of constant change of the DNA unit not only applies to major tissues such as muscle but to the study of kidney growth when the contralateral kidney is removed (renal compensatory growth). Species differences are noted in the pattern of cell growth in muscle, but emphasis is placed on cell replication rather than on cytoplasmic growth in the primate. Restriction of protein energy metabolism mainly affects cytoplasmic growth of muscle but restoration of growth to expected levels is the rule. Overnutrition and obesity relate to excessive growth of DNA units in number rather than size. Attention is drawn to factors other than calories, proteins and hormones that influence hormonal actions viz. trace metals such as zinc, chromium and vanadium. The cell mass of the body can readily be reached by relatively non-invasive methods and by monitoring the intracellular water. Muscle mass can be precisely measured by creatinine excretion. The cell mass of muscle constitutes 70% of the entire cell mass.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The control of cell mass and replication. The DNA unit--a personal 20-year study. 391 56

We studied insulin-like growth factors (IGF) I and II, prolactin, and the insulin response to arginine in 19 children with craniopharyngioma and documented growth hormone deficiency. Patients were divided into three groups according to their growth rate during the first postoperative year. Seven patients with excessive growth (Group A) had hyperinsulinism, normal IGF values, elevated basal prolactin levels, and a delayed thyrotropin response to thyrotropin-releasing hormone, which was compatible with hypothalamic lesions. In the six patients with normal growth (Group B), the insulin level was low; all other hormone values were similar to those of Group A. In the six patients with decreased growth (Group C), levels of IGF I, insulin, prolactin, and thyrotropin were low, indicating the presence of severe pituitary damage and explaining the failure to grow. Patients in all groups had low or undetectable basal levels of growth hormone. We conclude that in Group B, normal IGF permitted normal growth, and prolactin hypersecretion may have been responsible for normal IGF I values. Excessive growth in Group A may have been caused by hyperinsulinism associated with hyperphagia and obesity of hypothalamic origin.
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PMID:Insulin-like growth factors I and II, prolactin, and insulin in 19 growth hormone-deficient children with excessive, normal, or decreased longitudinal growth after operation for craniopharyngioma. 635 37

Twenty nine (1.8%) of a national cohort of 1600 patients with growth hormone deficiency presented before the age of 2 years. Sixteen of the 29 presented before 6 months of age--11 with symptomatic hypoglycaemia, four with failure to thrive, and one with obesity. Hypoglycaemia was persistent and difficult to control until growth hormone treatment was started. Ten of the 11 hypoglycaemic patients had multiple pituitary hormone deficiencies compared with two of the remaining five. Thirteen children presented between 6 months and 2 years of age; 12 had failure to thrive and one had spontaneous hypoglycaemia. Twelve of the 29 were boys and all but one of these had microgenitalia . Growth hormone deficiency should be considered in the differential diagnosis of infants presenting with refractory hypoglycaemia and in boys with failure to thrive and microgenitalia .
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PMID:Growth hormone deficiency presenting under age 2 years. 674 76


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