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

The present knowledge about the differentiation of preadipocytes into adipocytes is reviewed. The adipose conversion is initiated by an as yet unknown serum factor and is enhanced by various hormones including insulin, prostaglandin F2 alpha, steroids, and prolactin; prostaglandin E1 and phorbol diesters are inhibitors of differentiation. Adipose conversion of fibroblasts (preadipocytes) is associated with the coordinate induction of key enzymes of the lipogenetic and lipolytic pathways and is accompanied by profound changes in hormone responsiveness. Pathophysiological studies with preadipocytes of genetically obese mice show differences between adipocyte precursors of obese animals and lean controls which may be casually related to obesity. Regional differences in the hormonal regulation of fibroblast conversion might be important for the sex differences of fat deposition in human beings.
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PMID:[Preadipocytes: a new model in obesity research (author's transl)]. 625 26

Progressive left hemiparesis followed by face and trunk cutaneous vasodilation and hyperphagia developed in a 28-year-old man. He began eating five to six meals a day and gained 16 kg in 60 days. Computed tomography disclosed a neoplastic lesion involving the midline via the hypothalamus and reaching the contralateral lenticular nucleus. Findings from endocrine studies, including thyroid-stimulating hormone, growth hormone, prolactin, and cortisol serum levels, were normal. Hyperphagia and consequent obesity were associated with bilateral destruction of the ventromedial hypothalamic area; cutaneous vasodilation was related to involvement of the preoptic area.
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PMID:Hyperphagia and obesity. Relationship to medial hypothalamic lesions. 626 71

Twenty-six patients who were more than 35 per cent above their ideal weight were examined before the introduction of a weight reduction programme. At the end of a three-month period, seven patients had lost more than 10 per cent of their body weight. These patients had significantly lower triglyceride levels, fasting gastric inhibitory polypeptide levels (GIP) and prolactin levels. Fasting vasoactive intestinal polypeptide levels (VIP) before commencing diet were raised in six of the 19 patients who subsequently did not lose weight whereas the seven patients who lost weight had normal VIP levels (X2 = 3.07, P less than 0.05). Patients with high VIP levels had higher triglyceride levels, higher mean C-terminal glucagon-like immunoreactivity (C-GLI) and higher post glucose infusion secretin levels. There was a significant correlation between triglycerides and VIP. The significance of abnormally high VIP levels in obesity and the inability of these patients to lose weight is discussed.
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PMID:Vasoactive intestinal polypeptide in obesity. 634 22

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

The incidences of mammary tumors in female Sprague-Dawley rats injected with 7,12-dimethylbenz-(a)anthracene (DMBA) on day 50, ovariectomized 80 days later, and then maintained for 40 weeks on semipurified high-fat (20%) and low-fat (0.5%) high-fat diets, were 57% and 25%, respectively. In addition, the group exhibited significantly higher tumor multiplicities than the low-fat group (0.78 vs 0.25 tumors/total rats at risk). The weight gains of the HF and LF groups were similar, indicating that the differences in tumor yields were due to the fat content of the diet per se and not to caloric insufficiency or obesity. These results indicate that a high-fat diet has a tumor-enhancing effect in the absence of normal periodic ovarian secretions. Extragonadal estrogen production stimulated by high dietary fat intake may play a role, possibly by inducing secretion of the tumor-promoting hormone prolactin. The etiological, preventive, and therapeutic implications of these results with regard to human breast cancer are discussed.
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PMID:The role of a high-fat diet in enhancing the development of mammary tumors in ovariectomized rats. 678 Jan 83

17 women affected by essential obesity were examined, 9 of whom had become obese as adults (group A) and 8 had been obese since childhood (group B). In group A, fasting and after TRH, the PRL presented higher plasmatic levels than those found in the controls. In group B the hormone showed basal values and global secretory areas higher than those observed in the controls and in group A, while incremental areas did not result different from those found in the other groups examined. In no case did IRI, GH and glycaemia undergo changes in relation to TRH. In conclusion we think that the behaviour of prolactin can be an important physiopathological characteristic, expression of the different neuroendocrine hypothalamic homeostasis existent in the heterogeneous obese population.
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PMID:[Prolactin secretion in patients with essential obesity]. 678 37

Thirty-eight obese (13 prepubertal, 25 pubertal) boys, and 17 obese (16 prepubertal, 11 pubertal) girls underwent a thyroid-releasing hormone test with assay of prolactin. Obese pre-pubertal boys had prolactin levels that were significantly below those of the control group both under basal conditions and after stimulus. In the obese pubertal boys the difference was significant only after stimulus. The pituitary prolactin reserve in obese pubertal girls was lower than that of the control group. We conclude that in children and adolescents obesity may induce a hypothalamo-pituitary disorder that affects prolactin secretion.
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PMID:Disordered prolactin secretion in the obese child and adolescent. 678 79

Previous studies have indicated dysfunction of the hypothalamic-hypophyseal axis in obesity. We have studied 12 obese males to further characterize the extent of this dysfunction. The hypothalamic-hypophyseal-gonadal axis is normal as determined by the testicular response to human chorionic gonadotropin (hCG), the pituitary response to 200 micrograms gonadotropin-releasing hormone (GnRH), and the hypothalamic-pituitary-testicular response to clomiphene. Although L-dopa suppresses prolactin normally, the ability of thyrotropin releasing hormone (TRH) to stimulate the release of prolactin and thyroid stimulating hormone (TSH) is blunted. These latter responses are inversely related to the degree of obesity. The response to chlorpromazine, a hypothalamic stimulus for prolactin secretion, is also blunted, and to a greater extent than the prolactin response to TRH. These data indicate that exogenous obesity in males is associated with more extensive hypothalamic and pituitary dysfunction than previously realized. The abnormalities with regard to prolactin and TSH release become progressively worse when body weight exceeds 200 percent of ideal. In addition, when evaluating pituitary function with regard to gonadotropin release, obese males may have an abnormal response to 100 micrograms GnRH but respond normally to 200 micrograms.
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PMID:Hypothalamic and pituitary dysfunction in obese males. 680 59

We have carried out a prospective survey of 25 cases of male hypogonadism attending one hospital, and a retrospective study of 73 men attending other endocrine clinics in Manchester. In total, 47 had pituitary disorders, 15 isolated gonadotrophin deficiency (including 4 with Kallmann's syndrome), 10 testicular atrophy of unknown cause, 12 testicular damage, 10 with Klinefelter's syndrome, and 4 had miscellaneous disorders. Our survey emphasises the importance of adequate history and examination. Most patients presented with reduced libido, with marital problems in 62% of married men. Less common problems were facial flushing, osteoporosis and gross obesity. Several patients with pituitary disorders were asymptomatic, even in the presence of visual field defects. Klinefelter's syndrome, and testicular atrophy, may present with infertility or gynaecomastia rather than symptoms of androgen deficiency. On examination, the presence of gynaecomastia or obesity were of no help in differential diagnosis, whereas visual field defects clearly indicated a pituitary cause. Measurement of height/span was of little help. The precise diagnosis was usually established with basal plasma LH, FSH, testosterone and prolactin, with karyotype and pituitary radiology, and without more elaborate dynamic hormone tests. Testosterone esters given by intramuscular injection as "Sustanon 250" was the most commonly used replacement therapy. Improved libido usually resulted. Side-effect occurred in 10%, usually as muscle cramps, pain at the injection sites, acne, or excessive sex drive. One tragic case illustrates the potential dangers of androgen replacement therapy in an unrecognised psychopath, and where doubt exists a psychiatric opinion should be sought before starting therapy.
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PMID:Clinical aspects of androgen deficiency in men. 689 Jul 81

In comparison with matched nonvegetarian women, postmenopausal vegetarian women were found to have lower urinary levels of estriol and total estrogens, lower plasma prolactin levels, and higher plasma sex hormone-binding globulin (SHBG) levels. These differences were not explained by differences in body weight or obesity. Plasma SHBG levels were highly correlated with plasma high-density lipoprotein cholesterol levels, which were also higher in vegetarians than in nonvegetarians. These hormonal differences may explain the lower rates of endometrial and possibly breast cancer that have been observed previously in vegetarian women.
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PMID:Diet and reproductive hormones: a study of vegetarian and nonvegetarian postmenopausal women. 694 45


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