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

The authors carried out studies on 28 women with the syndrome of Stein-Leventhal with obesity. It was established that patients with hypothalamic genuine obesity of III degree predominated. The number of patients with liver steatosis was the largest among accompanying metabolic disturbances, followed by those with arterial hypertension and asymptomatic hyperuricemia. Menarche occurred on time, but it was succeeded by various menstrual disturbances. There was increased level of testosterone in sera of 12 out of 20 examined women patients, of LH-in 17, of 17-ketosteroids-in 8, of estrogens-in 6, of prolactin-in 8 patients. These data in parallelism between menstrual disturbances and hirsutism were interpreted by the authors as an expression of primary disturbances in hypothalamic-hypophysial-gonadal interrelationships with secondary changes in the ovaries. The role of fatty tissue in the metabolism of steroid hormones is discussed as well as the possibility for participation of genetic factors in the development of the syndrome of Stein-Leventhal and obesity.
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PMID:[The Stein-Leventhal syndrome with obesity]. 280 82

An increase in the number of diagnostic parameters (in addition to the determination of the urine level of 17-OCS, a study was also made of the level of 17-KS, blood concentrations of ACTH, prolactin, cortisol, and glucose before and after dexamethasone administration at a dose of 0.5 mg every 6 h for 2 days) and strict rules to be observed by examinees prepared for test performance made in possible to raise the differential-diagnostic role of Liddle's minor dexamethasone test. This conclusion was based on the examination of 34 persons without obesity, 25 patients with exogenous constitutional obesity, 75 patients with juvenile pubertal dyspituitarism, 107 patients with hypothalamic obesity, 8 patients with Cushing's syndrome determined by adrenal corticosteroma, one patient with ACTH-ectopic syndrome, and patients with Itsenko-Cushing disease (128 untreated patients, 99 patients with recurrence, 98 patients in remission). The comparison of clinico-instrumental results with the results of the test has shown its informative value for objective assessment of the gravity of disease. Stages of body responses to small doses of dexamethasone (the stage of lost responses, the stage of incomplete loss and the stage of recovered responses) were identified contributing to objective assessment of the gravity, course, presence, recurrence and remission of Itsenko-Cushing disease.
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PMID:[Use of the "extended" minor dexamethasone test in Itsenko-Cushing disease]. 285 54

We have previously reported an impaired growth hormone (GH) response and abnormal prolactin release to insulin-hypoglycaemia in obesity. We suggested that obese women with an absent prolactin response to hypoglycaemia ('non-responders') have a disorder of hypothalamic function. We have now investigated the GH response to i.v. growth hormone releasing factor, GHRF (1-29)NH2, in 14 obese women and nine age-matched normal-weight women. We found a significantly reduced GH response to GHRF in the obese women as compared with controls (mean peak +/- SEM: obese 8.9 +/- 2 mu/l, controls 28 +/- 2 mu/l; P less than 0.01). When the obese women were divided on the basis of their prolactin response to insulin-hypoglycaemia (seven 'non-responders', mean weight 102 +/- 5 kg; seven responders, mean weight 108 +/- 8 kg) a similar GH response to GHRF was found between the two groups but the GH response to hypoglycaemia was significantly less in the 'non-responder' women (mean peak 'non-responders' 10.5 +/- 3 mu/l, responders 27 +/- 4 mu/l; P less than 0.05). We conclude that obesity may be characterized by an impaired GH response to both i.v. GHRF and insulin-hypoglycaemia, which suggests altered hypothalamic-pituitary function. The finding that the GH response to hypoglycaemia is significantly less in the obese prolactin 'non-responder' women supports the hypothesis for a hypothalamic disorder.
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PMID:Impaired growth hormone response to growth hormone releasing factor and insulin-hypoglycaemia in obesity. 286 16

A group of oligomenorrhoeic women without obesity or hirsuties was investigated with high-resolution ultrasound, laparoscopy and biochemical parameters. In this series, polycystic ovaries (PCO), as defined by ultrasound and laparoscopy, are a common cause of oligomenorrhoea in women without the classic symptoms, and were strongly associated with an elevated free androgen index (FAI). Despite an elevated FAI, these women were not hirsute, It would seem reasonable to include a FAI in the investigation of the oligomenorrhoeic woman, along with the more 'standard' tests, such as thyroid function and a prolactin level.
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PMID:Elevated free androgen index as an indicator of polycystic ovaries in oligomenorrhoea without obesity or hirsuties. 297 54

Opiates stimulate the growth hormone and prolactin responses to stimuli in non-obese humans. Obese patients, however, show lowered growth hormone and prolactin responses and raised beta-endorphin levels. We therefore investigated the effect of the opiate antagonist naloxone on the stimulated growth hormone and prolactin secretions in a controlled double-blind study in obese patients. All patients received 200 micrograms TRH and 0.5 g/kg b.w. arginine together with 2 mg of naloxone or placebo i.v. in a randomized sequence. The TRH- and arginine-induced increases in prolactin and growth hormone were significantly greater after administration of naloxone (p less than 0.05). Naloxone also produced a significant increase in ACTH, cortisol and beta-endorphin when compared with placebo. TSH, triiodothyronine, thyroxine, insulin, glucagon and blood glucose showed no significant differences between both days of the trial. The effect of naloxone on growth hormone and prolactin secretions in obese humans can thus be regarded as a partial normalization. We therefore conclude that the hypothalamic regulatory disturbance of growth hormone and prolactin secretions in the obese could be caused by raised opiate levels.
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PMID:Naloxone increases the response of growth hormone and prolactin to stimuli in obese humans. 303 2

The aim of this article is to present evidence of hyperostosis frontalis interna in a 40-year-old female recovered from a Meroitic cemetery (ca. 300 A.D.) in Sudanese Nubia. A review of the literature concerning the Morgagni-Stewart-Morel (MSM) syndrome suggests that the changes in the skull fragment are consistent with this diagnosis. This case is the earliest example of the condition so far reported, and therefore, in archaeological time and space, this is a disease not only of modern civilization, but also of antiquity. Current endocrinological reports suggest that the hyperostosis is the hallmark of a generalized disorder of bone metabolism, with increased androgens, prolactin, and somatotropins. Hyperostosis frontalis interna is the central feature of a syndrome first described over 200 years ago by the early pathologist Giovanni Batistta Morgagni, professor of anatomy at Padua (1719). He found thickening of the internal tables of the frontal bones in association with virilism and obesity. Stewart (1928) and Morel (1929) independently added several neuropsychiatric problems to this complex and questioned the possibility of an endocrine basis for the syndrome.
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PMID:Hyperostosis frontalis interna: a Nubian case. 304 35

The regulation of testicular hCG binding and steroidogenesis in adult mutant mice with hereditary diabetes and obesity was studied. Low doses of hCG caused no change in hCG binding in obese (ob/ob) mice, whereas, in diabetic (db/db) mice, the increase in binding measured 24 h after hCG administration was not as great as in normal males. Intermediate doses of hCG caused a decrease in hCG binding in obese and normal mice, but not in diabetic animals. However, 72 h after injection of intermediate doses of hCG, a decrease in hCG binding also was observed in diabetic mice. Plasma testosterone was elevated 24 h after hCG injection in all types of mice studied, but the increase in diabetic mice was smaller than in normal animals. However, 72 h after treatment with hCG, plasma testosterone was still elevated in diabetic mice, but not in normal males. In vitro, hCG stimulated testicular testosterone synthesis in all groups of mice, but the observed increase was smaller in diabetic and obese than in normal animals. Plasma LH levels were higher in diabetic than in normal mice, whereas plasma FSH and prolactin levels were lower in obese mice than in normal animals. All parameters (i.e., LH receptors and circulating hormone levels) measured in yellow (Ay/a) mice were similar to those in normal (a/a) mice. The present study indicates that in these models for noninsulin-dependent diabetes, the testicular metabolism of LH receptors and capacity to secrete steroids is altered.
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PMID:Hormonal regulation of testicular human chorionic gonadotropin binding and steroidogenesis in adult mice with different forms of hereditary diabetes and obesity. 308 72

The mechanisms whereby growth hormone (GH) secretion is decreased in human obesity remain obscure. We studied the response of plasma GH and prolactin (PRL) to an I.V. dose of 0.5 mcg/kg of growth hormone releasing factor (GRF) in three groups of children: lean (N = 12), obese (N = 15) and GRF-deficient, i.e. children with complete GH deficiency on the basis of conventional provocative testing and evidence of hypothalamic dysfunction on the basis of thyrotropin-releasing hormone testing (N = 7). Mean (+/- SEM) peak plasma GH after GRF was blunted to the same extent in obese and in GRF deficient children (11.1 +/- 2.2 and 8.3 +/- 2.8 ng/ml) as compared to lean control children (34.7 +/- 4.7 ng/ml). The pattern of PRL response to GRF was however different in GRF deficient children, whose high basal PRL levels increased further after GRF injection, and in obese and lean children, who had n alpha acute change in PRL levels after GRF. Baseline plasma somatomedin C concentrations were low for age in GRF deficient children and tended to be high for age in obese children. On the basis of these discrepant patterns of response of PRL to GRF and plasma somatomedin C concentrations, we conclude that GRF deficiency does not account for the decreased GH secretion observed in obese children.
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PMID:Evidence against growth hormone-releasing factor deficiency in children with idiopathic obesity. 309 43

Our aim in the current study of 20 normal controls, 28 overweight, and 26 severely overweight (obese) subjects was to assess interrelationships of obesity, endogenous estradiol (E2) and testosterone (T), and the E2/T ratio with major independent explanatory variables for coronary heart disease (CHD), including lipids, lipoproteins, and apolipoproteins. Most of the lipid and lipoprotein variables (total, high-, low-, and very-low-density lipoprotein cholesterols) as well as apolipoproteins A1, A2, and B did not vary significantly with the presence of obesity. With increasing relative ponderosity, there were, however, increasing levels of total triglycerides and VLDL triglyceride. Levels of FSH, LH, prolactin, and testosterone did not differ significantly with obesity. The obese subjects had the highest E2 and E2/T levels; overweight subjects had intermediate levels which were also significantly higher than in the controls. Using multiple regression analyses, in obese subjects increasing T was associated with increasing apo B, and increasing E2 was correlated with decreasing apo A1. Opposite relationships were found in the normal controls where increasing T and increasing Quetelet indices were associated with diminished apo B and increasing E2 was associated with increasing A1. Obesity's association with increased CHD risk may be mediated through increasing E2 and apo B and reducing apo A1. Since obese subjects have higher E2 levels and often have lower T, they are likely to have a pattern of endogenous sex hormones (higher E2, lower T, higher E2/T ratios) similar to those observed in young men with premature myocardial infarction.
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PMID:Sex hormones, lipids, lipoprotein cholesterols, and apolipoproteins in normal and obese subjects: atherogenic relationships. 310 Apr 68

To elucidate further the role of opioid systems in the neuroendocrine alterations associated with obesity, we investigated the effect of the synthetic enkephalin analogue DAMME in 11 obese subjects and 10 lean controls. Prolactin responses to DAMME were similar in lean and obese, even in those obese subjects who had absent prolactin responses to insulin-induced hypoglycaemia. The obese showed impaired growth hormone release after both DAMME and insulin-induced hypoglycaemia compared to the lean subjects. The discordance of prolactin responses to DAMME and insulin-induced hypoglycaemia in the obese suggests that altered opioid systems are unlikely to account for the hypothalamic dysfunction present in obesity.
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PMID:The effect of enkephalin analogue on pituitary hormone release in human obesity. 310 84


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